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

The cerebrovascular permeability quantitatively determined by the retention of 131I-human albumin in the perfused brains was increased in SHR, especially in stroke-prone SHR compared with normotensive Wistar-Kyoto, and confirmed the macroscopical or microscopical findings on the leakage into the brain or trypan blue or peroxidase injected intravenously 2 to 3 hours before sacrifice. The localization of increased vascular permeability in SHR corresponded to the predilection sites of cerebral hemorrhage or softening, which developed likely following the increased cerebrovascular permeability.
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PMID:Experimental studies on the pathogenesis and prophylaxis of stroke in stroke-prone spontaneously hypertensive rats (SHR).(1) Quantitative estimation of cerebrovascular permeability. 115 93

Cerebrovascular permeability in stroke-prone spontaneously hypertensive rats (SHR) at various ages was histologically studied using horseradish peroxidase as a tracer and such was related to the cerebrovascular lesions in the animals. An increase in permeability was demonstrated in the brain of SHR, particularly in those animals with an extremely high blood pressure. Increased cerebrovascular permeability occurred in some animals without any organic vascular change or severe parenchymal changes, although edema was present. Histologically, the SHR brain with an increase in permeability showed mild focal edema, rarefaction of tissue and necrosis with cyst formation. Thus a transitional progress was evident. Localization of the increase in permeability corresponded well with the predilection sites of cerebrovascular lesions in SHR. Constrictions and dilatations of intracerebral arterioles and small arteries were also demonstrated by the peroxidase method, and the dilated arterial walls did reveal a darker staining. From these results it is strongly suggested that certain cerebrovascular lesions, especially necrosis with cyst formation in SHR are sequelae of the increased cerebrovascular permeability caused by a chronic hypertensive state.
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PMID:Changes in vascular permeability in stroke-prone spontaneously hypertensive rats studied with peroxidase as a tracer. 119 27

Eosinophilic endocarditis is a potentially lethal complication of chronic peripheral blood hypereosinophilia. We hypothesized that eosinophil peroxidase (EPO), an abundant eosinophil (EO) cationic granule protein, promotes eosinophilic endocarditis by binding to negatively charged endocardium, and there generating cytotoxic oxidants. Using an immunocytochemical technique, we demonstrated endocardial deposition of EPO in the heart of a patient with hypereosinophilic heart disease. Because EPO preferentially oxidizes Br- to hypobromous acid (HOBr) rather than Cl- to hypochlorous acid (HOCl) at physiologic halide concentrations, we characterized the Br(-)-dependent toxicity of both activated EOs and purified human EPO towards several types of endothelial cells and isolated working rat hearts. In RPMI supplemented with 100 microM Br-, phorbol myristate acetate-activated EOs, but not polymorphonuclear leukocytes, caused 1.8-3.6 times as much 51Cr release from four types of endothelial cell monolayers as in RPMI alone. H2O2 and purified human EPO, especially when bound to cell surfaces, mediated extraordinarily potent, completely Br(-)-dependent cytolysis of endothelial cells that was reversed by peroxidase inhibitors, HOBr scavengers, and competitive substrates. We further modeled eosinophilic endocarditis by instilling EPO into the left ventricles of isolated rat hearts, flushing unbound EPO, then perfusing them with a buffer containing 100 microM Br- and 1 microM H2O2. Acute congestive heart failure (evidenced by a precipitous decrement in rate pressure product, stroke volume work, aortic output, and MVO2 to 0-33% of control values) ensued over 20 min, which deletion of EPO, Br-, or H2O2 completely abrogated. These findings raise the possibility that EPO bound to endocardial cells might utilize H2O2 generated either by overlying phagocytes or endogenous cardiac metabolism along with the virtually inexhaustible supply of Br- from flowing blood to fuel HOBr-mediated cell damage. By this mechanism, EPO may play an important role in the pathogenesis of eosinophilic endocarditis.
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PMID:Bromide-dependent toxicity of eosinophil peroxidase for endothelium and isolated working rat hearts: a model for eosinophilic endocarditis. 198 18

The activity of peroxidases and the level of myeloperoxidase in the bone marrow of spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHR-SP) were determined in comparison with normotensive Wistar Kyoto rats (WKY). In the cetyltrimethylammonium bromide extract of bone marrow, the peroxidase activities using guaiacol or Kl as the electron donor of male and female WKY were different from those of SHR and SHR-SP. The peroxidase activity was also separately determined as myeloperoxidase and eosinophil peroxidase by the use of ion-exchange high pressure liquid chromatography. In males, SHR and SHR-SP contained a low activity of eosinophil peroxidase compared with WKY. Bone marrows of female SHR and SHR-SP contained a lower activity of myeloperoxidase, while SHR and SHR-SP possessed a higher activity of eosinophil peroxidase compared with WKY. No change of the level of myeloperoxidase in the bone marrow was observed among male animals. A significant decrease in the level of myeloperoxidase was observed in female SHR and SHR-SP. Therefore, these results indicate that the change in the activity of the peroxidases in the bone marrow is accompanied by the spontaneously hypertensive state.
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PMID:Bone marrow peroxidases of spontaneously hypertensive rats. 216 64

In members of the families whose parents had atherosclerosis complicated by macrofocal myocardial infarction or stroke, the serum level of lipid peroxidation products was correlated to enzymatic activity of neutrophil and red blood cells oxidation-antioxidation. In persons with hereditary predisposition to atherosclerosis both with clinical signs of atherosclerosis and phenotypically healthy against the control group there was elevated content of plasma acylhydroperoxides and hypoactivity of neutrophil myeloperoxidase. Determination of lipid peroxidation products by malonic dealdehyde showed this parameter to be higher in members of the families of the study group and in those with cardiovascular disorders. For those whose parents had atherosclerosis versus control subjects there were no differences in the activity of superoxide dismutase, glutation peroxidase and catalase in the blood red cells. Shifts in lipid peroxidation and activity of blood myeloperoxidase are identical in type and may represent a pathogenetic ling in formation of hereditary predisposition to cardiovascular disorders of atherosclerotic origin, the detection of which becomes feasible in a subclinical period.
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PMID:[Indicators of lipid peroxidation in the blood in hereditary predisposition to arteriosclerosis]. 233 43

We recorded regional cerebral blood flow, somatosensory evoked potentials, and auditory evoked potentials in the thalamic relay nuclei (ventral posterior lateral nucleus and medial geniculate body) and in the somatosensory and auditory cortices during and after 1 hour of transient left middle cerebral artery occlusion in nine cats. Regional cerebral blood flow was also measured in the thalamocortical tracts of five of these cats. Additionally, the integrity of thalamocortical connections was tested by retrograde labeling of the thalamic nuclei with horseradish peroxidase in eight cats (three of which experienced no ischemia). Regional cerebral blood flow was severely reduced during middle cerebral artery occlusion in the left primary auditory cortex (8.5 ml/100 g/min) and in white matter pathways (6.4-7.6 ml/100 g/min). In contrast, regional cerebral blood flow did not change significantly in the somatosensory cortex or in either thalamic nucleus. Evoked potentials were abolished in both cortices but remained unchanged in the thalamic nuclei. Cortical somatosensory evoked potentials disappeared 5-8 minutes later than auditory evoked potentials. Recirculation after 1 hour of ischemia resulted in rapid and almost complete recovery (94%) of somatosensory evoked potentials and little recovery (18.4%) of auditory evoked potentials. We conclude that in the auditory pathway both cortical and fiber tract ischemia are (perhaps synergistically) responsible for dysfunction, while in the somatosensory cortex evoked potentials are abolished due to white matter ischemia. The delayed disappearance and better recovery of somatosensory than of auditory evoked potentials indicate that ischemic tolerance is higher in fiber tracts than in cortex.
Stroke 1990 Jun
PMID:Functional impairment due to white matter ischemia after middle cerebral artery occlusion in cats. 234 96

We studied disruption of the blood-brain barrier after experimental subarachnoid hemorrhage induced by an injection of 4 ml autologous arterial blood into the cisterna magna of rabbits. The animals were killed at 40 minutes, 6 hours, 1 day, 2 days, 4 days, or 6 days after subarachnoid hemorrhage. We assessed the integrity of the barrier function of intraparenchymal vessels in the ventral brain stem and cerebral hemispheres morphologically with transmission electron microscopy, using horseradish peroxidase as a tracer. In the ventral brain stem, which was in direct contact with the cisternal clots, markedly increased peroxidase staining toward the core of the brain stem was observed on the first day after subarachnoid hemorrhage. In an area of the cerebral hemispheres distant from the clots, barrier disturbance was prominent in the 6-hour specimens, and permeation of the tracer was spotty. From the distribution and morphological findings of these lesions, permeability changes in the ventral brain stem may have been caused by a direct effect of the cisternal clots; in the cerebral hemispheres, hemodynamic factors and changes in intracranial pressure associated with the elderly stages of subarachnoid hemorrhage seemed to be responsible. These results suggest that barrier disturbance associated with subarachnoid hemorrhage may be multifactorial in time course and location.
Stroke 1990 Jul
PMID:Blood-brain barrier disturbance following subarachnoid hemorrhage in rabbits. 236 6

We studied functional disturbances following left middle cerebral artery occlusion in rats. Neuronal function was evaluated by [14C]2-deoxyglucose autoradiography 1 day after occlusion. We analyzed the mechanisms of change in glucose utilization outside the infarct using Fink-Heimer silver impregnation, axonal transport of wheat germ agglutinin-conjugated-horseradish peroxidase, and succinate dehydrogenase histochemistry. One day after occlusion, glucose utilization was remarkably reduced in the areas surrounding the infarct. There were many silver grains indicating degeneration of the synaptic terminals in the cortical areas surrounding the infarct and the ipsilateral cingulate cortex. Moreover, in the left thalamus where the left middle cerebral artery supplied no blood, glucose utilization significantly decreased compared with sham-operated rats. In the left thalamus, massive silver staining of degenerated synaptic terminals and decreases in succinate dehydrogenase activity were observed 4 and 5 days after occlusion. The absence of succinate dehydrogenase staining may reflect early changes in retrograde degeneration of thalamic neurons after ischemic injury of the thalamocortical pathway. Terminal degeneration even affected areas remote from the infarct: there were silver grains in the contralateral hemisphere transcallosally connected to the infarct and in the ipsilateral substantia nigra. Axonal transport study showed disruption of the corticospinal tract by subcortical ischemia; the transcallosal pathways in the cortex surrounding the infarct were preserved. The relation between neural function and the neuronal network in the area surrounding the focal cerebral infarct is discussed with regard to ischemic penumbra and diaschisis.
Stroke 1989 Sep
PMID:Neuronal network disturbance after focal ischemia in rats. 247 23

The ultrastructure and permeability of retinal arterioles, venules, and capillaries located near the optic disc of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats were studied using electron microscopy and tracer cytochemistry. A variety of structural changes were observed in arterioles of SHRSP. They include (1) narrowing of the lumen due to smooth muscle hyperplasia and/or fragmentation and thickening of the basal lamina, (2) fusiform aneurysms containing degenerated smooth muscle cells and reduplicated basal lamina, and (3) the presence of microfilament bundles under the luminal surface of the endothelium. In addition, the wall of venules was thickened due to accumulation of basal lamina material. Many capillary pericytes were also degenerated. Retinal vessels of age-matched normotensive rats did not show such changes. In SHRSP, after injection of peroxidase, extravasation of tracer was seen occasionally in retinal capillaries and in the central retinal vein at the optic nerve head. No changes in vascular permeability were observed in the normotensive rats.
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PMID:Ultrastructural and permeability characteristics of retinal vessels in stroke-prone spontaneously hypertensive rats. 320 83

We have tested the hypothesis that blood-borne substances released from a site of vascular thrombosis can lead to acute alterations in the blood-brain barrier. The right common carotid artery of rats was photothrombosed using a dye/light insult. Rats were given the photosensitizing dye rose bengal and irradiated for 4 minutes with an argon laser beam focused onto the exposed common carotid artery. During the irradiation, 3 ml of blood was taken from the right external carotid artery. After 10 minutes, the blood was infused into the external carotid artery of a recipient rat that had received horseradish peroxidase. Fifteen minutes after blood infusion, bilateral peroxidase extravasation was noted within cortical and subcortical areas of recipient rats, being most intense ipsilaterally. Ultrastructural studies demonstrated peroxidase reaction product within numerous endothelial vesicles of arteriolar segments. Infusion of blood from control rats did not produce similar changes. Thus, photoinduced vascular thrombosis of a large feeding artery leads to the formation of blood-borne factors that acutely alter cerebral vascular permeability.
Stroke 1988 Jul
PMID:Photochemically stimulated blood-borne factors induce blood-brain barrier alterations in rats. 338 56


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