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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stimulation of the cerebellar fastigial nucleus (FN) increases CBF but not metabolism and reduces the tissue damage resulting from focal cerebral ischemia. This effect may result from enhancing CBF in the ischemic tissue without increasing local metabolic demands. To test this hypothesis, we studied whether the reduction in tissue damage is restricted to the neocortex, a region in which the CBF increase is independent of metabolism, and whether stimulation of the dorsal medullary reticular formation (DMRF), a treatment that increases both cerebral metabolism and CBF, also protects the brain from ischemia. In halothane-anesthetized Sprague-Dawley rats, the middle cerebral artery (MCA) was occluded either proximally or distally to the lenticulostriate branches. The FN or DMRF were then stimulated for 1 h (50-100 microA; 50 Hz; 1 s on/l s off). Twenty-four hours later, the infarct volume was determined. FN stimulation substantially reduced the size of the infarct, an effect that was greater with distal (-69 +/- 8%; n = 6; p < 0.001; mean +/- SD) than with proximal (-38 +/- 8%; n = 8; p < 0.001) MCA occlusion. The reduction occurred only in neocortex (-43 +/- 9%; p < 0.001) and not in striatum (-16 +/- 21%; p > 0.05). Stimulation of the FN also enhanced recovery of EEG amplitude in the ischemic cortex (+48%; p < 0.003). DMRF stimulation (n = 7) did not affect the stroke size or EEG recovery (p > 0.05). Thus, stimulation of the FN, but not the DMRF, attenuates the damage resulting from focal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of the fastigial nucleus enhances EEG recovery and reduces tissue damage after focal cerebral ischemia. 140 Jun 50

The effects of gamma-hydroxybutyrate (GHB) on 1) monoamine metabolism, and 2) protein synthesis were examined in a gerbil stroke model. The monoamine metabolism was studied by occluding bilateral common carotid arteries for 15 minutes followed by GHB administered intravenously 3 hours later. Tissue monoamine concentration was examined up to 8 hours after recirculation. Three hours after GHB administration, dopamine (DA) had increased to almost twice that of the non-treated group, whereas homovanillic acid, a metabolite of DA, did not show any significant difference. These results may mean that GHB will facilitate DA synthesis but that it has no influence on its release. Therefore, a DA-mediated increase in cerebral blood flow in the cerebral cortex cannot be expected. Tryptophan, a precursor of 5-hydroxytryptamine (5HT), started to increase just after recirculation reaching a level of over four times that of the control value at 2 to 3 hours, and then starting to decrease in the non-treated group. This decline in tryptophan was markedly facilitated by GHB administration within 1 hour. On the other hand, 5HT administration within 1 hour. On the other hand, 5HT increased only very slightly in the cerebral cortex 1 hour after GHB administration, the change ratio being 1/30 of tryptophan. It can therefore be speculated, that the decrease in tryptophan brought about by GHB administration is due to the improvement in disturbed protein synthesis rather than to stimulation of 5HT synthesis. Protein synthesis was studied by administering GHB 2 minutes prior to a 5-minute temporal common carotid artery occlusion. Ninety minutes after recirculation animals were given a single dose of 14C-leucine and further 60 minutes were allowed to pass before sacrifice. Autoradiographs of the GHB-treated group were compared with those of the non-treated group. With GHB pretreatment, autoradiographs showed an increased uptake of 14C-leucine in at least the hippocampus, thalamus, and hypothalamus, and in two out of three animals, there was diffusely increased uptake. Thus, it is speculated that GHB is effective in improving the protein synthesis in the postischemic period. The favorable function of GHB during cerebral ischemia is regarded by many to be prevention of energy failure by reducing cerebral metabolism. On the other hand, the results derived from the present study suggest that GHB may improve protein synthesis in the postischemic period. Thus, we suggest that GHB is useful if given at the acute stage of cerebral ischemia such as during internal carotid artery or middle cerebral artery occlusion.
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PMID:[Effects of gamma-hydroxybutyrate on monoamine metabolism and protein synthesis after transient global cerebral ischemia]. 140 58

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

1. A wide range of therapeutic strategies has been explored in humans and experimental animals with the aim of improving outcome after brain ischaemia but few have shown convincing clinical benefit. 2. The massive increase in the extracellular concentration of glutamate which occurs in cerebral ischaemia is a key component in the sequence of neurochemical events which leads to neuronal death. Pharmacological blockade of the action of glutamate at the N-methyl-D-aspartate (NMDA) receptor, (the glutamate receptor subtype principally involved in the neurotoxic effects of the amino acid) provides a novel therapeutic approach to cerebral ischaemia. 3. The effects of NMDA receptor antagonists in animal models of focal cerebral ischaemia are uniquely consistent, viz, a marked reduction in the amount of irreversible ischaemic damage irrespective of the species, the model of cerebral ischaemia, when the animals are sacrificed after the ischaemic episode, whether ischaemia is permanent or temporary and followed by reperfusion and which particular NMDA antagonist was employed. 4. NMDA receptor antagonists have marked effects on brain function in normal animals. The balance between these potential adverse effects and the anti-ischaemic efficacy of these drugs will ultimately determine the clinical utility of this class of drugs. 5. The data which are reviewed provide the basis for the current clinical evaluation of NMDA receptor antagonists in stroke and head trauma.
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PMID:Excitatory amino acid antagonists and their potential for the treatment of ischaemic brain damage in man. 141 72

U74006F, a novel 21-aminosteroid, is an inhibitor of iron-dependent lipid peroxidation that is devoid of glucocorticoid and mineralocorticoid side effects. The efficacy of U74006F in reducing cerebral infarct size was investigated in a rabbit model of thromboembolic stroke. Each animal received either U74006F (3.0 mg/kg immediately before and 2 hr after embolization, n = 8) or vehicle control (n = 10). Hematocrit, mean arterial pressure, PCO2, PO2, and pH were measured and controlled both before and after the administration of an autologous clot into one internal carotid artery. Regional cerebral blood flow (in ml/100 g/min, mean +/- SEM) measured by hydrogen clearance was similar in both groups, being reduced from 68.2 +/- 9.6 to 5.2 +/- 1.9 in the control group immediately after clot embolization and from 73.3 +/- 14.9 to 7.0 +/- 1.7 in the U74006F group. Four hours after embolization the brain was harvested and cerebral infarct size was determined using the triphenyl-tetrazolium chloride technique (% hemisphere, mean +/- SEM). In the U74006F-treated group, the infarct size was significantly reduced (P < 0.05) to 14.8 +/- 6.4 from a control value of 36.0 +/- 6.4. Additionally, cerebral blood flow values after embolization were consistently higher in the U74006F group, although the differences were not statistically significant. This data suggests that the 21-aminosteroid U74006F may have a protective effect in cerebral ischemia.
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PMID:The effect of the 21-aminosteroid U74006F in a rabbit model of thromboembolic stroke. 143 19

1. Studies in animal models of stroke have provided an invaluable contribution to our current understanding of the pathogenesis of cerebral ischaemia. The strengths of stroke research in animals are: 1) the ability to control the severity, duration, location and cause of the ischaemia, variables which confound interpretation of human stroke data; 2) co-existent disease states and variations in cerebrovascular anatomy are avoided; and 3) physiological parameters such as blood pressure, blood gases, temperature and plasma glucose (all of which influence the magnitude of the ischaemic lesion) can be closely monitored and controlled. Taking all these things on board, it is possible to induce a consistent focal ischaemic lesion in animal models of stroke (e.g. the permanent occlusion of the middle cerebral artery (MCA) in the rat). This has resulted in the wide use of animal models for assessment of anti-ischaemic drug efficacy as well as for research into the pathophysiological sequelae of stroke. 2. Traditionally focal ischaemia models involved permanent occlusion of a major cerebral artery such as the MCA. However, since vessel occlusion is seldom permanent in human stroke more recent developments have incorporated reperfusion (following ischaemia) into the design of the animal model. This has been achieved by reversible occlusion of cerebral vessels using 1) intraluminal filaments; 2) microclips; 3) the abluminal application of potent and prolonged vasoconstrictors; or 4) the introduction of emboli into the cerebral circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New models of focal cerebral ischaemia. 145 62

Our recent finding that less than 50% of late postendarterectomy strokes are related to recurrent carotid stenosis led us to question the utility of routine postendarterectomy duplex surveillance (RpCEADS) in the prevention of late stroke. To evaluate our RpCEADS program, we reviewed our postoperative duplex studies and correlated their results with clinical data. A total of 1053 postendarterectomy scans was carried out on 348 carotid arteries (258 patients) (3.0 +/- 0.1 studies/artery) during an average follow-up of 52.6 (+/- 2.3) months. Less than 50% of recurrent carotid stenosis was documented throughout follow-up in 292 (83.9%) of 348 arteries. Recurrent carotid stenosis of greater than 50% or occlusion of either the common or internal carotid artery was noted in the remaining 56 arteries (16.1%). Of the 56 duplex-detected recurrent stenoses, only two (3.6%) resulted directly in an unheralded stroke, whereas eight (14.3%) underwent prophylactic reoperation, eight (14.3%) resulted in transient ischemia requiring reoperation, eight (14.3%) occluded without causing stroke, and 29 (51.8%) remained asymptomatic and did not progress to occlusion. Assuming that each of our eight patients who underwent prophylactic reoperation would have had a stroke if operation had not been carried out and our two unheralded strokes could have been prevented with more rigorous follow-up, RpCEADS might have prevented late stroke related to 10 (2.9%) of 348 arteries in 10 (3.9%) of 258 patients after surgery. All other cases of duplex-detected recurrent carotid stenosis or occlusion were asymptomatic or manifest by transient cerebral ischemia. Therefore RpCEADS cannot be justified as a means of preventing late strokes related to recurrent stenosis.
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PMID:Routine postendarterectomy duplex surveillance: does it prevent late stroke? 146 Jul 21

In vivo NMR techniques are currently well established in pharmaceutical research and will likely become increasingly important in the future, as they procure noninvasively morphological, physiological, and biochemical information. The status of magnetic resonance imaging (MRI) and spectroscopy (MRS) in drug development is discussed on the basis of the characterization and evaluation of a rat model of ischemic stroke and the development and profiling of drugs for cerebral ischemia in this model. It can be concluded that MRI is well suited for drug screening (quantitative determination of lesion size), while dynamic MRI and MRS techniques provide relevant information on the mechanism of drug actions. The possibility to follow changes, pathological and therapeutic, in the same individual is important from two points of view. First, variations due to interindividual differences may be eliminated, increasing the statistical power of the results. Second, dose and/or time dependence of a drug can be explored in the same individual. As a result, the number of animals required for a study will be reduced, which from both ethical and economic aspects is highly desirable.
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PMID:In vivo NMR in pharmaceutical research. 146 Oct 65

We evaluated leucocyte aggregation in 26 patients with ischemic stroke and in 10 patients with transient ischemic attacks (TIA), previously untreated, within 24 h from the onset of symptoms. The evaluation was also performed in 30 healthy subjects matched for age and sex. Leucocyte aggregation was significantly higher in patients than in controls (p < 0.01 post hoc Tukey test). Within patients, those with stroke showed a significantly higher aggregation than those with TIA (p = 0.01 post hoc Tukey test). Moreover, stroke patients with the poorest outcome showed significantly higher values of leucocyte aggregation. These results indicate an involvement of leucocytes in cerebral ischemia and suggest that changes in their aggregability may play a role in the evolution of the disease.
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PMID:Leucocyte aggregation in acute cerebrovascular disease. 148 25

1. The effects of acute bilateral superior cervical ganglionectomy on cerebral blood flow and metabolism were investigated in stroke-prone spontaneously hypertensive rats (SHRsp), before and during cerebral ischaemia. 2. The resting cerebral blood flow was comparable between the control and denervated animals. 3. There was no significant difference in cerebral blood flow or concentration of tissue energy metabolites (adenosine triphosphate [ATP], lactate and pyruvate) between the sham-operated control and denervated animals during ischaemia. 4. The results suggest that sympathetic innervation of cerebral vessels originating from superior cervical ganglia may not play a major role in the progression of cerebral ischaemia in SHRsp.
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PMID:Effects of acute superior cervical ganglionectomy on cerebral blood flow and metabolism in stroke-prone spontaneously hypertensive rats subjected to cerebral ischaemia. 149 46


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