bluuebunny/crossref_metadata_2025 huggingface dataset:
Progress in cerebrovascular disease: local cerebral blood flow by xenon enhanced CT.
Authors: Gur D , Wolfson S K , Yonas H , Good W F , Shabason L , Latchaw R E , Miller D M , Cook E E
Published: June 2011

A noninvasive technique for measuring local cerebral blood flow (LCBF) by xenon enhanced x-ray transmission computed tomography (CT) has been developed an reported quite extensively in recent years. In this method, nonradioactive xenon gas in inhaled and the temporal changes in radiographic enhancement produced by the inhalation are measured by sequential computed tomography. Time dependent xenon concentrations within various tissue segments in the brain are used to derive both local partition coefficient (lambda) and LCBF. An assessment of this method reveals that although it provides functional mapping of blood flow with excellent anatomic specificity, there are distinct limitations. The assumptions underlying this methodology are examined and problems associated with various potential applications of this technique are discussed.
High dose barbiturates in non-traumatic brain swelling: ICP reduction and effect on outcome.
Authors: Woodcock J , Ropper A H , Kennedy S K
Published: June 2011

High dose barbiturates were used to treat intracranial hypertension in 15 patients with nontraumatic brain lesions; (3 hypertensive hemorrhage, 4 subarachnoid hemorrhage, 5 infarction, 2 global anoxia-ischemia and 2 encephalitis). All had persistently raised intracranial pressure (ICP) while being treated with aggressive conventional therapy. The addition of barbiturates caused an initial lowering of ICP in 11 patients, but only 5 of these had sustained ICP reductions. Survival of the 5 patients with persistently lowered ICP and death of the remaining 10 may indicate an improvement in outcome attributable to the addition of high dose barbiturates to conventional therapy in non-traumatic brain swelling. Because of the resources required for their prolonged use, randomized studied in patients with intracranial hypertension are required to determine the effect of barbiturates on outcome.
Mechanisms of cerebral protection by pentobarbital and nizofenone correlated with the course of local cerebral blood flow changes.
Authors: Ochiai C , Asano T , Takakura K , Fukuda T , Horizoe H , Morimoto Y
Published: June 2011

The effects of delayed administration of pentobarbital and a novel imidazole derivative (Nizofenone or Y-9179) on the infarction size following the regional cerebral ischemia were studied using the permanent middle cerebral artery (MCA) occlusion model in cats. The courses of local cerebral blood flow (lCBF) before and after drug administration were also studied using the hydrogen clearance method. The extent of infarction one week after MCA occlusion was significantly smaller in the drug-treated groups than in the control group. Regarding the time-course of lCBF, there was no significant differences between the control and the Y-9179 groups. On the other hand, pentobarbital administration caused a significant lCBF increase in low-flow areas where the lCBF following MCA occlusion was below 40 ml/100g/min. In spite of this flow increase, the corresponding cortical areas underwent infarction. Histological examination of the state of vasogenic edema revealed that the perivascular exudation of plasma fluid in the infarcted area was definitely less in the Y-9179 treated group than in the other groups. Results indicate that redistribution of lCBF may not be involved in the mechanism of cerebral protection by pentobarbital or Y-9179.
Accuracy of death certification of stroke: the Framingham Study.
Authors: Corwin L E , Wolf P A , Kannel W B , McNamara P M
Published: June 2011

The validity of death certification of stroke was studied in the general population cohort at Framingham, MA. During the last 30 years, 5106 people aged 30 to 62 and free of CHD and stroke at entry have been followed for the development of cardiovascular disease including stroke. Of the 280 decedents with certified stroke 113 (40% false negative rate) had no mention of stroke on the death certificate. THe false negative rate increased significantly with increasing age at death and increasing interval from last stroke to death. Among the 216 certificates listing stroke there were 46 false positives (21%). Analysis by type of stroke disclosed marked over-reporting of cerebral hemorrhage and under-reporting of cerebral embolus. This comparison of prospectively collected data to death certificates should raise questions about the accuracy of studies dependent on ths source of information.
Intracranial internal carotid artery stenosis.
Authors: Craig D R , Meguro K , Watridge C , Robertson J T , Barnett H J , Fox A J
Published: June 2011

The advent of EC/IC Bypass surgery has focused attention on selected patients who might benefit from this innovative procedure. There is a poverty of natural history data pertaining to all such lesions. Two centres (Memphis, Tennessee and London, Ontario) pooled their resources to carry out a retrospective review of 58 patients with angiographically-proven intracranial internal carotid artery stenosis. Only 33% of the patients were alive and free from subsequent cerebral vascular events at the end of the mean follow-up of 30 months. Forty-three percent of the patients died during follow-up: 36% due to stroke and 44% because of cardiac disease. Forty-three percent of the patients suffered cerebral vascular events during the follow-up period: there were 17 strokes (29%) including 9 fatal strokes. The incidence of ipsilateral stroke was 19%; 65% of the strokes were appropriate to the stenotic intracranial carotid lesion under study. The annual ipsilateral stroke rate for patients with this lesion was 7.6% per year. This lesion detected on angiography is indicative of severe atheroma, and carries a serious risk of death due to ischemic heart disease or stroke.
The effect of intravenous dipyridamole on the cerebral and systemic circulations of the dog.
Authors: Boarini D J , Kassell N F , Olin J J , Sprowell J A
Published: June 2011

In 7 dogs anesthetized with halothane and nitrous oxide, dipyridamole was administered in a loading dose of 1 mg/kg supplemented with 0.5 mg/kg every 30 minutes. Cardiovascular parameters and organ blood flows (using the radioactive microsphere technique) were measured before and at 30 minute intervals after each administration of dipyridamole, for a total of 105 minutes. The administration of dipyridamole was associated with a 20% reduction in systemic arterial pressure, a 31% reduction in peripheral vascular resistance, and a 13% increase in cardiac index. Cerebrovascular resistance decreased 21%, but regional cerebral blood flow and metabolism were unchanged. Blood flow to the heart increased 355% in the right ventricle and 213% in the left ventricle. Blood flow to the jejunum decreased 52% while blood flow to the kidney and liver decreased slightly. The circulatory effects of dipyridamole are probably related to its interference with the inactivation of endogenous adenosine. The differential effects of dipyridamole on organ flow are similar to those seen following the IV infusion of adenosine.
Cerebral ischemia produced by four-vessel occlusion in the rat: a quantitative evaluation of cerebral blood flow.
Authors: Furlow T W
Published: June 2011

Cerebral ischemia was produced in the rat by simultaneous occlusion of the vertebral and carotid arteries according to the method of Pulsinelli and Brierley (Stroke 10: 267, 1979). Local cerebral blood flow (CBF) was determined by polarographic and autoradiographic techniques. Hydrogen-clearance measurements showed that mean CBF fell in four monitored regions of the hemispheres to between 0.11 and 0.18 ml/g/min, being least in deep rostal gray, intermediate in superficial gray, and greatest in deep caudal gray. However, individual animals had local CBF in excess of 0.20 and even 0.30 ml/g/min, and no animal showed zero CBF. When animals were rendered hypotensive (MABP of 50 Torr) during vascular occlusion, mean CBF ranged between 0.03 and 0.10 ml/g/min in the same regional order. With hypotension, total arrest of flow occurred. Autoradiographic data confirmed the above findings and indicated adequate CBF to the lower brainstem. During vascular occlusion, sufficient CBF may be present ot sustain cerebral tissue as in animals with a well developed spinal circulation or an inadvertently patent vertebral artery.
Flow and neuronal density in tissue surrounding chronic infarction.
Authors: Mies G , Auer L M , Ebhardt G , Traupe H , Heiss W D
Published: June 2011

In 6 cats, cerebral infarction was produced by transorbital occlusion of the left middle cerebral artery (MCA). Five animals developed typical cortical infarcts. Eight weeks later, cerebral blood flow (CBF) was determined by 14C-iodoantipyrine autoradiography and the number of intact neurons was counted histologically. Two non-operated cats served as controls. Cortical blood flow in the infarcted hemisphere was reduced by 24.6-74.4% when compared to the flow in the contralateral cortex and in controls. Averaged white matter flow was decreased by 39.1%. Regional cortical flow was gradually reduced from parasagittal regions towards the infarct. In the surrounding of the infarct, cortical perfusion was decreased to 24.8 +/- 9.7 ml/100 g/min, i.e. 19.7% of contralateral flow. Although the infarcts were sharply demarcated macroscopically, the number of cortical neurons decreased gradually from the midline to the peri-infarct zone. A significant linear correlation was found between absolute CBF-values and the number of neurons in areas of the infarcted hemisphere. The homolateral gyrus lateralis had normal neuronal density but flow was reduced by 20%. These findings suggest that the blood flow reduction in tissue surrounding chronic infarcts is due to neuronal cell loss and to functional inactivation caused by damage of afferent fibers.
Electron microscopic studies of ruptured arteries in hypertensive intracerebral hemorrhage.
Authors: Takebayashi S , Kaneko M
Published: June 2011

Eleven freshly removed brains and 20 lenticulostriate arteries (collected at emergency surgery for intracerebral hemorrhage) were examined by electron microscopy in a search for the mechanism of arterial rupture in hypertensive intracerebral hemorrhage. Forty-six of 48 ruptured arteries examined showed severe arteriosclerosis including degenerative changes of the media at or near bifurcations. Atrophy and fragmentation of smooth muscle cells gave them a moth-eaten appearance. Material resembling basement membrane and cell debris was also present in the arterial walls. The above findings were restricted to the middle and distal portions of the perforating arteries. Rupture from a miliary aneurysm was observed in only 2 of the 48 specimens examined. These resembled saccular aneurysms, ultrastructurally. They seemingly formed at a cavity which we strongly felt may have been formed by complete or incomplete subclinical hemorrhages; reabsorption of the hemorrhage from the dissection resulted in the aneurysms seen. Degeneration of smooth muscle cells may be the result of prolonged tension or spasm of the arterial wall as a result of longstanding hypertension.
Evaluation of the risk of immediate anticoagulant treatment in patients with embolic stroke of cardiac origin.
Authors: Lodder J , van der Lugt P J
Published: June 2011

We evaluated immediate anticoagulation of embolic stroke. Of 39 patients suffering a focal cerebral ischemia caused by a cardiac embolus, 38 were submitted to CT within 24 hours after onset. Twenty-one patients received direct full anticoagulation and, in 10 patients, treatment was delayed because of hemorrhagic infarction on initial CT (3 cases), cardiac cause 24 hours or more after stroke onset, or treatment delay without specific reason (6 cases). Eight patients with severe deficit were not anticoagulated because of hemorrhagic signs on initial CT, impaired consciousness, or general contra-indications to such treatment. Twenty-one follow-up CT-scans were performed under full anti-coagulation, and in only 2 cases hemorrhagic infarction was noticed without clinical deterioration. No clinical worsening attributable to anticoagulant treatment was observed during the three week observation period. It is concluded that direct anticoagulation therapy does neither induce hemorrhagic infarction nor cerebral hemorrhage in patients with embolic stroke nor does it cause clinical deterioration.
Delayed TIAs distal to bilateral occlusion of carotid arteries -- evidence for embolic and hemodynamic mechanisms.
Authors: Bogousslavsky J , Regli F
Published: June 2011

We studied 4 patients with bilateral carotid artery occlusion who suffered delayed TIAs in one of the occluded internal carotid or common carotid areas. Hemodynamic mechanisms were prominent in two patients, in head turning and orthostatic hypotension. In the other two cases, embolic phenomena through the homolateral external carotid collateral pathways were probable, because this artery (or the common carotid artery) showed atheromatous stenosis and major collateral supply to the brain and retina. Different mechanisms may be responsible for further ischemia after bilateral occlusion of carotid arteries.
Proton NMR imaging in experimental ischemic infarction.
Authors: Buonanno F S , Pykett I L , Brady T J , Vielma J , Burt C T , Goldman M R , Hinshaw W S , Pohost G M , Kistler J P
Published: June 2011

Proton nuclear magnetic resonance (NMR) images depict the distribution and concentration of mobile protons modified by the relaxation times T1 and T2. Using the steady-state-free-precession (SSFP) technique, serial coronal images were obtained sequentially over time in laboratory animals with experimental ischemic infarction. Image changes were evident as early as 2 hours after carotid artery ligation, and corresponded to areas of ischemic infarction noted pathologically. Resulting SSFP images in experimental stroke are contrasted to inversion-recovery NMR images in an illustrative patient with established cerebral infarction. Bulk T1 and T2 measurements were made in vitro in three groups of gerbils: normal, those with clinical evidence of infarction, and those clinically normal after carotid ligature. Infarcted hemispheres had significantly prolonged T1 and T2 (1.47 +/- .12 sec, 76.0 +/- 9.0 msec, respectively) when compared to the contralateral hemisphere (T1 = 1.28 +/- .05 sec, T2 = 58.7 +/- 3.9 msec) or to the other two groups. These data suggest that changes in NMR parameters occur and can be detected by NMR imaging as early as two hours after carotid artery ligation.
Pathophysiology of ischemic cell death: I. Time of onset of irreversible damage; importance of the different components of the ischemic insult.
Authors: Ames A , Nesbett F B
Published: June 2011

Rabbit retina was used as an example of organized central nervous tissue in in vitro experiments designed to characterize the onset of cell death from ischemia. Retinas were subjected to progressively longer periods of different types of ischemic insult and then given an opportunity to recover before being tested for irreversible damage, using failure to reinstitute protein synthesis as the principal criterion. Anoxia was more damaging than substrate deprivation, but they were synergistic in combination. Restricting the volume of extracellular fluid during the combined deprivation, to simulate complete circulatory arrest in vivo, caused irreversible damage to occur even sooner. The cells were able to recover from 20 min of the complete ischemia, but it took them more than 2 h to do so. After 30 min, there was extensive irreversible damage. Loss of viability was usually associated with failure to reinstitute energy metabolism, as assessed by 2-deoxyglucose uptake. Under some circumstances loss of viability may have been the consequence of the failed energy metabolism. Increasing medium Mg++, prior to ischemia, to levels that greatly reduce energy requirements caused a significant improvement in the recovery of 2-deoxyglucose uptake.
Pathophysiology of ischemic cell death: III. Role of extracellular factors.
Authors: Ames A , Nesbett F B
Published: June 2011

The purpose of this study was to determine the effect on cell survival of extracellular changes that occur during ischemia, over and above the depletion of O2 and substrate. Rabbit retinas were deprived in vitro of both O2 and substrate, and then returned to control medium for 4 h before recovery was assessed by measuring protein synthesis, glucose utilization, and tissue water. Experimental conditions were altered in various ways during the period of O2 and substrate deprivation in order to modify the changes taking place in the interstitial fluid as a result of the failure of energy metabolism. When O2-free, substrate-free extracellular electrolyte solution was added to the retinas to reduce the ischemia-induced changes in the interstitial fluid, there was marked reduction in irreversible damage. But when energy-deprived retinas were exposed to retinas that had already been ischemic, or to interstitial fluid from ischemic retinas, there was an increase in irreversible damage. Removing Ca++ from the extracellular fluid during the period of energy deprivation increased the damage due to short deprivations in a restricted volume of extracellular fluid, but reduced the damage from longer deprivations in a large volume of extracellular fluid. The results demonstrate that several changes occur in the extracellular fluid during ischemia that significantly affect recovery.
Blood flow and vascular reactivity in collaterally perfused brain tissue. Evidence of an ischemic penumbra in patients with acute stroke.
Authors: Olsen T S , Larsen B , Herning M , Skriver E B , Lassen N A
Published: June 2011

In a group of 48 patients with completed stroke, 8 patients had viable collaterally perfused brain tissue which was accessible for rCBF recordings with a two dimensional technique. All 8 had deep subcortical infarcts on CT-scan, and angiographic occlusion of the arteries normally supplying the infarcted territory. The brain tissue overlying the deep infarcts appeared normal on CT-scan and was supplied by collateral circulation. rCBF was measured in all within 72 hours after the stroke. The intra-carotid Xe-133 injection method and a 254 multidetector camera were used to study rCBF. Relatively ischemic low flow areas were a constant finding in the collaterally perfused tissue. In 6 of the patients, the collaterally perfused part of the brain had low flow values comparable to those of an "ischemic penumbra" (viable, but functionally depressed brain tissue due to inadequate perfusion). Autoregulation was impaired in all of the collaterally perfused areas while the CO2-response always was preserved. Steal phenomena were not seen. In the surrounding brain tissue, autoregulation was normal in 5 patients and impaired in 3 while the CO2-response seemed to be normal. The results confirm the experimental finding of an ischemic penumbra associated with acute cerebral infarcts and suggest that early restoration of the blood flow in acute stroke patients might improve recovery and prognosis in selected patients.
Mechanisms of the contractile effect induced by uridine 5-triphosphate in canine cerebral arteries.
Authors: Shirasawa Y , White R P , Robertson J T
Published: June 2011

This study was performed to elucidate mechanisms responsible for the contraction of isolated canine cerebral arteries induced by uridine 5'-triphosphate (UTP) and to ascertain whether UTP given intracisternally causes cerebral arterial constriction. The latter was proven arteriographically to be the case. In vitro, UTP (10(-4)M) and UDP were similar in potency, produced sustained contractions, and were more effective than other pyrimidine nucleotides or uridine. Unlike serotonin (5-HT), UTP was not antagonized by cinanserin and failed to cause constriction of mesenteric arteries. Adenosine similarly antagonized 5-HT and UTP. The Ca2+ antagonist nimodipine abolished contractions caused by high K+ but only incompletely antagonized 5-HT or UTP. On the other hand, procedures that hyperpolarize the cell membrane (low K+ followed by K+) abolished tonic contractions induced by UTP. Hyperpolarization prior to UTP (with or without nimodipine) did not, however, prevent the occurrence of a phasic contraction. Papaverine or lanthanum antagonized this phasic response. It was concluded that UTP selectively affects cerebral arteries, may initiate contraction by releasing membrane bound Ca2+, depolarizes the cell membrane to open receptor operated and potential sensitive calcium channels, but does not inhibit the electrogenic Na-pump nor specifically antagonize the vasodilator adenosine.
Angiographical analysis of acute cerebral infarction followed by "cascade"-like deterioration of minor neurological deficits. What is progressing stroke?
Authors: Irino T , Watanabe M , Nishide M , Gotoh M , Tsuchiya T
Published: June 2011

In order to understand the mechanism of clinical worsening in patients with cerebral infarction, attention was focused on the changes in cerebral angiograms obtained repeatedly before and after neurological deterioration. Among 212 stroke patients with minor neurological deficits, incomplete hemiparesis progressed to complete hemiplegia in 15 patients several days after the beginning of symptoms. On admission, 3 had internal carotid artery occlusion, 2 had stenosis of the internal carotid artery, 5 had occlusion of the middle cerebral arterial trunk, 2 had occlusion of the middle cerebral arterial branch, and 3 had no angiographically visible occlusion. The changes between the first and the second angiograms were of different varieties: another recurrent occlusion, progression of occlusion, new occlusion in the cerebral arteries opacified through the collateral pathway, recanalization of the initially occluded artery, and no change. Such different patterns of pathophysiological events show that the mechanism of neurological worsening in infarcted patients is not uniform. Based on the results from the present study, several problems which arose during the investigation and the somewhat vague definition of "progressing stroke" currently in use are discussed.
Clinicopathological study of pontine hemorrhage.
Authors: Nakajima K
Published: June 2011

This report concerns a clinico-pathological study of 60 patients afflicted with primary pontine hemorrhage. The illness was fatal in 43, 17 patients survived. Ophthalmic signs, autonomic disturbances and transient visual hallucination were observed and discussed. A ruptured microaneurysm within the border of a pontine hematoma was detected in this study, and in the first report of such a finding.
Hypertensive putaminal hemorrhage presenting as pure motor hemiparesis.
Authors: Tapia J F , Kase C S , Sawyer R H , Mohr J P
Published: June 2011

A 44 year old hypertensive man presented with a pure motor hemiparesis, and CT scan showed a putaminal hemorrhage. The clinical course was characterized by rapid resolution of the deficits. This case illustrates a variety of putaminal hemorrhage of good functional and vital prognosis, and stresses the value of CT scanning as a tool for diagnosis and prognosis.
Middle cerebral artery perfusion pressure in cerebrovascular occlusive disease.
Authors: Spetzler R F , Roski R A , Zabramski J
Published: June 2011

We measured the MCAP (middle cerebral artery pressure)/MSBP (mean systemic blood pressure) ratio in 76 patients who underwent an EIAB (extracranial-intracranial arterial bypass). Patients were divided into groups on the basis of angiographic findings. We found a definite correlation between increasing angiographic cerebral vascular occlusive disease and lower MCAP/MSBP ratios. Six of 32 patients with a preoperative neurologic deficit demonstrated mild but definite postoperative neurologic improvement. The mean MCAP/MSBP ratio in these six patients was significantly lower than that for the remainder of this group (p less than .05). Finally, postoperative filling of the middle cerebral artery territory through the graft was found to correlate in an inverse linear relationship with MCAP/MSBP. Evidence is presented that hypoperfusion produced by occlusion of major cranial vessels plays an important role in temporary and permanent neurological deficits seen in patients with cerebrovascular disease.
The effect of ischemia on biogenic amine concentrations in the central nervous system.
Authors: Zivin J A , Stashak J
Published: June 2011

A rabbit spinal cord ischemia model was used to study the effects of focal ischemia on the tissue concentrations of serotonin, 5-hydroxyindole acetic acid, and norepinephrine. Ischemia induced by abdominal aorta occlusion caused both serotonin and norepinephrine concentrations to decline in the most ischemic areas of the spinal cord by 55 minutes. In marginally perfused adjacent areas, serotonin concentrations transiently declined at 14 and 20 min. After the onset of ischemia and then returned to normal. The minimum was reached at the same time when previous studies showed damage had become irreversible in more ischemic regions. Concentrations of 5-hydroxyindole acetic acid did not change at any time and norepinephrine declined only in the most ischemic areas after damage was irreversible. Thus, permanent serotonin and norepinephrine decreases occur only in areas destined to be destroyed by infarction, but the serotonin returns to normal in marginal tissue that remains viable. These studies suggest that serotonin may be involved in the early stages of irreversible changes during central nervous system ischemia.
Ischemic brain edema with and without reperfusion: an experimental study in gerbils.
Authors: Iannotti F , Hoff J
Published: June 2011

Tissue water and rCBF from the same area of brain was measured in gerbils with cerebral ischemia. In one experiment we related the severity of ischemia that developed after one hour of carotid occlusion to the amount of edema which formed. In a second experiment brain made ischemic for one hour was reperfused for one hour to assess the effect of reperfusion of ischemic tissue upon edema formation. We identified a critical threshold (10-14 ml X 100g-1 min-1) for the reversibility of the ischemic process, above which edema can resolve upon reperfusion. When postocclusion rCBF was less than 10 ml X 100g-1 min-1, edema was maximal at the end of occlusion and did not resolve with reperfusion. Autoregulation was preserved in ischemic tissue in which the edema process resolved with reperfusion.
Regional cerebral glucose metabolism during and after bilateral cerebral ischemia in the gerbil.
Authors: Choki J , Greenberg J , Reivich M
Published: June 2011

Cerebral metabolic rate for glucose (CMRG) was measured using the 14C-deoxyglucose technique in a stroke model of the gerbil produced by bilateral common carotid artery occlusion. During 30 minutes of ischemia, 14C-deoxyglucose uptake in the brain was increased along the border zone between the ischemic and nonischemic area and decreased in the ischemic areas. During the early stage of reperfusion (2 or 3 to 30 minutes), CMRG increased 50 to 150% in the cerebral cortex, caudoputamen and thalamus and 270 to 320% in the hippocampus, globus pallidus and amygdala. During the late stage of reperfusion (15 to 45 minutes), heterogeneity of CMRG appeared in the cerebral cortex, caudoputamen and thalamus. CMRG decreased to less than 50% of the control value in the cerebral cortex but remained at 200 to 300% of control in the hippocampus, globus pallidus and amygdala. The latter structures exhibited a larger and more protracted increase in glucose metabolism than the other structures most probably due to the histological vulnerability to ischemia of these structures. The relationship between the transient increase of the glucose metabolism and cell function is discussed.
Regional cerebral blood flow during hypotension in normotensive and stroke-prone spontaneously hypertensive rats: effect of sympathetic denervation.
Authors: Sadoshima S , Heistad D D
Published: June 2011

This study was performed to determine whether, in hypertensive and normotensive rats, chronic sympathetic denervation impairs cerebral vasodilator responses during hypotension, and to determine whether there are regional differences in the autoregulatory response of brain vessels during hypotension. The superior cervical ganglion was removed on one side in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive (WKY) rats. Cerebral blood flow (CBF) was measured with microspheres when the rats were 5-6 months old. Chronic sympathetic denervation had little or no effect on cerebral vasodilator responses during acute hypotension in SHRSP and WKY. We suggest that the increase in incidence of ischemic infarction that we have observed previously after chronic sympathetic denervation in SHRSP probably is not the result of ischemia during episodes of hypotension. We also observed major regional differences in the response of cerebral vessels during acute hypotension in SHRSP: blood flow to brainstem was preserved better than flow to cerebrum and cerebellum. Thus the "lower limit" of the autoregulatory plateau differs in various regions of the brain in SHRSP.
Low protein fish vs low protein animal diet enhances the propensity for stroke in stroke-prone/SHR.
Authors: Wexler B C
Published: June 2011

Weanling male and female, stroke-prone, spontaneously hypertensive rats (SHR/SP) were fed: 1) regular commercial rat chow, 2) low protein fish diet, 3) low protein fish diet + 1% saline, 4) low protein animal diet, and 5) low protein animal diet + 1% saline. The blood pressure of all of the SHR/SP rose rapidly reaching 240 mmHg at 90 days of age; blood pressure of low protein fish diet + 1% saline-fed SHR/SP rose most rapidly, reaching levels ranging from 258 to 300 mmHg. All of these animals developed acute strokes by 90 days of age; none of the other diet-fed SHR/SP manifested cerebral damage. The protein poor diets prevented normal growth, caused hypogonadism, and severely reduced pituitary and adrenal gland weights. The low protein diets were stressful causing significantly increased secretion of adrenocorticotrophic hormone and marked increases in triglyceride, free fatty acid, cholesterol, glucose, and B.U.N. levels. The mixed hemorrhagic-thrombogenic cerebral lesions occurred ipsilaterally in the parietal lobe, involved basal ganglia, and appeared in areas of brain tissue nourished by the middle cerebral artery. It is concluded that the inclusion of 1% saline drinking water with a low protein diet of fish tissue origin specifically, was synergistic in enhancing the propensity of SHR/SP rats to develop their genetically-programmed hypertension and stroke.
Duration of atrial fibrillation and imminence of stroke: the Framingham study.
Authors: Wolf P A , Kannel W B , McGee D L , Meeks S L , Bharucha N E , McNamara P M
Published: June 2011

The role of Atrial Fibrillation (AF) as a precursor of stroke was examined in the Framingham cohort based on 30 years of follow-up during which time 501 strokes occurred. There were 59 persons who sustained stroke in association with AF excluding those with rheumatic heart disease. AF increased the risk of stroke five-fold and the excess risk was found to be independent of the frequently associated cardiac failure and coronary heart disease. The contribution of AF to stroke risk was also at least as powerful as that of the other cardiovascular precursors. Stroke associated with AF was not only independent and substantial but also imminent. There was a distinct clustering of stroke events at the time of onset of the AF. Thirty day case-fatality rates were no different in those with strokes accompanied by AF than not at 17% versus 19% respectively. Recurrences in those with AF were only slightly more frequent, 25% versus 20%, a difference that was not statistically significant. Stroke recurrence in the first 6 months following initial stroke was more than twice as common (47% versus 20%) in the AF group.
Factors contributing to stroke in patients with atherosclerotic disease of the great vessels: the role of diabetes.
Authors: Weinberger J , Biscarra V , Weisberg M K , Jacobson J H
Published: June 2011

The incidence of carotid artery disease and cerebrovascular symptoms were determined in 102 consecutive patients with peripheral arterial disease. Symptoms were correlated with risk factors of age, hypertension, smoking and diabetes and with the extent of disease at the carotid bifurcation. The incidence of stroke with permanent neurological deficit was twice as high in diabetics as in non-diabetics with equivalent atherosclerotic vascular disease (p less than .05). In women, the incidence of stroke was three times higher in diabetics (p less than .02). The number of transient ischemic attacks was significantly higher in non-diabetics (p less than .02). The total number of ischemic episodes in diabetics and non-diabetics was equivalent. This indicates that diabetics are more prone to irreversible destruction of ischemic brain tissue regardless of the nature of the circulatory disturbance.
A two-year longitudinal study of post-stroke mood disorders: findings during the initial evaluation.
Authors: Robinson R G , Starr L B , Kubos K L , Price T R
Published: June 2011

A consecutive series of 103 stroke patients capable of undergoing a psychiatric interview were evaluated for mood disorders. Nearly 50% of patients studied in the acute stroke period had clinically significant depressions and one fourth had symptom clusters found in major depressive disorders. We confirmed our previous findings that lesion location is most important in determining frequency and severity of depression. In addition, we have identified other variables including functional physical impairment, intellectual impairment, quality of social support, and age which contribute to or modify depression. Post-stroke depressive disorders are multifactorial in their determination and expression and include both neurophysiological-neurochemical mechanisms and psychological factors in their etiology.
Ataxic hemiparesis in patients with primary pontine hemorrhage.
Authors: Kobatake K , Shinohara Y
Published: June 2011

Two patients with small primary pontine hemorrhage developed a syndrome identical to ataxic hemiparesis, one of the lacunar syndromes of Fisher. The possible mechanisms of the homolateral cerebellar signs, pyramidal signs, and dysarthria are discussed. Lesions of the ipsilateral pontine nuclei may be responsible for the homolateral ataxia.
Effects of sphere size and injection site on regional cerebral blood flow measurements.
Authors: Chen R Y , Fan F C , Schuessler G B , Usami S , Chien S
Published: June 2011

Regional cerebral blood flows and shunting of microspheres with four different sizes (9,12, 16 and 25 microns) into the superior sagittal sinus were determined in twelve dogs. Venous blood was collected from the superior sagittal sinus for 120 min after the injection of microspheres, and the dogs were then sacrificed immediately. Results on blood flow measurements and venous shunting determinations were similar between left ventricular and left atrial injections. Blood flows measured by 12, 16 and 25 microns spheres were comparable in various brain tissues, except the choroid plexus. 9 microns spheres underestimated blood flows in all regions studied: by 13-19 percent in the cerebral cortex, midbrain, brain stem and cerebellum, by 34-42 percent in the cortical white matter, corpus callosum and cervical cord, and by 64-81 percent in pituitary gland and choroid plexus. These results probably reflect regional difference in microvascular architecture. Venous shunting of 9, 12, 16 and 25 microns spheres during a 24 hr period were 23.6 +/- 2.5, 12.6 +/- 1.2, 4.8 +/- 1.4, and 4.0 +/- 1.2 percent (mean +/- SEM), respectively, with respect to the arterial delivery. Although most of the venous shunting occurred during the first 3 min after the injection of microspheres, it continued 3-60 min after the injection. Beyond 60 min, the venous shunting became minimal for 16 and 25 microns spheres, while significant amount of 9 microns spheres continued to appear in sagittal sinus. This time dependent shunting indicates that some microspheres may be transiently trapped in the microcirculation and become gradually dislodged with time. Failure to consider this time dependence may underestimate the shunting of microspheres through the microcirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
Measurement of cerebral blood flow by washout of microwave induced heating.
Authors: Lawner P M , Oldendorf W H , Braun L D
Published: June 2011

A method is described for measurement of cerebral blood flow utilizing the washout of microwave delivered heating. Using a microwave source attenuated to achieve a brain temperature elevation of 0.5-0.75 degrees C after a 2 second exposure in the rat, cerebral blood flow was calculated from the temperature washout curve monitored by a small thermistor implanted in the brain. The results obtained with this method were comparable to those obtained using the [14C] butanol method. To our knowledge this represents the first description of a method to deliver a blood flow "indicator" atraumatically directly into brain tissue.
The role of ethanol in diluents of drugs that protect mice from hypoxia.
Authors: Moursi M M , Luyckx B A , D'Alecy L G
Published: June 2011

This study evaluates the hypothesis that ethanol alone, or in diluents for drugs used to protect hypoxic mice, is responsible in part for an increased tolerance to hypoxia (4-5% oxygen). The change in hypoxic tolerance following i.v. or i.p. administration of ethanol, diazepam, nimodipine and various diluent components was measured. Diazepam (50 mg/kg i.v.) increased hypoxic tolerance to 700 +/- 47% (n = 11) of saline control, its diluent increased hypoxic tolerance to 468 +/- 60% (n = 10) of saline control but the ethanol component of the diluent accounted for almost half of this diluent effect. Nimodipine (2 mg/kg i.p.), a calcium antagonist, increased tolerance to 180 +/- 18% of control (n = 19) and nimodipine diluent showed an even greater increase to 226 +/- 25% of control (n = 15). In this case essentially all of the protective effect of nimodipine diluent (81.3%) is accounted for by ethanol. Dose response curves indicate the maximum ethanol induced increase in hypoxic tolerance was approximately 335% of control at a dose of 2.4 g/kg. Buffers, etc. in the diluents evidently add to the protective effect of ethanol. Our data clearly indicate ethanol is the important component of some treatments which protect mice from hypoxia. The pharmacological activity of ethanol, even when used in a diluent, should not be ignored in evaluating therapeutic intervention for protection from hypoxia.
Double lumen dissecting aneurysms of the internal carotid artery in fibromuscular dysplasia: case report.
Authors: Garcia-Merino J A , Gutierrez J A , Lopez-Lozano J J , Marquez M , Lopez F , Liano H
Published: June 2011

A young man with cerebral infarction, skeletal, cardiac and renal malformations was found to have on angiography a rare lesion involving the cervical left internal carotid artery, formed by the superposition of two arterial lumina. Anti-platelet therapy did not prevent thrombosis of the lesion and reinfarction. Extracranial-intracranial bypass graft was performed, followed by excision of the arterial lesion. Pathological examination revealed fibromuscular dysplasia and dissecting aneurysm. The few reported cases associating fibromuscular dysplasia of the internal carotid artery with dissecting aneurysm are reviewed. Surgical therapy is recommended in such cases when symptomatology progresses. Fibromuscular dysplasia occasionally coexists with somatic malformations, suggesting a congenital origin of this condition.
Sequential computerized tomographic appearance of strokes.
Authors: Hakim A M , Ryder-Cooke A , Melanson D
Published: June 2011

Eighteen consecutive patients satisfying predefined clinical criteria for embolic strokes were prospectively studied by sequential computerized tomography (CT). Their findings were compared to CT scans obtained from patients presumed to have suffered thrombotic strokes. Our data reveal that the CT appearance of hemorrhagic infarction is likely to occur twice as frequently (22%) in CT scans of strokes presumed embolic than in those presumed thrombotic, where hemorrhagic infarction appeared at some time in 10% of the patients. No patient deteriorated with anticoagulation regardless of the CT appearance. In patients showing hemorrhagic infarction before anticoagulants, follow-up scans obtained after the administration of anticoagulants revealed resolution of the hemorrhagic aspect.
The effect of graded hypothermia on hypoxic-ischemic brain damage: a neuropathologic study in the neonatal rat.
Authors: Young R S , Olenginski T P , Yagel S K , Towfighi J
Published: June 2011

To investigate the relationship between neuropathologic damage and cerebral metabolic alterations during hypothermia in the neonatal animal, 7 day old Sprague-Dawley rats were subjected to unilateral common carotid artery ligation and hypoxia at 37 degrees C, 29 degrees C, and 21 degrees C. At 37 degrees C, animals had extensive infarction of tectum and ipsilateral cerebral hemisphere, and marked depletion of brain ATP. At 29 degrees C, there was no significant change in brain ATP; neuropathologic damage was limited to a few areas of necrosis in the deeper layers of cerebral cortex. No histologic injury was seen in the 21 degrees C group of rats. Profound hypothermia may prevent cerebral edema and visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing cerebral metabolic demands. Moderate hypothermia confers a partial, but incomplete degree of protection; whereas during normothermia, the full extent of hypoxicischemic injury is manifest.
Symmetric brainstem necrosis in an adult following hypotension: an arterial end-zone infarct?
Authors: Jurgensen J C , Towfighi J , Brennan R W , Jeffreys W H
Published: June 2011

A 44-year-old woman with prolonged coma and hypotension following drug overdosage developed bilateral hemorrhagic infarcts in the dorsolateral brainstem. The regional distribution of these paired lesions corresponds to the area of confluence of penetrating arteries in the brainstem. It is suggested that under exceptional circumstances brainstem arterial end-zones may be vulnerable to anoxic-ischemic insult.
A possible role of lipid peroxidation in cellular damages caused by cerebral ischemia and the protective effect of alpha-tocopherol administration.
Authors: Yamamoto M , Shima T , Uozumi T , Sogabe T , Yamada K , Kawasaki T
Published: June 2011

Incomplete global cerebral ischemia was induced by clamping the bilateral common carotid arteries of spontaneously hypertensive rats (SHR) and blood reperfusion was allowed by declamping the arteries after indicated times. To investigate the possible role of lipid peroxidation which causes irreversible ischemic cell injury during ischemia and subsequent reperfusion, cerebral energy metabolism, brain edema, neurological signs and cerebral and serum lipid peroxides were examined. The effect of alpha-tocopherol administration on these parameters was also studied from the standpoint of its action as a free radical scavenger. During ischemia up to 5 hours, cerebral ATP decreased and lactate increased rapidly, and concomitantly neurological signs, such as eye closure and jumping seizures, and slowly progressing brain edema were observed. The level of lipid peroxides in the brain and serum remained practically unchanged during ischemia, although an increasing tendency was noted. When blood reperfusion was allowed 3 hours after ischemia, tissue ATP level was restored only partially (67.4% of normal), but lactate returned to the normal level. The reperfusion resulted in a rapid rise in the lipid peroxide level both in cerebral tissue and serum and also caused a more severe expression of neurological signs. Intravenous injection of alpha-tocopherol (20 mg/kg body weight) 30 minutes prior to ligation of the carotid arteries significantly suppressed the rise in lipid peroxides both in the brain and serum, improved the severely expressed neurological signs, and promoted resynthesis of ATP. These improvements in the parameters were observed only after the reperfusion was made following ischemia for 3 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral blood flow during dihydralazine-induced hypotension in hypertensive rats.
Authors: Barry D I , Strandgaard S , Graham D I , Svendsen U G , Braendstrup O , Paulson O B
Published: June 2011

The cerebrovascular effects of graded, controlled dihydralazine-induced hypotension were studied in rats with renal hypertension (RHR) and spontaneous hypertension (SHR). Repeated measurements of cerebral blood flow (CBF) were made using the intraarterial 133Xenon injection technique in anaesthetised normocapnic animals. Dihydralazine was administered in single increasing i.v. doses (0.1 to 2 mg/kg), and CBF measured after each dose when a stable blood pressure had been reached. From a resting level of 145 +/- 7 mm Hg in RHR and 138 +/- 11 mm Hg in SHR, mean arterial pressure (MAP) fell stepwise to a minimum of around 50 mm Hg. CBF was preserved during dihydralazine induced hypotension, and remained at the resting level of 79 +/- 13 ml/100 g . min in RHR and 88 +/- 16 ml/100 g . min in SHR. Following 2 hours hypotension at the lowest pressure reached, the rats were sacrificed by perfusion fixation and the brains processed for light microscopy. Evidence of regional ischaemic brain damage was found in 4 of 11 animals: in 2 cases the damage appeared to be accentuated in the arterial boundary zones. Although the lower limit of CBF autoregulation in these rats is around 100 mm Hg during haemorrhagic hypotension, dihydralazine brought MAP to around 50 mm Hg without any concomitant fall in CBF. This was interpreted as being due to direct dilatation of cerebral resistance vessels. The combination of low pressure and direct dilatation may have resulted in uneven perfusion, thus accounting for the regional ischaemic lesions.
Patency of external and internal carotid artery in the presence of an occluded common carotid artery: noninvasive evaluation with combined cerebrovascular Doppler examination and sequential computertomography.
Authors: Keller H M , Valavanis A , Imhof H G , Turina M
Published: June 2011

The patency of the external carotid artery (ECA) and internal carotid artery (ICA) in the presence of an occlusion of the common carotid artery (CCA) was evaluated in 7 patients with a symptomatic CCA occlusion by the combined application of cerebrovascular Doppler examination (cv-Doppler) based on continuous-wave equipment and sequential computertomographic scans with intravenous bolus injection of contrast material (sequential CT-scans). Occlusion of the CCA was demonstrated by cv- Doppler and sequential CT-scans and confirmed by routine angiography. A patent ECA was found in all 7 patients by the combined method, but could not be demonstrated by routine angiography in one of these patients. A patent ICA was found in 2 patients by the combined method, while routine angiographic findings concerning the patency of the ICA were equivocal. An occluded ICA was found in 5 patients by the cv-Doppler-sequential CT-scans method, where routine angiographic findings also were equivocal. Operation to restore blood flow in the CCA was performed in 5 patients and successful in 3 patients in whom blood flow from the CCA to the ECA could be achieved in 2 patients, and to the ECA and ICA in one patient, as predicted by the combined cv-Doppler-sequential CT-scans method. Thus, the patency of the ICA in the presence of a CCA occlusion can be reliably evaluated by the combined diagnostic procedure. The method may help to decide for further diagnostic work-up, e.g., specific selective injections and projections in more than two plans during cerebral angiography, and/or successful surgical intervention in a given patient with a CCA occlusion, even if angiographic findings are equivocal.