bluuebunny/crossref_metadata_2025 huggingface dataset:
Degradation of phospholipid molecular species during experimental cerebral ischemia in rats.
Authors: Goto Y , Okamoto S , Yonekawa Y , Taki W , Kikuchi H , Handa H , Kito M
Published: June 2011

Previous investigators have shown that free fatty acids that accumulate during ischemia are an indicator of evolution in ischemic brain damage. Our study describes the temporal relations between free fatty acid accumulation and degradation of phospholipid molecular species after cerebral ischemia. Using the four-vessel occlusion model of adult Wistar rats, we analyzed quantitatively the cerebral phospholipid molecular species of diacyl phosphatidylcholine and diacyl phosphatidylethanolamine and released free fatty acids during ischemia. Total diacyl phosphatidylcholine molecular species decreased gradually but did not show any significant difference even at 60 minutes. By contrast, total diacyl phosphatidylethanolamine abruptly decreased after 5 minutes and continued to decrease significantly thereafter. Polyunsaturated molecular species showed a higher ratio of degradation than saturated and monounsaturated molecular species of either phosphatidylcholine or phosphatidylethanolamine. Total free fatty acid accumulated according to the time elapsed, and statistical significance was obtained after 10 minutes. Free arachidonic and docosahexaenoic acids were attributed to these significant accumulations at 10, 15, and 30 minutes. At 60 minutes, individual free fatty acids increased nonspecifically. Free fatty acids, which are hydrolyzed from phospholipid classes, are known to be further metabolized to bioactive substances such as prostaglandins and leukotrienes. Rapid degradation of phospholipid molecular species, especially of diacyl polyunsaturated molecular species, could be an important finding to membrane perturbation. Effective prevention of these changes might enhance tolerance to ischemic brain damage.
New model of cerebral thrombosis in dogs.
Authors: Hirschberg M , Hofferberth B
Published: June 2011

Experimental in situ thrombosis of the middle cerebral artery was produced in dogs by use of intravasally placed copper coils, which subsequently gave rise to an obstructing autologous thromboembolus. The resulting thrombosis was produced in the middle or rostral cerebral artery within 5-15 minutes after delivery of the thrombogenic device. The correlation of location of the coil in the intracranial vasculature of the internal carotid artery with the anatomic distribution of resulting cerebral infarcts suggests that this experimental model can produce a selective acute local occlusion of cerebral vessels in a high proportion of dogs without violating the cranium. The composition of the autologous thromboembolus, the low mortality rate, and the excellent reproducibility will make the correlative study of thrombolytic agents and their therapeutic efficacy possible.
Amnesia following thalamic hemorrhage. Another stroke syndrome.
Authors: Hankey G J , Stewart-Wynne E G
Published: June 2011

The clinical manifestations of thalamic hemorrhage frequently comprise hemiparesis, hemianesthesia, and oculomotor abnormalities. Since the advent of computed tomography, an amnestic syndrome following thalamic hemorrhage has been recognized, but the thalamic structures involved and the mechanism of amnesia have remained uncertain. We report a patient with sudden memory dysfunction following hemorrhage into the anterior nucleus of the left thalamus that was shown neuropathologically to disrupt the mamillothalamic fasciculus, one of the principal components of the limbic system. It is considered that the amnestic syndrome following thalamic (anterior nucleus) hemorrhage is due to interruption of the mamillothalamic fasciculus.
Ischemic cortical lesions after permanent occlusion of individual middle cerebral artery branches in rats.
Authors: Rubino G J , Young W
Published: June 2011

Our study describes the anatomy of the middle cerebral artery (MCA) in 65 Sprague-Dawley rats and the spatial distribution of ischemic cortical lesions caused by occluding major MCA branches. The rats characteristically had at least two major MCA branches, frontal and parietal. Many rats had additional branches supplying the pyriform and temporal cortexes. Permanent occlusion of the frontal or parietal branches combined with 30 minutes of bilateral carotid artery occlusion produced visible Evans blue dye uptake by ischemic cortical areas after 24 hours. No lesions distal to the occlusion were apparent in 38% and 43% of rats with frontal and parietal branch occlusions, respectively; small lesions contiguous with the occlusion site were observed in 38% and 32% of the rats. Only 6% of the frontal and 7% of the parietal branch occlusions produced isolated distal infarcts as expected if these branches were end-arteries. Blood flow was reversed in arteries distal to the occlusion. We conclude that extensive collateral connections of the frontal and parietal MCA branches with other arterial systems protect the anterior and posterior cortical regions. In contrast, occlusions of the pyriform branch of the MCA invariably caused infarcts in the frontopyriform region. In about one third of the rats, frontal or parietal branch occlusions produced lesions involving much of the proximal MCA territory; the frontopyriform region was most consistently affected. Combined, these data suggest that the pyriform MCA branch is an end-artery and that the cortical region it supplies is prone to ischemic damage resulting from any reduction of blood flow through the main MCA trunk.(ABSTRACT TRUNCATED AT 250 WORDS)
Metabolic alterations in rabbit cerebral arteries caused by subarachnoid hemorrhage.
Authors: Tsukahara T , Kassell N F , Hongo K , Lehman R M , Torner J C
Published: June 2011

The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.02 mumol/g wet wt in control rabbit basilar arteries (n = 6). The ATP content decreased significantly to 0.17 +/- 0.02 mumol/g wet wt 2 days after experimental subarachnoid hemorrhage (n = 6), although only a slight decrease was detected in the basilar arteries 2 days after cisternal injection of the same amount of artificial cerebrospinal fluid. Hypoxia significantly decreased ATP content in the control basilar arteries to 0.26 +/- 0.04 mumol/g wet wt (n = 6). The same degree of hypoxia did not decrease ATP content in the basilar arteries after subarachnoid hemorrhage. Release of L-lactate was significantly higher from the arteries after subarachnoid hemorrhage than from the control arteries under both aerobic and hypoxic conditions. Our results indicate that subarachnoid hemorrhage induced an alteration of metabolic rates in rabbit cerebral arteries. The oxygen-requiring pathways to synthesize ATP may be important in control cerebral arteries; however, after experimental subarachnoid hemorrhage, the main pathway in the cerebral arteries may shift from oxygen-requiring pathways to an anaerobic glycolytic pathway.
In vivo evidence that an adenylate cyclase-cAMP system dilates cerebral arterioles in mice.
Authors: Rosenblum W I
Published: June 2011

Pial arterioles of living mice anesthetized with urethane were monitored by television microscopy. I tested the existence of an adenylate cyclase-cyclic adenosine monophosphate (cAMP) system for dilating the arterioles by topically applying the following drugs: cAMP (10(-3) M), its more potent analogue dibutyryl cAMP (10(-3) and 10(-4) M), and forskolin (10(-6) M). Forskolin activates endogenous adenylate cyclase, which leads to increases in endogenous cAMP. Each drug was applied for 30 seconds; all three produced dilation. I then applied either cAMP or forskolin in the presence or absence of 10(-4) M isobutylmethylxanthine (IMX), an inhibitor of endogenous phosphodiesterase, which destroys cAMP. The presence of IMX significantly potentiated the dilation produced by exogenous cAMP and forskolin. These data indicate that cerebral surface arterioles of mice respond to cAMP with dilation and contain the enzymes for producing and inactivating this dilator. The existence of an adenylate cyclase-cAMP dilating mechanism in pial arterioles does not rule out the simultaneous existence of other dilating mechanisms.
Effects of aging and hypertension on endothelium-dependent vascular relaxation in rat carotid artery.
Authors: Hongo K , Nakagomi T , Kassell N F , Sasaki T , Lehman M , Vollmer D G , Tsukahara T , Ogawa H , Torner J
Published: June 2011

We evaluated the effects of aging and hypertension on endothelium-dependent relaxation of rat common carotid arteries using 14-week-old (young) and 11-month-old (old) Wistar-Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR). Isometric tension of common carotid artery ring segments was measured. With a resting tension of 2.0 g determined from the baseline tension-contraction curves, precontraction was induced by 10(-5) M 5-hydroxytryptamine and endothelium-dependent relaxation was measured by application of either acetylcholine or adenosine 5'-triphosphate (ATP). Mean arterial blood pressure was 73.1 +/- 3.0 mm Hg in WKY and 110.0 +/- 3.1 mm Hg in SHR. These baseline values were significantly different. Acetylcholine-induced maximal relaxations were 70.1 +/- 2.6% of the 5-hydroxytryptamine-induced contraction in young WKY, 45.6 +/- 2.1% in old WKY, 35.1 +/- 1.8% in young SHR, and 21.4 +/- 2.5% in old SHR. On the other hand, ATP-induced relaxations were 52.0 +/- 3.2%, 35.7 +/- 3.8%, 21.7 +/- 3.5%, and 17.0 +/- 1.8% in the groups, respectively. Acetylcholine-induced relaxations were significantly different between WKY and SHR, young and old, independently. On the other hand, ATP-induced relaxations were also significantly different between young and old WKY, although no significant difference was observed between young and old SHR. The fact that endothelium-dependent relaxation of a cephalic artery is impaired in old rats and in hypertensive rats suggests that aging and hypertension are risk factors that may augment the disturbance of the cerebral circulation in pathologic conditions.
Accumulation of intimal platelets in cerebral arteries following experimental subarachnoid hemorrhage in cats.
Authors: Haining J L , Clower B R , Honma Y , Smith R R
Published: June 2011

From 2 hours to 23 days following experimental subarachnoid hemorrhage, the accumulation of indium-111-labeled platelets on the intimal surface of the middle cerebral artery was studied in 23 cats. Subarachnoid hemorrhage was produced by transorbital rupture of the right middle cerebral artery. Of the 23 cats, 17 exhibited right middle cerebral artery/left middle cerebral artery radioactivity ratios of greater than 1.25. When these results were compared with those of 12 control cats, 0.001 less than p less than 0.005 (chi2 test). Thus, the results from the control and experimental groups are significantly different and indicate early (after 2 hours) preferential accumulation of intimal platelets in the ruptured right middle cerebral artery compared with the unruptured left middle cerebral artery and new platelet deposition continuing for up to 23 days. However, the experimental group did not reveal a clear pattern for platelet accumulation following subarachnoid hemorrhage. There was no simple correlation between the magnitude of the radioactivity ratios and the time after hemorrhage when the cats were killed although the ratios for 2 hours to 7 days seemed greater than those for 8 to 23 days. Assuming the pivotal role of platelets in the angiopathy of subarachnoid hemorrhage, the administration of antiplatelet agents as soon as possible following its occurrence may be of value.
Quantitative analysis of effects of kappa-opioid agonists on postischemic hippocampal CA1 neuronal necrosis in gerbils.
Authors: Hall E D , Pazara K E
Published: June 2011

The ability of the kappa-opioid receptor agonists U50488H and U62066E (spiradoline mesylate) compared with the non-kappa close structural analogue U54494A to affect postischemic necrosis of the selectively vulnerable hippocampal CA1 neurons was examined in male Mongolian gerbils. The gerbils were treated with either saline vehicle or 10 mg/kg i.p. of one of the test drugs 30 minutes before and again 2 hours after a 10-minute period of bilateral carotid artery occlusion or sham occlusion under light methoxyflurane anesthesia. Seven days after ischemia and reperfusion the brains were perfusion-fixed, and hippocampal CA1 cells were counted in a blind fashion. In ischemic gerbils that received only vehicle, there was a 78.9% loss of CA1 neurons compared with sham-occluded gerbils. In contrast, in U50488H-treated gerbils, mean cell loss was reduced to 33.9% (p less than 0.01 vs. vehicle-treated group). U62066E was even more effective in reducing postischemic CA1 degeneration to only 20.7% (p less than 0.0001 vs. vehicle-treated group). However, treatment with the non-kappa analogue U54494A did not cause any apparent protection; the gerbils in this group showed an 80.7% loss of CA1 neurons. Our results are consistent with the hypothesis that kappa-receptor stimulation is associated with improved postischemic neuronal preservation.
Effect of the ganglioside GM1 on neurologic function, electroencephalogram amplitude, and histology in chronic middle cerebral artery occlusion in cats.
Authors: Komatsumoto S , Greenberg J H , Hickey W F , Reivich M
Published: June 2011

The effect of the ganglioside GM1 on amplitude of the electroencephalogram, neurologic function, and histology has been studied in chronic middle cerebral artery occlusion in cats. Ischemia was produced by a 2-hour occlusion of the left middle cerebral artery and was followed by a 7-day observation period. GM1 was intravenously administered 30 minutes after occlusion and daily during the observation period. Using the reduction in the electroencephalogram amplitude to measure stroke severity, three cats with mild, three cats with moderate, and three cats with severe stroke were treated with 5 mg/kg GM1. Nine cats, three in each group, were treated with 30 mg/kg GM1, while nine cats, three in each group, received middle cerebral artery occlusion but no treatment. In all cats there was a precipitous fall in mean electroencephalogram amplitude during occlusion, followed by a secondary fall during the observation period. Treated cats showed better recovery of electroencephalogram amplitude during the first 4 hours of reperfusion and a smaller secondary fall than untreated cats. Treated cats, especially those treated with 5 mg/kg GM1, showed significant recovery of neurologic deficits compared with untreated cats. Histologic damage was less in treated cats than in untreated cats. Some cats treated with 30 mg/kg GM1 exhibited convulsions, whereas no untreated cat showed any seizure activity. Our findings suggest that gangliosides may improve the recovery of both neurologic deficits and morphologic damage in the central nervous system. These positive effects might be tentatively explained by stimulation of enzymatic activities such as Na+, K+-ATPase and adenyl cyclase.
Anticoagulant therapy in cerebrovascular disease: review and meta-analysis.
Authors: Jonas S
Published: June 2011

Sixteen acceptably randomized studies of anticoagulant therapy after cerebral or retinal ischemia or infarction are reviewed and the results among 1,046 anticoagulated patients and 1,071 controls are analyzed. The following conclusions are derived. 1) Anticoagulant therapy has not been shown to be better than control management after transient ischemia or nonprogressing ischemic stroke; this is true whether the control management was deliberately ineffectual treatment (generally studies completed in 1974 or earlier) or platelet antiaggregant therapy (pooled results of three recent studies). 2) Although a study done 30 years ago demonstrated no benefit, a recent study showed benefit from anticoagulant therapy in patients who had had cerebral emboli of cardiac origin; additional controlled data are needed. 3) There is evidence that patients with thrombosis in evolution might benefit from anticoagulant therapy; additional controlled data are needed.
Duplex scanner study of carotid artery dissection following surgical treatment of aortic dissection type A.
Authors: Zurbrügg H R , Leupi F , Schüpbach P , Althaus U
Published: June 2011

In patients suffering from aortic dissection, persistent perfusion of the false lumen distal to the implanted graft is frequent. Postoperative follow-up examinations of the carotid arteries of these patients were performed by duplex scanner and correlated with clinical symptoms. Thirty-nine patients who survived the surgical treatment of acute type A aortic dissection had duplex sonography of both common carotid arteries after an average postoperative follow-up of 53 months. In 21 cases a composite graft and in 18 cases a supracoronary prosthetic vascular graft were implanted. No sign of residual dissection of the common carotid arteries was seen in 23 patients; in nine there was a dissection of both common carotid arteries, and seven patients had a unilateral carotid dissection (five right, two left). There were nine symptomatic patients with the following symptoms: transient ischemic attack (four), amaurosis fugax (four), stroke with incomplete recovery (one). Two symptomatic patients had a corresponding dissection. The generally good prognosis of all these patients suggests a conservative nonoperative treatment.
Incidence of stroke in young adults in Florence, Italy.
Authors: Nencini P , Inzitari D , Baruffi M C , Fratiglioni L , Gagliardi R , Benvenuti L , Buccheri A M , Cecchi L , Passigli A , Rosselli A
Published: June 2011

A population-based study specifically addressing stroke in young adults (aged 15-44 years) was conducted in Florence, Italy, from 1983 to 1985. We identified 47 cases of first stroke by means of a daily check of the medical facilities of the city and nearby towns and a review of death certificates. Patients were assessed by a neurologist shortly after the onset of the stroke, and computed tomography or autopsy was performed in 96%. The average annual incidence rate for all stroke (cases per 100,000 population per year) was 9.0 (95% confidence interval 5.8-13.4) for males and 8.7 (95% confidence interval 5.5-13.0) for females. The average annual incidence rates for the pathologic types of stroke were 3.4 for cerebral infarction, 3.2 for subarachnoid hemorrhage, and 1.9 for intracerebral hemorrhage. The case-fatality ratio was 23.4% at 1 month. Among patients with ischemic strokes, atherosclerosis and cardiac disease accounted for 50% of the cases. Based on angiography or autopsy findings, aneurysm or arteriovenous malformation were demonstrated in 88% of the patients with subarachnoid hemorrhage. In 50% of the patients with intracerebral hemorrhage, no cause of bleeding was detected. Our study may supply information about stroke pathologic types in an unselected series of young adults.
Neuron-specific enolase is a marker of cerebral ischemia and infarct size in rat cerebrospinal fluid.
Authors: Hårdemark H G , Persson L , Bolander H G , Hillered L , Olsson Y , Påhlman S
Published: June 2011

Neuron-specific enolase concentrations were measured in samples of rat cerebrospinal fluid obtained repeatedly before and after occlusion of the middle cerebral artery. A method for reliable, repeated sampling of cisternal cerebrospinal fluid was developed for this purpose. Occlusion of the middle cerebral artery induced cerebral infarcts of slightly variable size with good correlation to raised neuron-specific enolase concentrations. Sham operation caused only superficial cortical damage at the site of surgery and was followed by an early, slight, and transient increase in neuron-specific enolase concentration. With our technique, the development of cerebral infarcts can be studied in individual rats under experimentally controlled conditions over an extended period of time. Analysis of neuron-specific enolase can be used in trials of drugs for mitigating the effect of ischemia. Information concerning the release of neuron-specific enolase from ischemic cerebral tissue to the cerebrospinal fluid is important because neuron-specific enolase in the cerebrospinal fluid can be determined in patients suffering from cerebrovascular insult.
Spontaneous internal carotid artery dissection presenting as hypoglossal nerve palsy.
Authors: Lieschke G J , Davis S , Tress B M , Ebeling P
Published: June 2011

A 42-year-old man presented with right temporal headache, dysarthria, and dysphagia. On examination, he had a right hypoglossal nerve palsy. The diagnosis of right internal carotid artery dissection was suggested by magnetic resonance imaging and confirmed by carotid angiography. A dynamic computed tomogram demonstrated enlargement of the carotid artery. In carotid dissection, the hypoglossal nerve may be compromised by local factors as it passes close to the carotid artery in the neck.
Cerebral Blood Flow Measurement as a Safeguard During Carotid Endarterectomy
Authors: BOYSEN GUDRUN
Published: June 2011

Intraoperative measurement of regional cerebral blood flow (rCBF) by the
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Xe intracarotid injection technique was performed in 17 patients operated on for stenosis of the internal carotid artery. Mean rCBF decreased from 51 ml/100 gm x minute before endarterectomy to 30 ml/100 gm x minute when the internal carotid artery was clamped, a reduction of 41%. Postoperative aggravation of neurological deficits was observed in five patients in whom rCBF was at or below 30 ml/100 gm x minute during the period of carotid clamping, indicating a critical lower limit of rCBF of this magnitude. Flow reduction below this limit was tolerated only if the occlusion time was short. A critical time/flow relation is suggested.

Distal internal carotid artery blood pressure during clamping (measured in eight cases) was poorly correlated to rCBF (r = 0.62, 0.1 > P > 0.05).
The Effect of Intra-arterial Papaverine on the Regional Cerebral Blood Flow in Patients with Stroke or Intracranial Tumor
Authors: OLESEN JES , PAULSON OLAF B.
Published: June 2011

The effect of intracarotid injection of 10 mg of papaverine on regional cerebral blood flow was measured in 27 patients. Most of the patients had cerebral infarction or intracranial neoplasm. The intra-arterial
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Xenon injection method was used and 16 or 35 regions of the diseased hemisphere were monitored. In patients without focal flow abnormalities an average flow increase of 93% followed the injection. In patients with focal abnormalities of cerebral blood flow the intra-arterial injection of papaverine produced a decrease in focal flow or less increase in flow than normal. It is concluded that vasodilator therapy presumably decreased flow in pathological tissue and that such treatment should not be employed in the therapy of cerebrovascular disease.
The Effect of Body Position and Forelimb Exercise on Cephalic Blood Flow
Authors: ANAZAWA WAKOU , SHIGENO KOJI , TOOLE JAMES F. , JANEWAY RICHARD
Published: June 2011

Flow through both common carotid, vertebral, and subclavian arteries was measured with "C-core" probes and square wave electromagnetic flowmeters in mongrel dogs. Exercise of the neurally isolated forelimb was simulated by electrical stimulation to obtain first clonic and then tetanic muscle contraction. Exercise was performed in the horizontal supine, 30° head-up, and 30° head-down positions. Bilateral forelimb exercise induced abrupt increase in subclavian artery flow and conductance. Cephalic arterial flow and conductance decreased at the onset of exercise and showed gradual recovery. Left subclavian artery flow and conductance decreased during right forelimb exercise. Right subclavian and brachiocephalic artery flow decreased during left forelimb exercise. Head-up position induced general decreases in cephalic blood flow in spite of increased mean arterial blood pressure. Response patterns of flow and conductance during bilateral exercise did not differ significantly from those in the horizontal supine position. Administration of gallamine triethiodide before stimulation eliminated all hemodynamic responses. Femoral artery flow and conductance decreased on the side contralateral to the side of the exercising limb.

The clinical implications of redistribution of blood are discussed.
Physiological Modification of Immediate Ischemia due to Experimental Middle Cerebral Occlusion-Its Relevance to Cerebral Infarction
Authors: HALSEY JAMES H. , CAPRA NORMAN F.
Published: June 2011

In cats subjected to middle cerebral artery occlusion, the resulting ischemia was unaffected by the blood pressure at the time of occlusion when arterial P

CO

CO
2

was normal or low. At normal and elevated blood pressures, hypercapnia established prior to occlusion minimized the ischemia and hypocapnia aggravated it. Re-occlusion during postischemic reactive hyperemia resulted in ischemia of the same severity as during the initial occlusion, provided P

CO

CO
2

and blood pressure were not changed. These observations suggest that a general determinant of the severity of immediate ischemia in this preparation is the competence of the collateral circulation.

This conclusion suggests that proper analysis of the pathogenesis of cerebral infarction requires consideration of immediate ischemia separately from the subsequent course of the ischemic lesion. There are so many variables bearing on the pathogenesis of cerebral infarction that a rational therapy of acute stroke can only be visualized when there is knowledge of the specific arterial lesion, frequent or continuous measurement of regional cerebral blood flow, regional metabolism or neuronal activity, intracranial pressure, and some way of distinguishing paralyzed but viable tissue from infarction.
The Treatment of Cerebral Ischemia with Hyperbaric Oxygen (OHP)
Authors: HART CDR. GEORGE B. , THOMPSON CDR. ROBERT E.
Published: June 2011

The treatment of a patient for three and one-half months, following occlusion of the right middle cerebral artery with the associated neurological sequelae, with hyperbaric oxygen combined with methyldopa and hydrochlorthazide is presented. Treatment scheduled was two and one-half atmospheres absolute. The treatment was interrupted after 15 treatments to rule out spontaneous remission for a period of 30 days, and no further improvement occurred until treatments were reinstituted. The dramatic return to a near normal state during treatment appears to indicate that he did benefit from therapy.
Contribution to the Hemodynamics of Arterial Venous Malformations
Authors: PROSENZ PIUS , HEISS WOLF-DIETER , KVICALA VLATISLAV , TSCHABITSCHER HELMUTH
Published: June 2011

In three cases of arteriovenous malformations (AVMs), and in one postoperative case, the passage of an I.V.-administered 99m-Technetium bolus through the brain and the
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Xenon clearance after intracarotid injection from different brain areas were observed, using a scintillation camera-1600 channel memorydigital magnetic tape unit. Regional cerebral blood flow values from contiguous areas down to 12 mm lateral lengths were calculated. In two cases computer-calculated cerebral blood flow maps are presented. Areas surrounding the AVMs revealed relatively high CBF values, while the blood flow in more distant parts of the hemisphere was decreased. Areas of low CBF values were detected also in the postoperative case with ligation of vessels. The initial part of the washout curves showed over all AVMs shunt peaks up to 88% of the initial activity. Shunt peaks detected also over most parts of the involved hemisphere are explained by arterio-arterial shunt connections. Their flow, centripetally directed to AVM, may cause the observed pattern of higher and lower flow values, indicating that the Xenon washout may be sensitive not only to capillary flow. Conclusions are drawn that the Xenon-clearance technique provides detection of the hemodynamic influence, but not of the shunt volume of AVMs.
Risk Factors in Stroke Due to Cerebral Infarction
Authors: KANNEL WILLIAM B. , BLAISDELL F. WILLIAM , GIFFORD RAY , HASS WILLIAM , McDOWELL FLETCHER , MEYER JOHN S. , MILLIKAN CLARK H. , RENTZ LEWIS E. , SELTSER RAYMOND
Published: June 2011

In 1968 the Council on Cerebrovascular Disease of the American Heart Association authorized the appointment of a subcommittee to produce a statement concerning "risk factors for Stroke." After working for over a year the Subcommittee reported that, because of inadequate data concerning "all or several of the factors," they had been unable to produce a statement satisfactory to each Subcommittee member. Some were reluctant to set down a policy statement until every loophole was plugged--a task made extraordinarily difficult by the complexity of Stroke and the fact that prospective studies of large population groups are necessary for the acquisition of some needed data. Another problem was that of interpreting the phrase risk factors. Does this phrase imply that eliminating or minimizing a "risk factor" (for example, maintaining successful control of hypertension) automatically reduces the risk of Stroke for that individual? This therapeutic consideration may await an answer for years, although it must be admitted that the term "risk factors for Stroke" does suggest that careful treatment of one or several risk factors can help to prevent Stroke. In any event, the Subcommittee was admonished by its chairman, Dr. William Kannel, to consider the task a never-ending one; that data are now available indicating that certain phenomena are more commonly followed by Stroke and that these phenomena (culprits) should be publicly identified as elements or risk factors for Stroke. The Subcommittee decided to work first with the profile of the candidate at risk of a cerebral infarction--and so state. The Subcommittee realistically writes: "Any statement arrived at will be subject to periodic revision as more information is accumulated!" Obviously, new data may make changes necessary! Under Dr. Kannel's talented and dedicated leadership the Subcommittee produced the statement which follows.
Neurogenic Control of Cerebral Circulation
Authors: ROSENBLUM WILLIAM I.
Published: June 2011

A review of recent literature provides evidence that cerebral vessels are innervated with myelinated and nonmyelinated nerves. Among the latter, adrenergic nerves are readily demonstrated. Stimulation of cervical sympathetics produces a reduction in cerebral blood flow attributable to constriction of vessels in the neck and on the cerebral surface. In vitro experiments indicate that cerebral vessels possess a mechanism responsive to sympathomimetic agents. Evidence indicates that neurogenic influences can alter cerebrovascular diameter without necessarily playing a role in maintaining resting tone. Data are also available which suggest that neurogenic influences may modulate the response of cerebral vessels to other more potent stimuli. Cerebral vessels are less sensitive and less responsive to neurogenic influences than are vessels elsewhere. However, available data suggest that this characteristic of the cerebral vasculature reflects specialization of vascular muscle or of perivascular nerves, rather than a vestigial basis for the existence of these nerves.
Effects of Acetazolamide on Cerebral Ischemia and Infarction After Experimental Occlusion of Middle Cerebral Artery
Authors: REGLI FRANCO , YAMAGUCHI TAKENORI , WALTZ ARTHUR G.
Published: June 2011

Acetazolamide was given to five of ten cats for 48 to 54 hours after extradural occlusion of a middle cerebral artery (MCA). At seven to eight days later, measurements of regional cerebral blood flow (CBF) and estimates of the sizes of the ischemic and infarcted areas of the brains were made. Neurological deficits were more severe and the ischemic and infarcted regions were larger in the cats given acetazolamide. Cerebral edema (brain swelling) was present and reactive hyperemia was common in the treated cats, even one week after MCA occlusion. The hypercapnia and decreases of pH of nonischemic brain tissue that are caused by acetazolamide are harmful for ischemic brain tissue, presumably because of vasodilatation in nonischemic brain tissue with resultant increases of intracranial pressure and decreases of CBF of ischemic regions.
Cerebral Spinal Fluid Lactic Acid Following Circulatory Arrest
Authors: PAULSON G. W. , LOCKE GEORGE E. , YASHON DAVID
Published: June 2011

CSF lactic acid rises quickly and then gradually declines toward normal after severe cerebral ischemia in the dog. In animals in whom recovery can be postulated, the increase in lactic acid would appear to be transitory, and more severe insults produce higher levels. The increase in blood levels of lactic acid occurs more rapidly than that in the CSF, and the blood level returns to normal sooner than the CSF.
Electrodiagnostic Study of Brainstem Strokes
Authors: KIMURA JUN
Published: June 2011

The orbicularis oculi reflex elicited by electrical stimulation of the supraorbital nerve was studied in 39 cases with vascular lesions of the brainstem (four mesencephalic, 14 pontine, 13 medullary and eight multilevel), six cases following severe anoxic episodes and two cases of traumatic brainstem lesions. The early reflex (normal latency: 10.6 ± 2.5 msec) was delayed in 20 out of 22 cases with pontine or multilevel brainstem strokes and in all the eight cases of anoxic or traumatic brainstem lesions. The direct (31 ± 10 msec) and consensual (32 ± 11 msec) late reflexes, analogously to the pupillary light reflex, were useful in distinguishing afferent, efferent, and other blocks. In all the seven comatose patients, the late reflex was virtually absent. However, a relatively normal early reflex was present in four of these. The findings of this study indicate that the brainstem conduction altered by vascular and anoxic lesions can be measured simply and objectively by the orbicularis oculi reflex. A delay of the early reflex is relatively specific to pontine lesions. The late reflex is not only altered by brainstem lesions but is also totally depressed in coma, presumably reflecting diffuse suppression in multisynaptic reticular system.
Effect of subarachnoid hemorrhage on calcitonin gene-related peptide-induced relaxation in rabbit basilar artery.
Authors: Hongo K , Tsukahara T , Kassell N F , Ogawa H
Published: June 2011

An isometric tension measurement of ring segments was performed in the rabbit basilar and common carotid arteries in vitro to investigate the regional differences in the calcitonin gene-related peptide (CGRP)-induced vasodilation and the effect of subarachnoid hemorrhage on CGRP-induced vasodilation. CGRP elicited vasodilation of the rabbit basilar artery in a dose-dependent fashion when the artery was precontracted by 10(-5) M 5-hydroxytryptamine, whereas almost no relaxation occurred in the rabbit common carotid artery. The relaxation of the basilar artery was 64.03 +/- 1.85% at 3 x 10(-8) M CGRP, with an EC50 of 8.46 +/- 0.08. Two days after experimental subarachnoid hemorrhage, CGRP-induced relaxation of the rabbit basilar artery was 53.96 +/- 8.08% of the 10(-5) M 5-hydroxytryptamine-induced contraction, not significantly different from that of the basilar artery of the control rabbit. Our findings suggest that CGRP induces potent vasodilation in the rabbit basilar artery and that no impairment of vasodilation occurred after experimental subarachnoid hemorrhage. We speculate that CGRP may have therapeutic potential in cerebrovascular disease such as vasospasm after subarachnoid hemorrhage.
Model of electrocardiographic changes seen with subarachnoid hemorrhage in rabbits.
Authors: Uchida M , Saito K , Niitsu T , Okuda H
Published: June 2011

We developed a new method for introducing drugs into the basal cistern of rabbits. With minimal surgical invasion, we used either the opening of the craniopharyngeal duct to access the chiasmatic cistern or the suture between the basisphenoid and basioccipital bones to access the interpeduncular cistern. With our method, 0.5 ml contrast medium injected into three rabbits was determined roentgenographically to remain in the basal cistern; histologically, all the brain tissue remained intact. Intracisternal injection of 0.5 ml physiological saline into five rabbits had no effect on the cardiovascular system. In 23 rabbits, injection of 0.5 ml 0.1% prostaglandin F2 alpha led to a variety of electrocardiographic changes, including sinus bradycardia (in 43.5%), premature atrial contractions (in 17.4%), and premature ventricular contractions (in 39.1%). In 15 rabbits with severe changes, arrhythmia was followed by ST depression (in 30.4%), ST elevation (in 8.7%), T wave inversion (in 4.3%), ventricular tachycardia (in 17.4%), or ventricular fibrillation (in 4.3%). Intracisternal injection of 0.5 ml 1.0% lidocaine into the 23 rabbits was very effective in overcoming bradycardia and arrhythmias. We conclude that the clinical features of electrocardiographic changes seen in patients with subarachnoid hemorrhage are reproducible in this rabbit model.
Rat striatal cation shifts reflecting hypoxic-ischemic damage can be predicted by on-line impedance measurements.
Authors: de Boer J , Klein H C , Postema F , Go K G , Korf J
Published: June 2011

We investigated the earliest time at which irreversible damage takes place after hypoxia-ischemia in the Levine preparation of rats. In 60 rats anesthetized with chloral hydrate and maintained at one of three body temperatures, we unilaterally ligated the left common carotid artery and placed electrodes in the striatum to measure impedance (reflecting the extracellular space) during hypoxia, recovery, and/or cardiac arrest. We measured blood gases and pH at regular intervals during hypoxia in 47 rats and assessed blood-brain barrier function with Evans blue and tissue damage using Na+:K+ ratios. Shortly after hypoxia, impedance normalized in 24 rats without brain damage (normal Na+:K+ ratios, 4 hours of recovery). Sustained elevation of striatal impedance during recovery in six rats was related to an elevated Na+:K+ ratio and a disrupted blood-brain barrier. Damage was not obviously related to blood gases, pH, or the net reduction of the extracellular space during hypoxia. Hypothermia in 17 rats prevented impedance changes, and no striatal damage was found. Thus, irreversible brain damage very likely occurs during or very shortly after hypoxia. Persistent reduction of the extracellular space indicates tissue damage and can be used to monitor potential in vivo therapeutic measures.
Corticofugal axonal degeneration in rats after middle cerebral artery occlusion.
Authors: Iizuka H , Sakatani K , Young W
Published: June 2011

We used the Fink-Heimer method to study degenerating corticofugal axons after unilateral middle cerebral artery occlusion in 14 adult male Long-Evans hooded rats. Axonal degeneration in the pyramidal tracts was prominent at 1-3 weeks, manifesting in well-defined silver-impregnated axonal bundles coursing from the internal capsule to the pyramids and crossing completely to the contralateral spinal cord. In half of eight rats examined at 1-3 weeks, the cortical infarct included the forelimb region of the sensorimotor cortex, and degenerating corticospinal axons could be traced to the lower cervical segments; in rats with involvement of the hindlimb cortical area as well, axonal degeneration extended to the lumbosacral segments. Terminal degeneration products were present in the forebrain, midbrain, and brainstem within 2 days after arterial occlusion; the number of degenerating terminals peaked at 7 days and decreased gradually thereafter up to 6 weeks. Dense terminal degeneration was observed in the trigeminal nuclear complex of all seven rats studied at 2 and 7 days. In these seven rats, five had small cortical infarcts, and silver-impregnated terminals were observed in the lateral reticular formation; in two rats with large cortical lesions, terminal degeneration was prominent in the medial reticular formation as well. We conclude that infarcts produced by middle cerebral artery occlusion cause axonal degeneration in the brainstem and spinal cord. The Fink-Heimer method may be useful for evaluating the rat middle cerebral artery occlusion model.
Cardioembolic stroke in primary oxalosis with cardiac involvement.
Authors: Di Pasquale G , Ribani M , Andreoli A , Zampa G A , Pinelli G
Published: June 2011

Primary oxalosis is a rare disorder of oxalate metabolism, characterized by nephrocalcinosis, nephrolithiasis, and extrarenal deposition of calcium oxalate in several tissues, including the heart. We report the case of a 34-year-old man with sudden right hemiparesis and aphasia from the occlusion of the left middle cerebral artery. Clinical features and the results of laboratory investigations led to the diagnosis of primary oxalosis. Two-dimensional echocardiography disclosed the presence of massive intracardiac calcifications compatible with deposition of calcium oxalate. The absence of other causes of stroke strengthened a cause-and-effect relation between cardiac oxalosis and cerebral infarction. Consequently, cardiac oxalosis should be considered among possible occult cardiac sources of cerebral embolism.
Serum cholesterol and hemorrhagic stroke in the Honolulu Heart Program.
Authors: Yano K , Reed D M , MacLean C J
Published: June 2011

During an average 18 years of follow-up for 7,850 Japanese-American men in Hawaii who were free of stroke at entry, 116 developed hemorrhagic stroke (subarachnoid hemorrhage or intracerebral hemorrhage). There was a significant (p = 0.001) inverse association between serum cholesterol and the risk of intracerebral hemorrhage but not of subarachnoid hemorrhage. This inverse association was nonlinear, with a higher incidence rate only for men with serum cholesterol in the lowest quintile (less than 189 mg/dl). The relative risk (lowest quintile/other four quintiles) was 2.55 (95% confidence interval 1.58-4.12) after controlling for age, blood pressure, serum uric acid, cigarette smoking, and alcohol consumption. There was no evidence for an interaction between blood pressure and serum cholesterol, although the inverse association was stronger for normotensive than for hypertensive men. Public health implications would differ in different countries depending on the relative frequency of intracerebral hemorrhage and on the distribution of serum cholesterol levels in the population.
Arterial disease risk factors and angiographic evidence of atheroma of the carotid artery.
Authors: Schneidau A , Harrison M J , Hurst C , Wilkes H C , Meade T W
Published: June 2011

We conducted a prospective study of serial intravenous digital subtraction angiography to determine the relation of arterial disease risk factors and hemostatic variables with the presence of visible atheroma at the carotid bifurcation. Of the 492 patients with cerebrovascular disease or ischemic heart disease who entered the study, 354 had hematologic studies, including platelet aggregation in 230. Abnormal angiograms were associated with greater age, treated hypertension, current smoking, and lower hemoglobin levels but with higher uric acid, factor VIII, and fibrinogen concentrations. In patients presenting with isolated transient ischemic attacks, abnormal angiograms were also associated with higher levels of cholesterol and triglycerides. To study atheroma progression, the 230 patients with complete data at entry were recalled 2 years later. Repeat angiography in 209 patients showed progression of visible bifurcation disease in 13.4%. There was some evidence that progression was linked to higher age, hypertension, and more severe disease at entry, but further analysis was hampered by the small number of patients showing increased plaque size. The possible role of risk factors and hemostatic variables, especially fibrinogen, is discussed. Factors that did not correlate with progression of angiographically visible disease may also influence clinical end points by other mechanisms, such as thrombogenesis.
A radiologic study of dynamic processes in lacunar dementia.
Authors: Tanaka Y , Tanaka O , Mizuno Y , Yoshida M
Published: June 2011

Using magnetic resonance imaging and digitized brain computed tomography, we evaluated 33 elderly patients with documented lacunar stroke and divided them into three groups (nondemented, n = 15; borderline, n = 9; and demented, n = 9) by neuropsychological assessments and DSM III criteria. We evaluated the extent of white matter lesions and the degree of atrophy of specific anatomic structures, such as the corpus callosum, using magnetic resonance imaging and quantified the volumes of the ventricles, the subarachnoid spaces, and the brain parenchyma using digitized brain computed tomography. Our results show that both borderline and demented patients had significantly more extensive white matter lesions than nondemented patients, indicating a significant relation between the extent of white matter lesions and intellectual decline. In addition, borderline and demented patients had significantly larger ventricles and more brain atrophy than nondemented patients; demented patients also had significantly larger subarachnoid spaces than nondemented patients and more brain atrophy than borderline patients. Our findings suggest that in most patients with lacunar stroke, periventricular and subcortical white matter lesions with subsequent white matter atrophy first induce ventricular enlargement, followed by generalized brain atrophy, resulting in dementia.
Effects of middle cerebral artery occlusion on cerebral cortex choline and acetylcholine in rats.
Authors: Scremin O U , Jenden D J
Published: June 2011

We measured regional cerebral blood flow and acetylcholine and choline concentrations in tissue fragments of normally perfused and ischemic cortical regions from 10 rats. Tissue uptake of [14C]iodoantipyrine was used to indicate regional cerebral blood flow, and gas chromatography-mass spectrometry was used to measure acetylcholine and choline concentrations. Cerebral cortical ischemia was induced by permanent occlusion of the middle cerebral artery, and variables were measured 2.5 or 24 hours later. A close correlation was found between tissue choline concentration and the reciprocal of regional cerebral blood flow. A large increase in tissue choline concentration was observed in the ischemic cortex. Choline production rate was estimated by plotting choline concentration against the reciprocal of regional cerebral blood flow. This rate was independent of choline concentration. Acetylcholine concentration, on the other hand, was constant in ischemic and normally perfused regions, except in the center of the ischemic region 2.5 hours after middle cerebral artery occlusion, where a significant decrease was observed.
Endothelin acts in feline and canine cerebral arteries from the adventitial side.
Authors: Mima T , Yanagisawa M , Shigeno T , Saito A , Goto K , Takakura K , Masaki T
Published: June 2011

We investigated the in vivo vasoconstrictor effect of endothelin, a recently characterized vasoconstrictor peptide from vascular endothelium, in the basilar arteries of five cats and five dogs. Basilar artery caliber was angiographically measured under anesthesia before (control) and after either vertebral artery infusion or cisternal injection of the peptide. In cats, 5-500 pmol endothelin induced a dose-dependent basilar artery contraction in vivo when injected intracisternally; within 3 minutes after injection of 500 pmol endothelin, basilar artery caliber was decreased by 73 +/- 4% compared with control diameter before injection. The vasoconstriction was extremely long-lasting; no significant recovery of basilar artery caliber was observed for up to 2 hours after injection. In contrast, infusion of up to 3,000 pmol endothelin into the vertebral artery had no appreciable effect on basilar artery caliber. Similar results were obtained in dogs; vasoconstriction was maintained for as long as 12 hours. Our observations suggest that endothelin acts in cerebral vessels from the adventitial side, not from the luminal side, possibly due to the presence of the blood-arterial wall barrier. The long-lasting nature of endothelin-induced constriction of the cerebral arteries in vivo suggests that the peptide might be involved in the pathogenesis of cerebral vasospasm.