Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rapid occlusion of the middle cerebral artery (MCA) was undertaken in 5-6 week old rats to determine whether or not the young spontaneously hypertensive rat (SHR) or the normotensive Sprague-Dawley rat (SD) is protected against cerebral infarction by collateral circulation. Rats were killed 3 days after MCA occlusion and administration of Evans blue. As compared to SD, the SHR had elevated blood pressure prior to MCA occlusion, large cortical infarcts marked with Evans blue, and motor deficits contralateral to the occluded MCA. SHR did not develop an adequate collateral circulation, but SD were protected from infarction by it. Because the cerebral lesions were in young spontaneously hypertensive rats living prior to the established form of hypertension, the increased susceptibility to infarction was not secondary to it. Since normotensive rats usually do not infarct after sudden MCA occlusion, the infarction trait may be linked to the mechanism causing elevated blood pressure in spontaneously hypertensive rats.
Stroke
PMID:Different susceptibilities to cerebral infarction in spontaneously hypertensive (SHR) and normotensive Sprague-Dawley rats. 371 54

Severe hypertension in humans may lead to fibrinoid necroses of cerebral blood vessels with small hemorrhages and cystic necroses. Similar lesions have also been reported in the experimental model of stroke-prone spontaneously hypertensive rats (SHRSP). We examined the genesis and spreading pattern of the brain oedema in SHRSP. The extravasation of plasma proteins was visualized with the Evans-Blue or the immunoperoxidase method. Most commonly the leakage occurred in the grey matter of the cerebral cortex or basal ganglia. The spreading pattern followed that of vasogenic brain oedema with a local spread in the grey matter and an extensive one in the white matter. In addition, we detected a novel pathway upwards along the perivascular spaces of the penetrating vessels as well as laterally in the subpial zone. This route is likely to serve also as a drainage channel for the oedema into the cerebrospinal fluid in the subarachnoidal space. Transfer of the extravasated proteins from the white matter to the ventricles was also observed, confirming that this previously described pathway for the resolution of oedema fluid exists in the SHRSP model of vasogenic brain oedema.
 ...
PMID:The spread of brain oedema in hypertensive brain injury. 374 21

Nimodipine is a calcium slow channel blocker with several pharmacologic properties suggesting the potential to favorably modify outcome in focal cerebral ischemia. Thirty adult cats underwent unilateral middle cerebral artery (MCA) occlusion for 4 hours. Seventeen cats were treated with an ipsilateral intracarotid infusion of nimodipine (1 microgram kg-1 min -1) beginning 15 minutes before MCA occlusion and continuing throughout the occlusion period. Eight nimodipine treated cats maintaining MAP greater than 90 mmHg were assigned to a Higher Pressure Nimodipine (HPN) group. The remaining nine treated cats with MAP less than 90 mmHg were assigned to the Lower Pressure Nimodipine (LPN) group. Thirteen cats were untreated, receiving an isovolumetric amount of vehicle through the ipsilateral carotid artery. Local cerebral blood flow (ICBF) was continuously monitored using thermal diffusion probes. The brains, assessed for colloidal carbon perfusion, fluorescein and Evans blue staining, electroencephalographic activity (EEG), and histological changes, revealed no significant differences by any of these methods between the HPN and control animals with the exceptions of: HPN treated cats exhibited a preservation of EEG activity at 15 minutes post-occlusion compared to the untreated cats, and Post-ischemic surface colloidal carbon perfusion was better preserved in the treated cats than in the untreated cats. Mild hypotension, as demonstrated by the LPN group, negated these two positive effects. Prior to MCA occlusion, ICBF was bilaterally significantly increased after nimodipine infusion in the HPN group as compared to vehicle infusion. Intra-arterially infused nimodipine did not reduce infarct size.
Stroke
PMID:Effects of nimodipine on acute focal cerebral ischemia. 376 59

To study the effects of antithrombotic therapy in experimental stroke, we have characterized a baboon model of acute cerebrovascular thrombosis. In this model an inflatable silastic balloon cuff has been implanted by transorbital approach around the right middle cerebral artery (MCA), proximal to the take-off of the lenticulostriate arteries (LSA). Inflation of the balloon for 3 hours in six animals produced a stereotypic sustained stroke syndrome characterized by contralateral hemiparesis. An infarction volume of 3.2 +/- 1.5 cm3 in the ipsilateral corpus striatum was documented by computerized tomographic (CT) scanning at 10 days following stroke induction and 3.9 +/- 1.9 cm3 (n = 4) at 14 days by morphometric neuropathologic determinations of brain specimens fixed in situ by pressure-perfusion with 10% buffered formalin. Immediate pressure-perfusion fixation following deflation of the balloon was performed in 16 additional animals given Evans blue dye intravenously prior to the 3 hour MCA balloon occlusion. Light microscopy and transmission electron microscopy consistently confirmed the presence of thrombotic material occluding microcirculatory branches of the right LSA in the region of Evans blue stain, but not those of the contralateral corpus striatum. When autologous 111In-platelets were infused intravenously in four animals from the above group prior to the transient 3 hour occlusion of the right MCA, gamma scintillation camera imaging of each perfused-fixed whole brain demonstrated the presence of a single residual focus of 111In-platelet activity involving only the Evans blue-stained right corpus striatum. Focal right hemispheric activity was equivalent to 0.55 +/- 0.49 ml of whole blood, and the occlusion score derived from histologic examination of the microcirculation of the Evans blue-stained corpus striatum averaged 34.8 +/- 2.8. Similar 111In-platelet imaging and histologic scoring experiments carried out in four animals pretreated with the antithrombotic combination heparin and ticlopidine showed marked reduction of both 111In-platelet activity (0.01 +/- 0.03 ml vs. 0.55 +/- 0.49 ml; p less than 0.01) and thrombotic occlusion of the microcirculation (10.8 +/- 7.4 units vs. 34.8 +/- 2.8 units; p less than 0.01) in the right corpus striatum following 3 hours of MCA occlusion. In separate control experiments 111In-labeled autologous platelets were infused after the 3 hour period of right MCA occlusion and subsequent balloon deflation in two animals; no focus of 111In-platelet activity was demonstrated in fixed whole brain.(ABSTRACT TRUNCATED AT 400 WORDS)
Stroke
PMID:Experimental acute thrombotic stroke in baboons. 381 Jul 30

In this study we determined whether the decline in exercise stroke volume (SV) observed when endurance-trained men stop training for a few weeks is associated with a reduced blood volume. Additionally, we determined the extent to which cardiovascular function could be restored in detrained individuals by expanding blood volume to a similar level as when trained. Maximal O2 uptake (VO2max) was determined, and cardiac output (CO2 rebreathing) was measured during upright cycling at 50-60% VO2max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692 ml; P less than 0.01) during upright exercise, due primarily to a 12% lowering (P less than 0.01) of plasma volume (PV; Evans blue dye technique). SV was reduced by 12% (P less than 0.05) and VO2max declined 6% (P less than 0.01), whereas heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P less than 0.01) and 8% (P less than 0.05), respectively. When blood volume was expanded to a similar absolute level in the trained and detrained state (approximately 5,500 +/- 200 ml) by infusing a 6% dextran solution in saline, the effects of detraining on cardiovascular response were reversed. SV and VO2max were increased (P less than 0.05) by PV expansion in the detrained state to within 2-4% of trained values. Additionally, HR and TPR during submaximal exercise were lowered to near trained values. These findings indicate that the decline in cardiovascular function following a few weeks of detraining is largely due to a reduction in blood volume, which appears to limit ventricular filling during upright exercise.
 ...
PMID:Effects of detraining on cardiovascular responses to exercise: role of blood volume. 394 49

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
Stroke
PMID:Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia. 400 66

The present studies were performed to determine whether cerebral edema will develop as a consequence of arterial hypertension and/or craniectomy. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta, and a parietal craniectomy was performed. The cerebral edema noticed was evaluated by macroscopic and microscopic observations, BBB permeability of HRP and Evans blue and water content. In addition, ICP was measured in the cisterna magna and ICPP by a catheter-tip transducer. In arterial hypertension or craniectomy alone, some small areas of Evans blue extravasation with increased water content were seen in the cortex, which corresponded to the occipito-parietal parts of the arterial boundary zones. In contrast, when arterial hypertension was combined with craniectomy, these lesions extended further into underlying white matter with increased water content. Forty-eight hours later, extensive brain edema with a shift of midline structures developed on the side of craniectomy which differed from that in arterial hypertension or craniectomy alone. It is suggested that some hydrostatic pressure gradients, particularly between blood vessel and surrounding extracellular space and among different areas within the brain parenchyma, may play an important role in the development of brain edema.
Stroke
PMID:Cerebral edema associated with craniectomy and arterial hypertension. 402 78

Topographic distribution of barrier function in normal canine cervico-cephalic arteries was studied using horseradish peroxidase (HRP) and Evans blue as tracers. The carotid sinus of the internal carotid artery (ICA) was conspicuously permeable to HRP when compared to other areas of major cervical arteries. The cavernous portion of the ICA also showed prominent permeation of HRP, especially through the outer surface, which is covered with venous endothelial cells. On the luminal side of the cavernous portion of the ICA, barrier deficiency was noted at angulated segments such as the carotid siphon. Intracranial segments of both ICA and vertebral arteries demonstrated incomplete barrier function of the first 1 to 4 mm from the origin of the intradural segments. These areas were considered to be transitional sites in barrier function between extra- and intracranial arteries. Focal, but definite, barrier disruption was also noted at the distal ends of the ICA and other arterial branching sites of major intracranial arteries. While opening of the interendothelial junctions was considered to be one of the mechanisms causing increased permeability in the cavernous ICA, the mechanisms for the permeation of HRP into the major cerebral arteries could not be confirmed ultrastructurally.
Stroke
PMID:Topographical distribution of barrier function in cervico-cephalic arteries of dog. Major cerebral arteries possess definite barrier function? 404 52

The cerebrovascular lesions of severe chronic hypertension were studied by light microscopy in perfusion-fixed, subserially sectioned brains from stroke-prone spontaneously hypertensive rats (SHRSP). The leakage and spread of plasma proteins were visualized by immunohistochemical detection of extravasated fibrinogen and by using an exogenous marker (Evans blue injected i.v.) for blood-brain barrier (BBB) dysfunction. In most SHRSP the hypertension did not lead to major BBB lesions in spite of a mean arterial pressure around 200 mm Hg at 6-9 months of age. Multifocal BBB damage occurred in a minor group of SHRSP, particularly within the cortex and the deep gray matter. A close spatial correlation was found between the leakage-spread of plasma constituents and the neuropathologic alterations. Fibrinoid degeneration of penetrating arterioles was found within the leakage sites. The surrounding gray matter showed petechial hemorrhages and abundant proteinaceous exudates rich in antifibrinogen-positive material. The current leakage of Evans blue and wide spread of fibrinoid substances suggested long-lasting damage to the BBB. Most neurons within the edematous gray matter had well preserved nuclei surrounded by a rim of cytoplasm with ill-defined outline as if vacuolation or lysis of the peripheral cytoplasm had occurred. The sponginess of the tissue progressed in severe cases to formation of necrotic cysts. Condensed acidophilic neurons were seen in the border zone between the edematous and more compact gray matter. The appearance and distribution of the gray matter lesions deviated in many respects from those commonly seen in regional ischemic infarcts. The fibrin thrombi found close to the cysts might be regarded as secondary events. The extensive spread of antifibrinogen-positive material within the white matter seemed to originate mainly from the chronic leakage sites in the gray matter. Increased number of large astrocytes were seen within the leakage sites and along the spreading pathways for the edema constituents. The white matter showed a rarefied texture with widely dispersed nerve fiber tracts, volume expansion, and occasional cyst formation. The results indicate a crucial pathophysiologic role for the egress, spread, and accumulation of vasogenic edema in the development of the cerebrovascular lesions in SHRSP.
 ...
PMID:Cerebrovascular lesions in stroke-prone spontaneously hypertensive rats. 409 Sep 40

The object of this investigation was to study the effects of prostacyclin (PGI2) upon the evolution of acute focal cerebral ischemia in the cat. Twenty-five fasted adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion. Eleven cats received an intracarotid infusion of PGI2 in buffered saline pH 10.5 (100 ng/kg/min at 0.01 ml/kg/min), and 11 cats received intracarotid buffered saline pH 10.5 (0.01 ml/kg/min) without therapeutic agents. Treatment with PGI2 was started upon MCA occlusion and continued for 6 hours. Thirty minutes prior to perfusion, the animals were given fluorescein and Evans blue by intravenous injection. The cats were perfused-fixed in vivo with carbon and buffered formalin 6 hours after MCA occlusion. Another 3 cats received tritium labeled intracarotid PGI2, and peripheral venous samples were collected and assayed for PGI2 plasma levels. Mean arterial pressure was stable in PGI2 treated animals during 6 hours of MCA occlusion, while untreated cats had significant progressive hypertension during that period. The rCBF (measured by the intracarotid 133Xe method) decreased markedly in all animals immediately upon MCA occlusion. However, untreated animals had a significant progressive improvement in rCBF during the occlusion period, while PGI2 treated animals had no such improvement. Quantitative EEG changes, gross edema, areas of fluorescein extravasation, patterns of carbon perfusion, and infarct size were not significantly different in the two groups. While most untreated animals had marked Evans blue extravasation after 6 hours of MCA occlusion, most PGI2 treated animals had no such extravasation, indicating some protection of the blood-brain barrier in these animals.
Stroke
PMID:Treatment of acute focal cerebral ischemia with prostacyclin. 634 Feb 54


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>