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

Activities of catalase, superoxide dismutase, glyceraldehyde phosphatedehydrogenase and glucose-6-phosphate dehydrogenase implicated in the process of hemoglobin oxygenation were studied and compared in 40 patients with ischemic and in 30 patients with hemorrhagic brain strokes in the most acute disease period (days 1-2). A well-defined relationship was revealed between the brain stroke pattern and enzymatic activity which is likely to be determined by varying degree of body adaptation under hypoxia developing in ischemic and hemorrhagic brain strokes. It is assumed that the clinico-enzymatic correlations discovered might be employed as additional criteria in the differential diagnosis of the brain stroke pattern.
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PMID:[Value of the study of various erythrocyte enzymes in determining the nature of cerebral stroke in the acute period]. 217 84

The goal was to describe the metabolic profile of ganglionic and cortical arteries and arterioles in aging normotensive male rats. Five enzymes indicative of key metabolic pathways in the vessel walls were semiquantitatively evaluated using bright-field histochemical microscopy. Lactate dehydrogenase showed significant reactivity which increased with vessel diameter in cortical and ganglionic vessels in all age groups tested. Succinate dehydrogenase and cytochrome oxidase showed little reactivity in both cortical and ganglionic vessels, suggesting a reduced role for aerobic metabolic pathways. Myosin ATPase reactivity was high in cortical and ganglionic vessels. Only this enzyme showed an increased reactivity that was correlated with the age and diameter of the vessel. Glucose-6-phosphate dehydrogenase reactivity was more pronounced in cortical than ganglionic vessels, suggesting that the hexose-monophosphate-shunt may be more active in the cortical vessels. There were no regional differences in enzyme reactivity throughout the caudatoputamen. In conclusion, both the cortical and ganglionic vessels are metabolically active, with significant anaerobic glycolysis, and reduced, but observable capacity for aerobic metabolism. The decreased myosin ATPase reactivity and the low level of glucose-6-phosphate dehydrogenase reactivity in the ganglionic arterioles of senescent rats may contribute to the susceptibility of these vessels to cerebrovascular accidents.
Stroke
PMID:A histochemical study of cerebral cortical vessels and ganglionic vessels of the caudatoputamen in aging normotensive rats. 315 35

We studied energy metabolism after experimental subarachnoid hemorrhage in rats. Four different cerebral areas were tested: frontal cortex, occipital cortex, hippocampus, and brainstem. Vmax of the following enzymatic activities was evaluated: in the homogenate: hexokinase, phosphofructokinase, and lactate dehydrogenase for the glycolytic pathway, and glucose-6-phosphate dehydrogenase for the hexose monophosphate shunt; in the purified nonsynaptic mitochondria: NAD+-isocitrate dehydrogenase, citrate synthase, and succinate dehydrogenase for the Krebs cycle, and cytochrome oxidase for the electron transfer chain. We also evaluated some parameters related to the respiration of nonsynaptic mitochondria (State 3, State 4, uncoupled state, respiratory control ratio, and ADP:O ratio). Subarachnoid hemorrhage did not significantly affect Vmax of the enzymatic activities related to anaerobic and aerobic metabolism; however, mitochondrial respiration was affected, particularly in the presence of NADH-producing substrates (glutamate + malate).
Stroke 1988 Mar
PMID:Bioenergetics of different brain areas after experimental subarachnoid hemorrhage in rats. 335 25

The effects of 1 microgram/mL of vanadium, given for 12 mo as sodium metavanadate in drinking water, on cardiovascular and biochemical indices of male rabbits were investigated. At the end of the exposure period, vanadium was more accumulated in bones and kidneys than in spleen and liver; the cardiac ventricles and the aorta contained similar amounts of this element. Blood pressure and heart rate were unchanged in the vanadate-exposed animals since the observed decrease of both cardiac inotropism and stroke volume was counteracted by an increase of peripheral vascular resistance, with reduction of arterial blood flow. The arterial levels of sodium, potassium and aldosterone were unmodified by vanadate which, however, strongly raised those of noradrenaline, adrenaline, L-DOPA, and dopamine. Vanadate caused a marked increase of the activity of monoamine oxidase in renal tubules and liver (probably in relation to the increased plasma catecholamine levels) and a reduction of that of glucose-6-phosphate dehydrogenase in the kidney. There was also evidence that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. It was concluded that vanadium may represent an environmental factor of altered cardiovascular homeostasis.
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PMID:Vanadate as factor of cardiovascular regulation by interactions with the catecholamine and nitric oxide systems. 883 75

Stroke, or ischaemic brain damage, is of great geriatric importance being the third most common cause of death after cancer and heart diseases in developed countries. Despite such high frequency, its management has received inadequate attention. Many studies have shown the role of free radicals in the pathogenesis of ischaemic brain damage. Search for safe and effective antioxidant and free radial scavenger agents, therefore, appear to be a promising approach for stroke therapy. Gold, widely used in modern medicine for the treatment of rheumatoid arthritis, is highly valued for various medicinal uses in Indian systems of medicine. Traditional gold preparations are attributed with tonic/rejuvenating and antioxidant properties. Our earlier studies revealed interesting analgesic, immunostimulant, adaptogenic and glycogen sparing properties in these preparations, but their effects in cerebral ischaemia have not been investigated. This prompted us to initiate the present study using global and focal models of ischaemia in albino rats. Enzymatic parameters (lipid peroxidase, reduced glutathione, catalase, glutathione reductase, glutathione-S-transferase, glutatione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase) were employed to assess ischaemic brain damage and its modulation. Significant restoration of altered values to near normal levels by Ayurvedic Swarna Bhasma and Unani Kushta Tila Kalan (25 mg/kg, orally for 10 days), suggest potentials for gold preparations in cerebrovascular diseases. The preparations deserve more scientific attention for possible therapeutic exploitation.
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PMID:Antioxidant/restorative effects of calcined gold preparations used in Indian systems of medicine against global and focal models of ischaemia. 1207 6

We intended to determine whether or not dietary canola oil (CO) elevates plasma lipids and oxidative stress, since both of these are, possibly, related to the CO-induced life shortening through exacerbation of hypertension-associated vascular lesions found in stroke-prone spontaneously hypertensive rats (SHRSP). Spontaneously hypertensive rats (SHR) were used in this study to avoid a potential bias in the results due to the irregular death by stroke seen in SHRSP. SHR were fed for 26 weeks on a chow containing either, 10 wt/wt% of CO or soybean oil (SO), i.e., the control. Elevated plasma lipids and glucose-6-phosphate dehydrogenase (G6PD) activation in the liver and erythrocyte were found in SHR fed CO compared to that fed SO, while anti-oxidative enzymes other than G6PD were not activated. The CO diet brought about significant vascular lesions in the kidney, in which abundant cyclooxygenase-2 (COX-2) positive foci were immunochemically located in the juxtaglomerular apparatus. These results suggest that dietary CO induces a hyperlipidemic condition, in which G6PD may serve as an NADPH provider, and aggravates genetic diseases in SHR (also, probably, in SHRSP). The increased COX-2 expression indicates a role of renin-angiotensin-aldosterone system activation in the increased vascular lesions, whereas the effects of oxidative stress remain unclear.
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PMID:Different effects of 26-week dietary intake of rapeseed oil and soybean oil on plasma lipid levels, glucose-6-phosphate dehydrogenase activity and cyclooxygenase-2 expression in spontaneously hypertensive rats. 1850 77

Asia, the largest continent in the world, is heterogeneous in the ethnic, socioeconomic, and developmental status of its populations. A vast majority of it is poor with no adequate access to modern health care, making an accurate estimation of the nature and extent of acute kidney injury (AKI) difficult. Community-acquired AKI in otherwise healthy individuals is common, and the population developing AKI is younger compared with its counterparts in Europe or North America. The etiologic spectrum varies in different geographic regions of Asia depending on environmental, cultural, and socioeconomic factors. Some of the etiologic factors include AKI in relation to infectious diseases, intravascular hemolysis caused by glucose 6-phosphate dehydrogenase deficiency, poisonings caused by industrial chemicals or copper sulphate, animal venoms, natural medicines, heat stroke, and after complications of pregnancy. Preventive opportunities are missed because of failure to recognize the risk factors and early signs of AKI. Patients often present late for treatment, leading to multi-organ involvement and increased mortality. The exact etiologic diagnosis cannot be established in many instances because of a lack of appropriate laboratory support. Modern methods of renal replacement therapy are not universally available; and intermittent peritoneal dialysis is still widely practiced in many areas.
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PMID:Community-acquired acute kidney injury in Asia. 1862 Sep 56

Canola oil (CO) given as a dietary fat deteriorates hypertension-related condition and shortens the life of stroke-prone spontaneously hypertensive rats (SHRSP). Although substances other than fatty acids have been presumed as causatives, CO mimics consisting of oils other than CO also shorten the life. In this study we intended to examine whether or not fatty acid composition unique to CO participates in the adverse effect. CO or an interesterified CO mimic (ICOM) consisting of safflower oil, flaxseed oil and erucic acid was fed as a dietary fat for 13 weeks to Wistar Kyoto (WKY) rats, and clinical and pathological signs were compared. WKY rats were used to avoid the difficulty in evaluating the results in SHRSP due to irregular deterioration in conditions by stroke. Compared to a standard diet, both diets containing CO or ICOM similarly elevated blood pressure, increased plasma lipids, activated hepatic glucose-6-phosphate dehydrogenase, decreased platelets, shortened blood coagulation times and induced abnormalities in the kidney. Thus, CO-specific fatty acid composition appeared to affect the pathophysiology of the rat and produce consequent aggravation of pathological status, especially in SHRSP. However, the existence of causative factors other than fatty acids was suggested by increased neutrophil count exclusively induced by CO.
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PMID:Similar changes in clinical and pathological parameters in Wistar Kyoto rats after a 13-week dietary intake of canola oil or a fatty acid composition-based interesterified canola oil mimic. 1902 30

Free radicals are known to cause secondary neuronal damage in cerebral ischemia/reperfusion (I/R). We investigated here the neuroprotective effect of resveratrol, a potent antioxidant present in grape seed, against cerebral I/R-induced mitochondrial dysfunctions in hippocampus. Transient rat middle cerebral artery occlusion (MCAO) model of brain ischemia was used to induce brain infarction. Resveratrol (10(-7) g/kg) was given twice intravenously: 15 min pre-occlusion and at the time of reperfusion (2 h post-occlusion). Resveratrol significantly restored ATP content and the activity of mitochondrial respiratory complexes in resveratrol treated group which were severely altered in MCAO group. Western blot analysis showed a marked decrease in cytochrome c release as a result of resveratrol treatment. Electrophoretic migration of hippocampal genomic DNA showed a marked decrease in DNA fragmentation after resveratrol treatment. Notably, expression of Hsp70 and metallothionein (MT) was significantly higher in MCAO group but their expression was more significant in resveratrol treated group. The status of mitochondrial glutathione (GSH), glucose 6-phosphate dehydrogenase (G6-PD) and serum lactate dehydrogenase (LDH) was restored by resveratrol treatment with a significant decrease in mitochondrial lipid peroxidation (LPO), protein carbonyl and intracellular H(2)O(2) content. Resveratrol significantly improved neurological deficits assessed by different scoring methods. Also, the brain infarct volume and brain edema were significantly reduced. Histological analysis of CA1 hippocampal region revealed that resveratrol treatment diminished intercellular and pericellular edema and glial cell infiltration. The findings of this study highlight the ability of resveratrol in anatomical and functional preservation of ischemic neurovascular units and its relevance in the treatment of ischemic stroke.
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PMID:Resveratrol exerts its neuroprotective effect by modulating mitochondrial dysfunctions and associated cell death during cerebral ischemia. 1902 23

Ischemic brain is highly vulnerable to free radicals mediated secondary neuronal damage especially mitochondrial dysfunctions. Present study investigated the neuroprotective effect of S-allyl L-cysteine (SAC), a water soluble compound from garlic, against cerebral ischemia/reperfusion (I/R)-induced mitochondrial dysfunctions in hippocampus (HIP). We used transient rat middle cerebral artery occlusion (MCAO) model of brain ischemia. SAC (300 mg/kg) was given twice intraperitoneally: 15 min pre-occlusion and 2 h post-occlusion at the time of reperfusion. SAC significantly restored ATP content and the activity of mitochondrial respiratory complexes in SAC treated group which were severely altered in MCAO group. A marked decrease in calcium swelling was observed as a result of SAC treatment. Western blot analysis showed a marked decrease in cytochrome c release as a result of SAC treatment. The status of mitochondrial glutathione (GSH) and glucose 6-phosphate dehydrogenase (G6-PD) was restored by SAC treatment with a significant decrease in mitochondrial lipid peroxidation (LPO), protein carbonyl (PC) and H2O2 content. SAC significantly improved neurological deficits assessed by different scoring methods as compared to MCAO group. Also, the brain edema was significantly reduced. The findings of this study suggest the ability of SAC in functional preservation of ischemic neurovascular units and its therapeutic relevance in the treatment of ischemic stroke.
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PMID:S-allyl L-cysteine diminishes cerebral ischemia-induced mitochondrial dysfunctions in hippocampus. 1940 Nov 83


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