bluuebunny/crossref_metadata_2025 huggingface dataset:
Butanediol induced ketosis increases tolerance to hypoxia in the mouse.
Authors: Kirsch J R , D'Alecy L G , Mongroo P B
Published: June 2011

In previous studies from our laboratory a positive correlation between elevated blood ketone levels and the survival time (ST) during hypoxia (4-5% oxygen) was observed in fasted and alloxan diabetic mice. To test the hypothesis that ketosis was somehow increasing the tolerance of mice to hypoxia, we induced ketosis by either oral (PO), intraperitoneal (IP), or intravenous (IV) 1,3-butanediol (BD). Blood beta-hydroxbutyrate increased from 0.33 +/- 0.06 mM to 3.32 +/- 0.08 mM for PO, 1.2 +/- 0.2 mM for IV and 0.83 +/- 0.15 mM for IP. BD was associated with an increase in ST to 458% (n = 19) when given PO, 217% (n = 12) by IP route, and 560% (n = 13) by the IV route. The effect of ambient temperature (Ta) on this phenomenon was evaluated at 12, 22, 32, and 34 degrees C. At each Ta, IV BD at 1.4 mmole/mouse was associated with an increase in ST to 525, 559, 151, and 145% of control, respectively. The absolute ST of both control and treated mice was greater at Ta of 12 and 22 degrees C. Hypoxia, however, was associated with a decrease in body temperature in each group. It is concluded that the artificial induction of ketosis by BD is associated with an increase in ST of mice exposed to hypoxia.
Histochemical changes of brain dopamine in an acute stage of cerebral ischemia in gerbils.
Authors: Ahagon A , Ishikawa M , Handa H
Published: June 2011

The fluorescence histochemical method of Falck et al. was applied to 40 gerbil brains after ligation of a unilateral common carotid artery to investigate alterations of brain dopamine in the acute stage of cerebral ischemia. The distribution of dopaminergic terminals and cell bodies in gerbils is the same as in other mammals. On the ligated side after one hour of ischemia, diffuse green fluorescence of dopaminergic terminals showed only a slight decrease in intensity when compared to the nonligated side. But white matter and bundles of myelinated fibers adjacent to and in the dopamine-rich regions had an intense green fluorescence in contrast to the non-ligated side where they are normally non-fluorescent. This is considered to indicate the extraneuronal leakage and diffusion of dopamine. The intensity of extraneuronal green fluorescence was especially high in glial cells. Occasionally, there was also an unusual green fluorescence in the lumen of small vessels in dopamine-rich regions on the ligated side. Dopaminergic cell bodies in the substantia nigra on the ligated side revealed a conspicuous reduction in the fluorescence intensity in severely affected cases. After 2 or 3 hours of ischemia, there was a marked reduction or disappearance of the diffuse green fluorescence on the ligated side. This may be attributed in part to further diffusion of leaked dopamine.
Effect of unilateral common carotid artery occlusion on levels of prostaglandins D2, F2 alpha and 6-keto-prostaglandin F1 alpha in gerbil brain.
Authors: Gaudet R J , Levine L
Published: June 2011

The concentrations of the arachidonic acid metabolites, PGD2, PGF2 alpha and 6-keto-PGF1 alpha, were measured in the cerebral hemispheres of gerbils subjected to unilateral carotid occlusion. Approximately 37 percent of the animals with occlusion had symptoms of cerebral ischemia. In those animals PGD2 and PGF2 alpha levels were elevated in both hemispheres. The levels of 6-keto-PGF1 alpha increased only slightly. There was no change of prostaglandin levels in asymptomatic animals. Indomethacin inhibited the increase in the levels of these arachidonic acid metabolites but did not alter brain swelling as judged by a decrease in specific gravity after 6 hours occlusion.
Cerebrovascular reactivity and metabolism after subarachnoid hemorrhage in baboons.
Authors: Mendelow A D , McCalden T A , Hattingh J , Coull A , Rosendorff C , Eidelman B H
Published: June 2011

Subarachnoid hemorrhage (SAH) was induced in baboons by puncturing the middle cerebral artery. Four to seven days later cerebral blood flow (CBF) responses to changing PaCO2 and to intracarotid infusion of 1.0, 2.5 and 5.0 micrograms of 5-hydroxytryptamine (5-HT)/kg/min were studied using the intracarotid 133xenon clearance technique. Indices of cerebral metabolism were determined by measuring arterio-venous differences for oxygen, pyruvate, lactate and glucose. The results were compared with those from sham-operated baboons. In the sham-operated group normal CO2 reactivity was seen, and 5-HT infusion did not produce any significant change in CBF or cerebral metabolism. By contrast, the group in which SAH was induced showed a significant decrease in CBF and cerebral oxygen utilization, and attenuated CO2 reactivity.
Serial measurements of positron-emitting isotope activity in rat brain.
Authors: Lockwood A H , Kenny P J
Published: June 2011

This report describes the construction and performance characteristics of a device capable of making rapid serial measurement of rat brain radioactivity following the administration of a positron emitting isotope. Two bismuth germanate oxide (BGO) scintillation detectors in a coincidence detection circuit are used to achieve the necessary degree of collimation. Data from the device can be used to characterize cerebral biochemical and physiological processes using computer-assisted mathematical models.
Hemodynamic and clinicopathologic verification of a stroke model in the dog.
Authors: Lawner P M , Laurent J P , Simeone F A , Fink E A
Published: June 2011

Twenty-five mongrel dogs had intracranial internal carotid and proximal middle cerebral artery occlusions. The animals were followed for one week and subsequently sacrificed. This method of clipping produced a mean drop in cortical cerebral blood flow of 48.4% as measured by the 85Kr washout technique. Cerebral blood flow was not affected by the brain retraction necessary for clip placements. Mortality in the first week was 16% and neurological deficits were observed in 73% of the animals. Infarction was present in 80% of the animals, and the mean percent infarction of the affected hemisphere was 17.00 +/0 3.98SE. This is a useful stroke model in an animal which is easily available, inexpensive, and suitable for microvascular intracranial surgery research.
Arterial air embolism: structural effects on the gerbil brain.
Authors: Garcia J H , Klatzo I , Archer T , Lossinsky A S
Published: June 2011

Air injection into the carotid artery of adult mongolian gerbils caused, within 10 minutes, multifocal brain lesions. The extracellular spaces were widened and neurons, oligodendrocytes and myelin sheaths remained unchanged. The "delayed" effects of air embolism (first seen after 3 h) were similar to those observed in gerbils after unilateral carotid ligation. The histologic alterations after 3 h consisted of astrocytic swelling and shrinkage/necrosis of neuronal soma. The observations reported here illustrate the temporal and spatial separations that exist between a) brain water retention, and b) intraparenchymal entry of horseradish peroxidase. Both alterations can be a consequence of either decreased blood flow or arterial air embolism. Edema and protein leakage in each situation may be initiated by different mechanisms.
Mapping local blood flow of human brain by CT scanning during stable xenon inhalation.
Authors: Meyer J S , Hayman L A , Amano T , Nakajima S , Shaw T , Lauzon P , Derman S , Karacan I , Harati Y
Published: June 2011

Non-invasive methods are described for estimating local cerebral blood flows (LCBF) and partition coefficients (L lambda) during inhalation of 35% stable xenon gas (Xes) in oxygen during CT scanning. After denitrogenation by 100% oxygen breathing, 35% Xes is breathed for 7-8 minutes to minimize subanesthetic effects. Mean changes in brain Hounsfield units extrapolated to 15 minutes were 7.7 units for white matter and 5.3 units for gray matter. They were measured from volumes 80 cubic mm (10 mm2 area x 8 mm), or larger with an EMI 1010 scanner at 1 minute intervals. These data were used for computing LCBFs and L lambdas. Irradiation measured at the center of brain slices was 1 rad per minute. To calculate L lambdas about 6 exposures are necessary, thereafter, each 1 minute scan provides LCBF measurements for 2 adjacent 8 mm slices. Reproducibility for LCBF was r = 0.85 (P less 0.001). Mean L lambdas were 0.86 +/- 0.08 for gray and 1.34 +/- 0.10 for white matter. Normative mean flows (mls/100 g brain/min) were: basal ganglia = 79.6 +/- 9.3, cortex = 82.3 +/- 8.5, white matter = 29.2 +/- 5.9, midbrain tegmentum = 94.3 +/- 14.8, cerebellar cortex = 80.1 +/- 10.9, dorsal pons = 89.3 +/- 4.7, brachium pontis = 35.0 +/- 4.2. Subject finger exercises produced increases of LCBF in contralateral pre-central and post-central gyri. Eye closure decreased flow values limited to the visual system. Gray matter flow values diffusely decreased in non-REM sleep but increased above normal in REM sleep. Cerebral infarction and hemorrhage resulted in zones of zero flow with borders having reduced lambdas and low flows attributed to edema.
Reversal of focal "misery-perfusion syndrome" by extra-intracranial arterial bypass in hemodynamic cerebral ischemia. A case study with 15O positron emission tomography.
Authors: Baron J C , Bousser M G , Rey A , Guillard A , Comar D , Castaigne P
Published: June 2011

Tomographic images of cerebral blood flow (CBF) and oxygen extraction fraction (OEF) using the 15O continuous inhalation technique, and positron emission tomography, were obtained from a patient with cerebral ischemia distal to an occluded left internal carotid artery. There was a focal mismatch between CBF and oxygen metabolism in the brain supplied by the middle cerebral artery where CBF was decreased and OEF increased ("misery-perfusion syndrome" as opposed to "luxury-perfusion syndrome"). These abnormalities were most marked in the parieto-occipital watershed area. After left superficial temporal to middle cerebral artery anastomosis, the clinical attacks ceased and a repeat study did not demonstrate the previous CBF and OEF abnormalities. This suggests that this pattern of abnormalities indicates potential viable tissue. The concept of "misery-perfusion" may be of some importance in the pathophysiological mechanisms of hemodynamic cerebral ischemia and serve as a rational basis for revascularization procedures.
CSF serotonin concentrations and cerebral arterial spasm in patients with ruptured intracranial aneurysm.
Authors: Voldby B , Engbaek F , Enevoldsen E M
Published: June 2011

In 26 patients with recent rupture of an intracranial saccular aneurysm the CSF concentrations of serotonin (5-HT) were measured repeatedly by a radioimmunoassay. The 5-HT level in ventricular CSF collected between the 2nd and 15th day after SAH ranged between less than 2 and 5 nmol/l. These did not differ from the levels found in the ventricular CSF (less than 2-3 nmol/l) and lumbar CSF (less than 2-3 nmol/l) of control patients. 5-HT concentrations did not correlate with the severity of angiographical vasospasm, nor with CSF pressure or clinical grade. In two patients with severe postoperative vasospasm, however, cisternal CSF collected during operation and contaminated by fresh blood showed 5-HT concentrations exceeding 25 nmol/l. Thus, although these results do not support the conception that 5-HT plays a major role in sustaining delayed vasospasm, they suggest that 5-HT liberated from platelets may be operative in the initiation of cerebral arterial spasm.
Epileptic seizures in cerebral arterial occlusive disease.
Authors: Cocito L , Favale E , Reni L
Published: June 2011

The occurrence of epileptic seizures was investigated in 141 patients with angiographically proven carotid or MCA occlusive disease. Epileptic seizures occurred some time during the clinical course of the disease in 17.3% of carotid patients and in 10.8% of MCA patients, being mainly represented by partial motor seizures. The pattern of occurrence of seizures in the natural history of cerebral arterial disease was different in the two groups. In the carotid group, epilepsy was the presenting symptom in 6.7% of patients, whereas no MCA patient had seizures prior to the appearance of a neurological deficit. Since epileptic seizures may complicate an otherwise asymptomatic carotid obstruction, angiography should be performed whenever the other standard investigations, including CT-scan, fail to reveal the cause of late-onset epilepsy.
Intracranial dissecting aneurysms in childhood.
Authors: Nass R , Hays A , Chutorian A
Published: June 2011

Children presenting after trauma with headache, seizures, hemiplegia and coma may have an intracranial dissecting aneurysm. Specific angiographic findings provide confirmation of this diagnosis. The dissection occurs subintimally and differs clinically and pathologically from dissecting aneurysms of extracranial arteries. The course in children beyond infancy is catastrophic, justifying consideration of potentially life saving surgical intervention.
Factors limiting regeneration of ATP following temporary ischemia in cat brain.
Authors: Welsh F A , O'Connor M J , Marcy V R , Spatacco A J , Johns R L
Published: June 2011

Cerebral ischemia was induced in cats using bilateral carotid artery occlusion coupled with hemorrhagic hypotension. Thirty minutes of ischemia, which depleted levels of ATP and phosphocreatine throughout the cerebral cortex, was followed by 2-4 hours of recirculation. During the recovery period, cortical perfusion and NADH fluorescence were monitored through a cranial window. Postischemic perfusion, as indicated by transit time, was initially higher than control, but declined to subnormal levels by 60 minutes. NADH fluorescence transients, induced by brief anoxia, also decreased steadily during recirculation, indicating a failure of oxidation-reduction capability. The disappearance of anoxic-NADH transients usually preceded the decline of flow, suggesting that O2 delivery was not the factor limiting redox reactions. Furthermore, tissue levels of NADH, which were nearly normal after 2-4 hours of recirculation, did not indicate tissue hypoxia. In spite of normalization of NADH, resynthesis of high energy phosphates were severely impaired. The degree of ATP recovery varied widely in different cortical regions; however, there were two general groups of ATP values--one at 5% and the other at 70% of control levels. In the energy-depleted areas, NADH levels were normal, but the total pool of NAD (NADH + NAD+) and the tissue content of K+ were 43% lower than control. In contrast, the NAD pool and K+ content were only slightly diminished in the regions with greater ATP restitution. The results suggest that postischemic resynthesis of ATP may be limited not by inadequate delivery of O2, but rather by defective production of NADH.
Long-term prognosis of hypertensive intracerebral hemorrhage.
Authors: Douglas M A , Haerer A F
Published: June 2011

The diagnosis of intracerebral hemorrhage (ICH) has become precise with the advent of computerized tomography (CT). Little, however, is known concerning the long-term prognosis. Seventy consecutive patients with primary intracerebral hemorrhage (all known etiologies except hypertension excluded) proven by CT scan were studied. Follow up, averaging 2 1/2 years, was successful in all cases. The status of alertness, EKG, and clinical impression on admission were significant prognostic factors. As expected, mortality increased with size of the hematoma and ventricular rupture. Acute in hospital mortality was 40%. Another 17% died during the long-term follow up, but none of them from cerebrovascular disease. Ninety-two percent of the survivors were ambulatory at follow up. Hypertensive intracerebral hemorrhages, unlike aneurysms, rarely, if ever, rebleed. Patients are not likely to have a second bleed in another location. Hypertensive intracerebral hemorrhage is more common in blacks, especially young adult males with severe hypertension, but overall mortality is lower than thought prior to the CT scan. Most survivors can achieve independence and deserve aggression rehabilitation efforts.
The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain.
Authors: Shohami E , Rosenthal J , Lavy S
Published: June 2011

Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB2, on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.
The effects of a calcium antagonist, nimodipine, upon physiological responses of the cerebral vasculature and its possible influence upon focal cerebral ischaemia.
Authors: Harris R J , Branston N M , Symon L , Bayhan M , Watson A
Published: June 2011

The effects of a calcium antagonist, nimodipine, were tested on the response of the cerebral circulation to arterial pCO2 and blood pressure changes. The effects of reduced blood flow upon oedema formation and extracellular ion homeostasis under nimodipine preloading were studied. Both open and closed skull primate models were used, with alpha-chloralose anaesthesia. Nimodipine infusion increased basal blood flow in the open skull, but not the closed skull animals. Autoregulation to increased blood pressure was little affected. Responses to arterial pCO2 changes and autorerulation to reduced blood pressure were severely imparied. Residual blood flow after middle cerebral artery occlusion was significantly higher with nimodipine than in controls. The threshold levels of blood flow for the development of cortical oedema and for disturbance of ion homeostasis were, however, increased, suggesting that nimodipine interferes with cellular energy metabolism and increases the susceptibility of tissue to ischaemic damage.
Mechanisms of perioperative cerebral infarction.
Authors: Hart R , Hindman B
Published: June 2011

Perioperative cerebral infarction occurs in less than 1% of general surgical procedures; the mechanism is usually unknown. The clinical features of 12 consecutive perioperative strokes were retrospectively reviewed. Although intraoperative hypotension was frequent, onset of deficit occurred postoperatively in 83% and intraoperatively in 17%. Cardiogenic embolism was a common cause of stroke (42%), with atrial fibrillation present in 4 patients (33%) at the time of stroke. The potential roles of hypercoagulability, hypotension and carotid occlusive disease are discussed. Future reports concerning perioperative stroke should consider the multiple mechanisms and temporal relationship of stroke to the operative procedure.
Treatment of ischaemic stroke with prostacyclin.
Authors: Gryglewski R J , Nowak S , Kostka-Trabka E , Kusmiderski J , Dembinska-Kiec A , Bieron K , Basista M , Blaszczyk B
Published: June 2011

Ten patients with ischaemic stroke were treated with prostacyclin (2.5-5.0 ng/kg/min i.v. in 6 h courses 4-10 times during 1-2.5 days). In all patients a dramatic regression of hemiplegia, or hemiparesis, or aphasia occurred in the first few hours of prostacyclin infusion. Four to eight weeks later 6 patients left the clinic without neurological deficit; 3 patients had minor residual hemiparesis in upper limbs. In one patient, the occlusion of the contralateral carotid artery led to his death. It is considered that an antagonism may exist between endogenous cerebral prostanoids and prostacyclin and may have been responsible for the beneficial effects of prostacyclin therapy.
Mechanisms of relaxant action of nicardipine, a new Ca++-antagonist, on isolated dog cerebral and mesenteric arteries.
Authors: Yamamoto M , Ohta T , Toda N
Published: June 2011

In helically-cut strips of cerebral and mesenteric arteries contracted with prostaglandin (PG) F2 alpha, carbocyclic thromboxane A2 (cTxA2) or K+, the addition of nicardipine caused a dose-related relaxation. Nicardipine-induced relaxation was greater in cerebral than in mesenteric arteries when contracted with PGF2 alpha and cTxA2, but did not appreciably differ in the arteries contracted with K+. Cerebral arteries contracted with hemolysate and PGF2 alpha relaxed in response to nicardipine to a similar extent. The contractile response to PGF2 alpha was attenuated by pretreatment with nicardipine, the attenuation being greater in cerebral than in mesenteric arteries. Ca++-induced contractions in cerebral and mesenteric arteries previously exposed to Ca++-free media and depolarized by excess K+ were attenuated by nicardipine to a similar extent. PGF2 alpha-induced contractions of cerebral arteries exposed to Ca++-free media were attenuated by nicardipine, whereas those of mesenteric arteries were unaffected. Attenuations by nicardipine of the Ca++-induced contraction in PGF2 alpha-treated cerebral arteries were greater than those seen in mesenteric arteries. It may be concluded that nicardipine produces a greater relaxation of cerebral arteries than mesenteric arteries, possibly due to a greater inhibition of the Ca++-influx and to a decrease in the release of Ca++ from intracellular storage sites in cerebral arteries. As far as the concentrations used are concerned, nicardipine appears to attenuate the inward movement of Ca++ across cell membrane in mesenteric arterial smooth muscle, but not the release of intracellularly stored Ca++.
Heparin for lacunar stroke in progression.
Authors: Dobkin B H
Published: June 2011

Four patients with mild hemiparesis were treated with heparin for presumed progressing stroke. All worsened to hemiplegia with pure motor deficits and lacunar infarcts despite this medical intervention. Clinical distinction between large artery and small, penetrating vessel thrombotic disease is needed to best evaluate any benefit of anticoagulation for stroke in progression.
Cardiac abnormalities in ischemic cerebrovascular disease studied by two-dimensional echocardiography.
Authors: Nishide M , Irino T , Gotoh M , Naka M , Tsuji K
Published: June 2011

In the study of cardiac abnormalities responsible for the development of cerebral embolism two-dimensional echocardiography was performed on 350 patients with ischemic cerebrovascular disease. The results were compared with those obtained from 350 controls without any history of stroke. Atrial fibrillation was detected on ECG in 115 cases (33%) of the patients and in 35 cases (10%) of the controls (p less than 0.001). The structural cardiac diseases observed in stroke patients were: rheumatic heart disease (RHD) in 37, congestive cardiomyopathy (CCM) in 7, hypertrophic cardiomyopathy (HCM) in 19, mitral annulus calcification (MAC) in 29, mitral valve prolapse (MVP) in 9, and myocardial infarction (MyI) in 10 patients. Controls were found to have these lesions in 11, 2, 3, 12, 4 and 9 patients respectively. RHD (p less than 0.001), HCM (p less than 0.01) and MAC (p less than 0.01) were significantly more frequent in patients with ischemic cerebrovascular disease, but not MyI, CCM or MVP. Intracardiac thrombi were diagnosed in 29 cases of patients and in 4 cases of controls (p less than 0.001). Our data suggested that nonrheumatic heart diseases such as MAC and HCM could also be considered as causes of embolic stroke. The reasons for the variable frequencies of cardiac abnormalities reported in the literature for stroke patients are discussed.
Amaurosis fugax: the results of arteriography in 59 patients.
Authors: Adams H P , Putman S F , Corbett J J , Sires B P , Thompson H S
Published: June 2011

Fifty-nine patients had arteriography because of episodes of amaurosis fugax. Only one third of them had atherosclerotic lesions potentially treatable by carotid endarterectomy. Another third had normal arteriograms, some of these had migraine, heart disease or platelet disorders presumed to be the cause of their symptoms. Patients with amaurosis fugax are a heterogeneous group, and their visual symptoms should not be considered a specific indicator of stenosis of the internal carotid artery.
Regional blood flow in canine brain during nicotine infusion: effect of autonomic blocking drugs.
Authors: Crystal G J , Downey H F , Adkins T P , Bashour F A
Published: June 2011

Radioactive microspheres (15 mu) were used to measure regional cerebral blood flow during intravenous infusion of nicotine (36 micrograms/kg/min) in anesthetized, open chest dogs. Experiments were conducted with uncontrolled mean aortic pressure and intact autonomic receptors (Series I; n = 9), and in four groups of dogs with mean aortic pressure held constant (Series II); 1) with intact autonomic receptors (n = 6), 2) after beta adrenergic blockade (n = 8), 3) after alpha and beta adrenergic blockade (n = 6), 4) after alpha and beta adrenergic and cholinergic blockade (n = 4). In Series I, nicotine raised mean aortic pressure (+ 72%) and increased flow in cerebral cortex (+ 67%), cerebellum (+ 38%), pons (+ 46%), medulla (+ 39%), and spinal cord (+ 48%). In all regions, but cortex, increases in vascular resistance limited nicotine-induced increases in flow. In Series II, nicotine changed flow only in cortex. Without blockade, nicotine increased cortical flow (+ 38%); but beta blockade abolished this increase in flow. After alpha and beta blockade nicotine again raised cortical flow (+ 29%), and additional cholinergic blockade had no effect on this response. It is concluded that nicotine causes predominant beta receptor mediated vasodilation in cerebral cortex, although it also activates alpha (vasoconstrictor) receptors and a non-adrenergic, non-cholinergic vasodilator mechanism in this region of brain.
The effect of chronic propranolol therapy on regional cerebral blood flow in hypertensive patients.
Authors: Globus M , Keren A , Eldad M , Granot C , Tzivoni D , Lavy S , Stern S
Published: June 2011

In 31 hypertensive patients the effect of chronic oral administration of the beta blocking agent propranolol on regional cerebral blood flow (rCBF) was studied, using the non-invasive 133Xenon inhalation technique. The results of the measurements were compared to the rCBF obtained in an age-matched normal control group. Our study shows that during long-term therapy with low doses of propranolol (less than 120 mg/daily) the rCBF is unaffected, but it is increased significantly if higher doses (greater than 120 mg/daily) are used. In all six patients who served as their own control, as they had basic rCBF measurements before or during low-dose propranolol, the rCBF on high-dose propranolol became significantly increased. The possible mechanisms which may cause the increased rCBF on high-dose propranolol are discussed.
Role of tissue lactate and substrate availability in 1,3-butanediol-enhanced hypoxic survival in the mouse.
Authors: Kirsch J R , D'Alecy L G
Published: June 2011

Previously we found that 1,3-butanediol-treated mice live longer during hypoxia. We hypothesized that 1,3-butanediol could reduce the brain's accumulation of potentially cytotoxic lactate and/or elevate brain substrate availability (ketones or glucose) and thus maintain the brain's energy producing capability even during reduced oxygen availability. To test these hypotheses, whole brain metabolites from normoxic and hypoxic mice, pretreated with 1,3-butanediol or insulin, were compared to saline controls. During hypoxia both pretreated groups had lower brain lactate than controls. If lactate accumulation was the sole factor responsible for hypoxic tolerance, insulin should have increased brain lactate since insulin has been shown previously to reduce hypoxic tolerance. In normoxic mice the ratio of lactate to pyruvate and the level of malate and fumarate were not changed by 1,3-butanediol as is found with other agents known to protect the hypoxic animal. When substrate availability was directly elevated by beta-hydroxybutyrate and glucose administration hypoxic survival time increased thus implicating substrate availability as an important factor in hypoxic tolerance. We conclude that reduced brain lactate and augmented substrate availability both contribute to 1,3-butanediol-enhanced hypoxic tolerance in this animal model.
Early changes in blood brain barrier permeability to small molecules after transient cerebral ischemia.
Authors: Sage J I , Van Uitert R L , Duffy T E
Published: June 2011

Brain unidirectional extraction and flux of leucine were measured simultaneously with cerebral blood flow (CBF) at various times after transient global cerebral ischemia in the rat. The results permit an evaluation of blood-brain barrier permeability in the postischemic period independent of alterations in CBF at the time of measurement. Leucine extraction was higher (p less than 0.001) than that of CBF-matched controls at 15 min and 6 hr after 30 min of global cerebral ischemia, but was not different from control at 30 min and 1 h after ischemia. Leucine flux into brain was increased only at 15 min after reperfusion of the brain. Cerebral edema occurs 15-30 min after reperfusion in this ischemia model, but the permeability of the blood-brain barrier to large molecules is unaltered during this period (Petito et al: J Neuropath Exp Neurol 41:423-436, 1982). Increased barrier permeability to small molecules such as leucine may contribute to the production of this early postischemic edema.
Role of intrinsic arachidonate metabolites in the vascular action of erythrocyte breakdown products.
Authors: Okamoto S , Handa H , Toda N
Published: June 2011

In helically-cut strips of dog basilar and mesenteric arteries, the isometric tension developed by application of ghost-free hemolysate from dog erythrocytes was recorded. The hemolysate contracted basilar arteries in a concentration-dependent fashion, the response being attenuated by treatment with either aspirin or polyphloretin phosphate, a prostaglandin antagonist. Mesenteric arteries were contracted only slightly by high concentrations of hemolysate. When the mesenteric arteries had partially been contracted with prostaglandin F2 alpha or norepinephrine, the hemolysate induced relaxations, which were abolished by aspirin in approximately half the preparations used. Studies on rat stomach strips exposed to superfusate of dog cerebral arteries showed a release of prostaglandin-like substance by the hemolysate application. It may be concluded that the hemolysate contracts basilar arteries and relaxes mesenteric arteries, mainly through prostaglandins synthesized in and released from the vascular wall. Such a mechanism may be involved in the pathogenesis of cerebral vasospasm following a subarachnoid hemorrhage.
Stable xenon CT CBF measurements in prevalent cerebrovascular disorders (stroke).
Authors: Meyer J S , Okayasu H , Tachibana H , Okabe T
Published: June 2011

Local cerebral blood flow (LCBF) and local tissue: blood partition coefficient (L lambda) values were measured for small volumes of gray or white matter by CT CBF. Single compartment analysis was used but fitted to infinity in normal volunteers aged between 20 to 100 years (N = 20). Hemispheric LCBF and L lambda values were compared to those of 61 age matched patients with transient ischemic attacks (TIAs, N = 10), reversible ischemic neurologic deficits (RINDS, N = 10), acute and chronic cerebral infarctions associated with emboli from atherosclerotic plaques or complete occlusion of internal carotid or middle cerebral arteries (n = 9) or of cardiac origin (N = 3), cerebral hemorrhage (N = 1), multi-infarct dementia (MID) (N = 11) and arteriovenous malformations (AVM) (N = 17). In normal aging, L lambda s were normal, but LCBF showed diffuse age-related declines. Symptomatic cerebrovascular disease was characterized by accentuation of age-related LCBF declines. TIAs with unilateral ICA occlusion showed bilateral reductions of LCBF more evident in ischemic hemispheres. TIAs due to fibrino-platelet emboli from ulcerated, non-occlusive ICA plaques were characterized by transient unilateral, localized LCBF reductions. All TIAs showed normal L lambda values. RINDS showed both LCBF and L lambda reductions. Larger embolic infarctions of ICA origin, whether acute or chronic, showed zones of zero flow with surrounding reductions of LCBF and L lambda values. Recent cerebral embolism of cardiac origin likewise exhibited zones of zero flow surrounded by reduced LCBF and L lambda values; but in chronic stages LCBF and L lambda values adjacent to zero flow zones were normal. MID was characterized by patchy reductions of LCBF and L lambda values throughout both hemispheres. Brain tissues surrounding AVM showed normal L lambda values but LCBF values were reduced due to steal.
Autoradiographic determination of brain pH following middle cerebral artery occlusion in the rat.
Authors: Kobatake K , Sako K , Izawa M , Yamamoto Y L , Hakim A M
Published: June 2011

A method of quantitative autoradiography using 14C-labelled 5,5-dimethyl-2, 4-oxazolidinedione 14C-DMO to evaluate the local changes in brain pH after ischemia is described. In normal control rats the calculated tissue pH values in gray matter were slightly lower than those in white matter, and there was no significant difference in the calculated pH among the various structures in cortical and subcortical gray matter. Four hours after a left middle cerebral artery (MCA) occlusion, marked reductions in 14C-DMO concentrations were demonstrated in the anterior two-thirds of the cerebral cortex and in the lateral part of the caudate nucleus indicating tissue acidosis in these areas. Although several assumptions are required for the calculation of pH in brain tissue, this method would appear very useful in the investigation of the altered metabolic state in ischemic brain.
A double blind trial of naloxone in the treatment of acute stroke.
Authors: Fallis R J , Fisher M , Lobo R A
Published: June 2011

Naloxone has been reported to have potential benefit in the treatment of stroke. We evaluated the effect of naloxone in a double-blind trial conducted with 15 stroke patients whose deficits ranged from 8 to 60 hours in duration. All but one patient sustained a cerebral infarction. Neurologic function was assessed before and five minutes after each of two injections given to each patient in a double-blind fashion. The injections consisted of naloxone (0.4 mg in 3 patients and 4.0 mg in 12 patients) and saline. Prior to the trial, samples of plasma were obtained for determination of immunoreactive beta-endorphin for each patient. Four patients showed minimal improvement following injection of naloxone, while five patients exhibited a slightly greater improvement following saline injection. There were no significant elevations of plasma beta-endorphin among stroke patients. We conclude that naloxone may not have a significant therapeutic role for stroke in the clinical setting.
Demonstration of adenosine receptors on mouse cerebral smooth muscle membranes.
Authors: Beck D W , Vinters H V , Moore S A , Hart M N , Henn F A , Cancilla P A
Published: June 2011

Adenosine receptors have been identified on brain cortical membranes and microvascular preparations. However, they have not been demonstrated on specific microvascular elements in isolation. 2-3H-chloroadenosine was used as a ligand to investigate the presence of adenosine receptors on isolated mouse cerebral smooth muscle membranes. The binding studies reveal the presence of a high affinity binding site with a Kd value of 33.3 nM and a maximal binding capacity (Bmax) of 283 fmol/mg protein. These findings demonstrate that there is an adenosine receptor on cerebral smooth muscle membranes.
CT-CBF correlations of cognitive deficits in multi-infarct dementia.
Authors: Kitagawa Y , Meyer J S , Tachibana H , Mortel K F , Rogers R L
Published: June 2011

Fifteen right-handed patients with Multi-Infarct Dementia underwent cognitive testing by the Jacobs Mini-Mental Scale (MMQ), and xenon contrast CT scanning. Local cerebral blood flow (LCBF) and local partition coefficient (L lambda) values were measured by stable xenon contrast CT scanning and potential methodological errors were discussed. Reduced values were graded: 0 = normal, 1 = mild, 2 = moderate, 3 = severe. Graded values were pooled and plotted on composite brain maps to display locations of abnormal L lambda and LCBF values. Topographic brain maps, showing most frequent locations of reduced L lambda values, confirmed the common anatomical locations of multiple cerebral infarcts to be distributed in both thalami, temporal lobes, basal ganglia, left internal capsule and right cingulate cortex. Gray matter flow values were reduced in similar cortical and subcortical regions. There were no correlations between MMQ scores and reduced LCBF values for caudate and lenticular nuclei. Direct and statistically significant correlations were found between reduced MMQ scores and mean LCBF values for left or right frontal cortex, left or right temporal cortex and left or right thalamus. Subgrouping MMQ tests according to functions assessed, indicated that left mid-temporal ischemia correlated with dyscalculia and memory disturbances while ischemia of both frontal lobes correlated with disorientation to time and place.
Myocardial damage from acute cerebral lesions.
Authors: Kolin A , Norris J W
Published: June 2011

Autopsy findings in 58 patients with intracranial lesions were compared with those in 50 control patients for myocardial damage, characterised by a change from a myofibrillar to a granular staining pattern, using a histochemical method for succinic dehydrogenase. Transmurally scattered foci of damaged myocardial fibres were significantly more common (p less than 0.01) in patients with intracranial lesions (62%) compared to controls (26%). No victims of sudden violent deaths showed these cardiac lesions. Focal myocardial damage required at least six hours to develop after onset of the acute neurological event and was not observed after the second week. It was associated with lesions producing a rapid increase in intracranial pressure and was usually absent in patients with slowly enlarging or small cerebral lesions. Similar myocardial changes were seen in patients in the control group dying from prolonged shock or other forms of acute circulatory or metabolic failure. The postulated mechanism of cardiac damage in these patients is increased levels of plasma catecholamines secondary to rapidly increasing intracranial pressure, irrespective of the cerebral pathology.
Effect of recirculation and regional counting rate on reliability of noninvasive bicompartmental CBF measurements.
Authors: Herholz K
Published: June 2011

Based on data from routine intravenous Xe133-rCBF studies in 50 patients, using Obrist's algorithm the effect of counting rate statistics and amount of recirculating activity on reproducibility of results was investigated at five simulated counting rate levels. Dependence of the standard deviation of compartmental and noncompartmental flow parameters on recirculation and counting rate was determined by multiple linear regression analysis. Those regression equations permit determination of the optimum accuracy that may be expected from individual flow measurements. Mainly due to a delay of the start-of-fit time an exponential increase in standard deviation of flow measurements was observed as recirculation increased. At constant start-of-fit, however, a linear increase in standard deviation of compartmental flow parameters only was found, while noncompartmental results remained constant. Therefore, and in regard to other studies of potential sources of error, an upper limit of 2.5 min for the start-of-fit time and usage of noncompartmental flow parameters for measurements affected by high recirculation are suggested.
Limb shaking--a carotid TIA.
Authors: Baquis G D , Pessin M S , Scott R M
Published: June 2011

Eight patients are described with an unusual form of carotid transient ischemic attack, limb shaking. The basic features included a brief, involuntary, coarse, irregular, wavering movement or tremble involving arm-hand alone, or arm-hand and leg together. In 2 patients limb shaking was the initial manifestation of carotid occlusive disease, and all but one patient had other typical carotid transient ischemic attacks. Major atheromatous carotid occlusive disease was present in all patients on the side opposite the limb movements. Four patients had bilateral carotid occlusive disease. Cerebral ischemia from a carotid territory low-perfusion state may be the pathogenesis of these limb movements, an idea supported by the apparent benefit of surgical revascularization in abolishing or reducing the limb shaking in 6 patients. There was no clinical or EEG evidence to document an epileptiform etiology. Recognition of this uncommon form of carotid transient ischemic attack may be important in the early diagnosis and treatment of carotid occlusive disease.
Digital subtraction angiography: current clinical applications.
Authors: Pelz D M , Fox A J , Vinuela F
Published: June 2011

The applications of digital subtraction angiography (DSA) in neurologic diagnosis have been evolving as clinical experience with this technology accumulates. Initial enthusiasm with the intravenous contrast material injections has been tempered by often equivocal results. Intravenous DSA (IV-DSA) is still an accurate screening technique for extracranial carotid atherosclerosis, comparable to duplex ultrasound. Intracranial imaging is less satisfying with intravenous injections but reliable information is available in the assessment of the venous sinuses and parasellar internal arteries. The future of DSA lies with intraarterial contrast injections, as this technique substantially decreases the risks and costs of definitive cerebrovascular investigation.
Subarachnoid haemorrhage in the rat: effect on the development of vasospasm of selective lesions of the catecholamine systems in the lower brain stem.
Authors: Svendgaard N A , Brismar J , Delgado T J , Rosengren E
Published: June 2011

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic vasospasm. Lesioning at the level of the mesencephalon of the ascending catecholamine pathways from locus coeruleus in the pons and the A1 and A2 nuclei in the medulla oblongata prior to cisternal blood injection prevents the development of both acute and late spasm. Selective lesioning in the medulla oblongata of ascending fibres from A1 and A2 also prevents development of spasm, indicating that these nuclei, which project to the hypothalamus-pituitary, are essential for the spasm syndrome. It is suggested that a substance vasospasm is produced by a substance liberated either by the hypothalamus or by the pituitary is involved in the occurrence of spasm.
Progression of stroke after arrival at hospital.
Authors: Britton M , Rödén A
Published: June 2011

In order to investigate the frequency, extent and importance of progression of stroke symptoms after arrival at hospital, 402 consecutive patients were studied. Speech ability, extremity and facial pareses were evaluated and graded on four occasions during hospitalization. Deterioration was noted in 43% of the patients; it was fairly marked in 25%. The frequency among the few patients with cerebral haemorrhage was much the same as in those with infarction. Limb motor function was affected in most cases. Half of the progressions occurred within the first 24 h after admission. Patients with progression stayed longer in hospital, were more disabled at discharge and more often needed further institutional care than those without progression, although the initial dysfunction was similar in the two groups. No characteristics were found that would help to identify a risk of deterioration. Thus, progression of stroke symptoms after arrival at hospital is a common and serious problem, whose solution calls for vigorous research.
Somatosensory evoked potentials in pure sensory stroke and related conditions.
Authors: Robinson R K , Richey E T , Kase C S , Mohr J P
Published: June 2011

Somatosensory evoked potentials were reviewed for their correlation with CT scan and clinical features of ischemic "pure sensory stroke" and "pure sensorimotor stroke". Somatosensory evoked potentials were normal in all 11 cases of pure sensory stroke, and CT was normal in ten. The N2-P2 components of the somatosensory evoked potentials were abnormal in all 4 cases of pure sensorimotor stroke, and all had low density CT lesions in the lateral thalamus and/or posterior limb of the internal capsule. It is concluded that somatosensory evoked potentials and CT scans are routinely abnormal in pure sensorimotor stroke, but they are consistently normal in pure sensory stroke, and should not be interpreted as evidence against a clinical diagnosis of pure sensory stroke.
Regional cerebral blood flow, glucose metabolism, protein synthesis, serum protein extravasation, and content of biochemical substrates in stroke-prone spontaneously hypertensive rats.
Authors: Paschen W , Mies G , Bodsch W , Yamori Y , Hossmann K A
Published: June 2011

Stroke-prone spontaneously hypertensive rats with arterial blood pressure above 210 mmHg were taken for the present study after appearance of neurological symptoms. Regional cerebral blood flow, glucose metabolism, and protein synthesis rate were evaluated on the same brain section by means of triple-labelled autoradiographic techniques. Consecutive sections were used in the pictorial presentation of glucose, ATP, and serum protein extravasation. In addition, NADH-fluorescence was recorded. Two different patterns of hypertension-induced brain lesions could be distinguished: in two animals sharply demarcated cysts were visible in the cortical grey matter. In these animals no regional inhomogeneities of flow and metabolism were present remote from the infarct. In contrast, in three animals cysts were located in the white matter, leading to pronounced hemodynamic and metabolic disturbances throughout the brain. It is concluded that edema-induced brain swelling was the main cause for reduction in blood flow and metabolism.
The significance of intensity of rehabilitation of stroke--a controlled trial.
Authors: Sivenius J , Pyörälä K , Heinonen O P , Salonen J T , Riekkinen P
Published: June 2011

Of the 373 stroke patients 95 were admitted to the feasibility study of stroke rehabilitation. The patients were divided into two groups, an intensive and a normal treatment group. In this study, the functional recovery of stroke, measured by ADL and motor function was significantly better in the intensive treatment group. There was no difference in institutionalization or incidence of death between the groups. The gain of ADL and motor function was greatest during the first three months after stroke in the intensive treatment group. The conclusion is that intensified physiotherapy seems to improve the functional recovery of stroke patients.