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

While oxygen-derived free radicals have been implicated in the pathogenesis of myocardial injury, the exact nature of this injury is still unclear. To test the hypothesis that oxygen-induced injury may influence the recovery of cardiac function from ischemic damage, we used an oxygen free radical scavenger, superoxide dismutase (SOD), together with catalase, during the reperfusion of isolated canine heart which had been subjected to 15 min of normothermic ischemic arrest followed by 2 hr of hypothermic cardioplegic preservation using a modified Collins solution. Determinations of thiobarbituric acid reactive substances and coenzyme Q10 within the myocardium showed that the treatment with SOD and catalase was capable of inhibiting lipid peroxidation induced by reperfusion. This inhibition was apparently associated with the improvement of myocardial energy metabolism and cardiac performance. Coronary flow was significantly higher in the heart treated with SOD and catalase during the working stage with a corresponding increase in oxygen consumption. Myocardial adenosine triphosphate (ATP) was partially, but significantly restored during reperfusion in these hearts whereas no restoration was observed in the heart without the enzymes. The treatment with SOD and catalase also improved left ventricular stroke work index and left ventricular maximum dp/dt at an early stage of the working mode. These results suggest that the use of SOD and catalase during reperfusion can protect the ischemic heart against reperfusion injury by scavenging oxygen-derived free radicals.
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PMID:Protection against oxygen-induced reperfusion injury of the isolated canine heart by superoxide dismutase and catalase. 376 23

We examined the relationship between the biological protective mechanisms of scavengers and free radicals that are elicited by subarachnoid hemorrhage (SAH) in the pathogenesis of prolonged vasospasm following ruptured intracranial aneurysm. The study included 25 patients treated by early surgery (within 72 hours after SAH). Lipid peroxides concentrations and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px) in the cerebrospinal fluid (CSF) were measured. The concentration of lipid peroxides increased significantly more (p less than 0.05) during the first 4 days after SAH in patients with symptomatic vasospasm than in those without. Patients with symptomatic vasospasm had a marked decrease in SOD activity on Days 3 and 4 followed by a gradual decrease, whereas the patients without spasm showed little change (difference between the groups, p less than 0.05). There was a significant difference in catalase activity reversal to SOD activity, but no difference in GSH-px activity. Thus, correlation was close between the increased lipid peroxides concentration and the decrease in SOD activity in CSF (p less than 0.05), suggesting an important mechanism in the pathogenesis of vasospasm.
Stroke
PMID:Biological defence mechanism in the pathogenesis of prolonged cerebral vasospasm in the patients with ruptured intracranial aneurysms. 396 28

A new histofluorescence method by HPAA (p-hydroxyphenyl acetic acid) for free radicals in the brain tissue was devised to study neuronal damage induced by ischemia. Cerebral ischemia was produced in rats by injection of plastic microspheres and arachidonic acid (AA) into the right carotid artery. The concentration of malondialdehyde (MDA; free radical) in cerebral cortex of aminotriazol (an H2O2-dependent inhibitor of catalase) treated rats 2 h after stroke was 6.33 times the level before infarction, while the concentration of MDA in h-r SOD (free radical-scavenging enzyme) treated rats 2 h after stroke was significantly lower than in untreated rats. The histochemical findings demonstrated marked H2O2 production around blood vessels occluded by microspheres in the cerebral cortex of the aminotriazole treated rats 2 h after stroke together with disruption of the BBB. Light microscopical findings demonstrated extensive edematous changes in the aminotriazole treated rats 2 h after stroke, while pathological damage in SOD treated rat brains was absent or minimal. We conclude that free radicals are formed during ischemia, and that AA appears to be a major source of activated oxygen radicals. The findings indicate that SOD is protective against ischemia-induced neuronal damage.
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PMID:Histochemical demonstration of free radicals (H2O2) in ischemic brain edema and protective effects of human recombinant superoxide dismutase on ischemic neuronal damage. 797 74

This study tests the hypothesis that reoxygenation injury is produced when cardiopulmonary bypass is initiated in immature hypoxemic piglets and that it causes cardiopulmonary dysfunction that can be avoided by intravenous metabolic treatment before and during cardiopulmonary bypass. Of 18 immature Yorkshire-Duroc piglets (aged < 3 weeks), six were anesthetized, instrumented, and observed for 5 hours (control animals). Twelve piglets underwent up to 2 hours of hypoxemia (arterial oxygen tension = 20 to 30 mm Hg) before initiation of reoxygenation on cardiopulmonary bypass. Six received an intravenous metabolic infusion solution (mercaptopropionyl glycine, catalase, aspartate, glutamate, glucose/insulin), which was started before and continued during cardiopulmonary bypass. Hypoxia produced an initial hyperdynamic response (39% increase in cardiac index; p < 0.05) followed by progressive hemodynamic deterioration, necessitating premature initiation of bypass in 8 of 12 hypoxemic piglets (67%). Reoxygenation-induced injury (assessed 30 minutes after cardiopulmonary bypass) was characterized by 39% reduction of stroke work index (p < 0.05), increased myocardial lipid peroxidation (79% increase of conjugated dienes; p < 0.05), 254% increase in pulmonary vascular resistance index (p < 0.05), 22% decrease in static lung compliance (p < 0.05), and 50% decrease in arterial/alveolar oxygen tension ratio (p < 0.05). These reoxygenation changes were avoided by intravenous metabolic treatment. We conclude that the reoxygenation of immature hypoxemic piglets by initiating cardiopulmonary bypass results in cardiopulmonary dysfunction that may increase vulnerability to subsequent ischemia (i.e., aortic crossclamping). The cardiopulmonary reoxygenation changes are preventable by intravenous metabolic treatment before and during cardiopulmonary bypass needed for cardiac repair.
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PMID:Cardiopulmonary dysfunction produced by reoxygenation of immature hypoxemic animals supported by cardiopulmonary bypass. Prevention by intravenous metabolic pretreatment. 809 11

The effects of diabetes on levels of lipid peroxides and glycolipids in brain were studied in alloxan (18 mg/100 g body weight) diabetic rats. Free fatty acid (FFA) and malondialdehyde (MDA) levels were increased in the brains of diabetic animals. On the other hand, activities of the antioxidative enzymes catalase and superoxide dismutase (SOD) were decreased. The study also showed elevated levels of most of the glycolipid fractions except gangliosides, which were found to decrease in diabetic brain. Administration of insulin to diabetic animals results in the restoration of these parameters to normal levels. These changes observed in diabetic brain may be responsible for the increased frequency of stroke in diabetes.
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PMID:Effect of diabetes on levels of lipid peroxides and glycolipids in rat brain. 823 39

The increased production of reactive oxygen metabolites in the central nervous system may result in cellular damage and vascular-parenchymal injury. Vascular injury is also a cause of the vasoregulation deficiency. In this case report, a 60-year-old woman was admitted to the department of neurology, with a diagnosis of cerebrovascular accident. During 18 days of follow-up, the status of the antioxidant system was determined by measuring red cell superoxide dismutase and catalase activity. Red cell and plasma copper, zinc and magnesium concentrations were also measured. Red cell superoxide dismutase activity increased markedly by Day 2, reached a peak on Day 6 before decreasing to normal 18 days after the injury. Red cell catalase activity was below normal values during the whole of the 18-day study period and was at its lowest between days 6 and 7. Plasma copper, zinc and magnesium concentrations showed corresponding alterations.
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PMID:Antioxidant defence system in a patient with cerebrovascular accident. 885 93

In order to investigate the role of two free radical detoxificant enzymes in patients with aging brain disorders, superoxide dismutase (SOD) and catalase (CAT) activities have been measured in blood from male and female human patients of different ages with several types of aging brain disorders. When compared with activities in the normal population, we have detected: 1) SOD and CAT activities are decreased in patients with Parkinson disease. 2) SOD activity seems to be normal and CAT activity is decreased in patients with dementia. 3) In the patients with stroke, SOD activity is normal, while CAT activity is decreased. SOD activity was measured in red blood cells using the Minami and Yoshikawa method. CAT activity was measured in hemolysates by the method of Aebi. We can conclude that SOD and CAT activities in patients with Parkinson disease are decreased.
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PMID:Human aging brain disorders: role of antioxidant enzymes. 889 40

Changes in oxidative stress status play an important role in tissue injury associated with ischemia -- reperfusion events such as those that occur during stroke and myocardial infarction. Endothelial cells (EC) from human saphenous vein and aorta were incubated for 22 h and found to take up vitamin E from media containing 0-60 mM vitamin E in a dose-dependent manner. EC supplemented with 23 or 28 mM vitamin E in the media for 22 h were maintained at normoxia (20% O2, 5% CO2, and balance N2) or exposed to hypoxic conditions (3% O2, 5% CO2, and balance N2) for 12 h, followed by reoxygenation (20% O2) for 30 min. Saphenous EC supplemented with 23 mM vitamin E produced less (p < 0.05) H2O2 than unsupplemented controls, both at normoxic condition (supplemented: 4.9 +/- 0.05 vs. control: 10.9 +/- 1.3 pmol/min/10(6) cells) and following hypoxia/reoxygenation (supplemented: 6.4 +/- 0.78 vs. control: 17.0 +/- 2.7 nmol/min/10(6) cells). In contrast, aortic EC, which were found to have higher superoxide dismutase and catalase activity than EC from saphenous vein, did not produce any detectable levels of H2O2. Following hypoxia/reoxygenation, the concentration of vitamin E in supplemented saphenous EC was 62% lower than cells maintained at normoxia (0.19 +/- 0.03 vs. 0.5 +/- 0.12 nmoles/10(6) cells, p < 0.001); in aortic EC vitamin E content was reduced by 18% following reoxygenation (0.86 +/- 0.16 vs. 0.70 +/- 0.09 nmoles/10(6) cells, p < 0.05). Therefore, enrichment of vitamin E in EC decreases H2O2 production and thus may reduce the injury associated with ischemia-reperfusion events.
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PMID:Effect of vitamin E on hydrogen peroxide production by human vascular endothelial cells after hypoxia/reoxygenation. 890 85

It is well-known that, in ischemic cerebral injury, a free radical and its byproducts are generated by xanthine-xanthine oxidase system and eliminated by scavengers such as superoxide dismutase (SOD), catalase, uric acid and ascorbic acid. To investigate the possible involvement of the xanthine-xanthine oxidase system in hypertensive cerebral injury, we examined chronological changes in uric acid level in the cerebral cortex and the effects of the inhibition of xanthine oxidase or catalase using stroke-prone spontaneously hypertensive rats (SHRSP). In young SHRSP, uric acid content was lower than age-matched Wistar-Kyoto rats (WKY), but in mature SHRSP strongly exposed to oxidative stress uric acid content had risen dramatically. Administration of allopurinol, an inhibitor of xanthine oxidase, caused a marked decrease in uric acid content. In these SHRSP, cerebral injury was much more intense compared to the control group. On the other hand, administration of aminotriazole, an inhibitor of catalase, did not affect the brain pathology of SHRSP, in spite of a mild reduction in tissue uric acid content. These results suggest that the xanthine-xanthine oxidase system is not the major source of free radical generation in hypertensive cerebral injury. Moreover, the results also suggest that tissue uric acid may have a key role for the incidence of hypertensive cerebral injury in SHRSP.
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PMID:Acceleration of hypertensive cerebral injury by the inhibition of xanthine-xanthine oxidase system in stroke-prone spontaneously hypertensive rats. 914 Jul 8

The effects of photoactivation of fluorescein 5'-isothiocyanate (FITC)-dextran on lymphatic pump activity of rat mesenteric collecting vessel were studied in vivo. Rats were anesthetized with intraperitoneal alpha-chloralose and urethane, and the mesenteries were studied by using intravital videomicroscopic techniques. The diameter of the collecting lymph vessels were continuously monitored and lymphatic pump parameters (end diastolic diameter, end systolic diameter, stroke volume index, ejection fraction, contraction frequency, and pump flow index) were calculated. FITC-dextran (42 nmol/100 g body wt) without illumination caused no disturbance of lymphatic pump activity. Photoactivated FITC-dextran significantly increased end systolic diameter and decreased stroke volume index, ejection fraction, contraction frequency, and pump flow index. End diastolic diameter was not changed throughout the experiment. Superoxide dismutase (120 U/ml) and catalase (5000 U/ml) had no protective effect on photoactivated FITC-induced pump dysfunction, while histidine (singlet oxygen quencher, 10 mM) significantly prevented the disturbance of pump parameters. These results indicate that photoactivation of FITC induces negative chronotropic and negative inotropic effects in lymphatic pump activity through generation of singlet oxygen in the mesentery.
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PMID:Inhibitory effects of fluorescein isothiocyanate photoactivation on lymphatic pump activity. 932 81


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