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

Catalase-like activity was determined in the cerebrospinal fluid of 16 patients with cerebral haemorrhage, 24 cases od encephalomalacia due to thrombosis, and 10 controls. It was demonstrated that catalase-like activity in the cerebrospinal fluid of patients with cerebral stroke is significantly raised in relation to the activity observed in controls. This rise is patricularly evident in the first 24 hours after the onset. The rise was statistically significant only in the group of encephalomalacia.
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PMID:[Catalase-like activity in cerebrospinal fluid in patients with cerebral stroke]. 120 96

Bradykinin produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats than in normotensive Wistar-Kyoto rats. The goals of this study were to determine the mediator of bradykinin-induced dilatation in cerebral arterioles of rats and to determine whether responses to this mediator are altered in hypertensive rats. Diameter of pial arterioles (20-65 microns) was measured using intravital microscopy in 18 normotensive and 17 hypertensive rats. Superfusion of 3 x 10(-7) M bradykinin dilated pial arterioles by 53 +/- 4% (mean +/- SEM) in normotensive rats but only 33 +/- 6% in hypertensive rats (p less than 0.05 versus normotensive rats). Vasodilatation in response to bradykinin was almost completely inhibited by 280 units/ml catalase in both normotensive and hypertensive rats (n = 7 and n = 7, respectively) whereas 150 units/ml superoxide dismutase (n = 6 and n = 5, respectively) and 1 mM deferoxamine (n = 5 and n = 5, respectively) did not attenuate bradykinin-induced vasodilatation. These findings suggest that hydrogen peroxide is the mediator of bradykinin-induced dilatation in cerebral arterioles of rats. We also examined responses of cerebral arterioles to hydrogen peroxide in five normotensive and six hypertensive rats. Dilator responses of cerebral arterioles to 3.2 x 10(-5) M to 1.6 x 10(-4) M hydrogen peroxide did not differ in normotensive and hypertensive rats, which suggests that impaired dilatation of cerebral arterioles in response to bradykinin is not related to altered responsiveness of smooth muscle to an endothelium-derived relaxing factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Sep
PMID:Mechanisms of impaired endothelium-dependent cerebral vasodilatation in response to bradykinin in hypertensive rats. 192 61

Thirteen immature puppies (2 to 4 kg) underwent 1 hour of acute hypoxia (oxygen tension 25 to 30 mm Hg), followed by 45 minutes of normothermic global ischemia on total vented bypass with normal blood reperfusion. Ventricular function was assessed by inscribing Starling function curves and measuring stroke work indices before hypoxia and after reperfusion. Seven puppies (control) received normal saline infusion at 4 ml/kg/hr. Six other puppies received a 4 ml/kg/hr intravenous infusion of glutamate/aspartate, glucose-insulin-potassium, mercaptopropionyl glycine, carnitine, and catalase during hypoxia and reperfusion. In control hearts, acute hypoxia depleted myocardial glutamate and aspartate by 52% (p less than 0.05 versus prehypoxia) and 48% (p less than 0.05 versus prehypoxia) and caused severe hemodynamic deterioration (55% decrease of stroke work index) (p less than 0.05 versus prehypoxia); three of seven (43%) required premature institution of bypass. Postischemic left ventricular function recovered to only 40% of control levels (p less than 0.05 versus prehypoxia). In contrast, intravenous metabolic infusions maintained tissue glutamate (p less than 0.05 versus control group) and aspartate (p less than 0.05 versus control group) in treated hearts during hypoxia and allowed cardiac index to rise 20% (p less than 0.05 versus prehypoxia); all treated hearts tolerated 1 hour of hypoxia, and stroke work recovered 70% (p less than 0.05 versus control group) of stroke work index after subsequent ischemia. Impaired tolerance of immature hearts to acute hypoxia and subsequent ischemia is due to substrate depletion. This impairment can be reduced by intravenous metabolic support during hypoxia and reperfusion and leads to improved recovery of postischemic function.
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PMID:Studies of myocardial protection in the immature heart. IV. Improved tolerance of immature myocardium to hypoxia and ischemia by intravenous metabolic support. 149 25

It is now becoming increasingly clear that free radicals contribute to brain damage in several conditions, such as hyperoxia and trauma. It has been more difficult to prove that free radical production mediates ischemic brain damage, but it has often been suggested that it may be a major contributor to reperfusion damage, observed following transient ischemia. Recent results demonstrate that cerebral ischemia of long duration, particularly when followed by reperfusion, leads to enhanced production of partially reduced oxygen species, notably hydrogen peroxide (H2O2). It has also been suggested that postischemic hyperoxia, e.g. an increased oxygen tension during the recirculation period, adversely affects recovery following transient ischemia. Other data support the notion that brain damage caused by permanent ischemia (stroke) is significantly influenced by production of free radicals. The present study, however, fails to show that recirculation following brief periods of ischemia (15 min) leads to an enhanced H2O2 production, and that hyperoxia aggravates the ischemic damage. This study was undertaken to reveal whether variations in oxygen supply in the postischemic period following forebrain ischemia in rats affect free radical production and the brain damage incurred. To that end, rats ventilated on N2O/O2 (70:30) were subjected to 15 min of transient ischemia. Normoxic animals were ventilated with the N2O/O2 mixture, hyperoxic animals with 100% O2, and hypoxic ones with about 10% O2 (balance either N2O/N2 or N2) during the recirculation. At the end of this period, the animals were decapitated for assessment of H2O2 production with the aminotriazole/catalase method. This method is based on the notion that aminotriazole interacts with H2O2 to inactivate catalase; thus, the rate of inactivation of catalase in aminotriazole treated animals reflects H2O2 production. In a parallel series, animals ventilated with one of the three gas mixtures in the early recirculation period, respectively, were allowed to recover for 7 days, with subsequent perfusion-fixation of brain tissues and light microscopical evaluation of the brain damage. Animals given aminotriazole, whether rendered ischemic or not, showed a reduced tissue catalase activity, reflecting H2O2 production in the brain. Hyperoxic animals failed to show increased tissue H2O2 production, while hypoxic ones showed a tendency towards decreased production. However, all three groups (hypo, normo- and hyperoxic) had similar density and distribution of neuronal damage. These results suggest that although postischemic oxygen tensions may determine the rates of H2O2 production, variations in oxygen tensions do not influence the final brain damage incurred.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Free radical production and ischemic brain damage: influence of postischemic oxygen tension. 205 15

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

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

To determine which biochemical entity of the red cell is responsible for preventing augmented postischemic myocardial oxygen consumption (MVO2), 28 canine hearts instrumented with ultrasonic dimension crystals underwent simultaneous determination of stroke work (SW) and MVO2 during incremental volume loading on right heart bypass before and 30 min after 2 hr of 10 degrees C cardioplegic arrest with unmodified oxygenated crystalloid cardioplegia (OC), OC with histidine of equal buffering capacity as 18% hematocrit blood (OC + H), or OC with 200 units/ml of superoxide dismutase and catalase (OC + SOD/C). In all groups, the slope of the linear SW vs end-diastolic volume relationship, Mw, and the slope of the linear SW vs MVO2 relationship, Me, were unchanged after cardioplegic arrest. The intercept of the SW vs MVO2 relationship, Eo, was augmented an average of 22.2% in the OC group, but both OC + H and OC + SOD/C prevented this subtle expression of ischemic injury. The characteristic of the red cell most likely responsible for the myoprotective efficacy of blood cardioplegia is buffering capacity; however, since the effects of tissue acidosis are partially mediated by free radicals, the use of free radical scavengers can also ameliorate ischemic damage incurred during cardioplegic arrest.
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PMID:Upgrading acellular to sanguineous cardioplegic efficacy. 273 17

The role of reactive oxygen metabolites in extrapancreatic organ dysfunction associated with acute hemorrhagic pancreatitis was studied in dogs. Experimental pancreatitis was induced by the intraductal infusion of activated trypsin and taurocholate. Cardiac output, pulmonary and systemic blood pressure, pulmonary wedge pressure, central venous pressure, heart rate, blood gases and serum amylase were measured. Cardiac index, pulmonary and systemic vascular resistance, and the right and left stroke work were calculated. Systemic arterial and venous blood pressure and cardiac index gradually declined over 6 hr, while pulmonary mean blood pressure and pulmonary vascular resistance increased. Pretreatment of pancreatitis with catalase and superoxide dismutase prevented the rise in mean pulmonary blood pressure, moderated the rise in pulmonary vascular resistance, and decreased the rate and extent of the fall in cardiac index. These data suggest that reactive oxygen metabolites may play some role in the extraabdominal organ manifestations of acute pancreatitis.
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PMID:Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis. 279 9

The present study has examined early cellular effects of chronic adriamycin administration to dogs using a protocol (1 mg/kg/week to a total cumulative dose of 240 mg/m2) producing significant but small reductions in ejection fraction and stroke volume as determined echocardiographically prior to the development of clinical or radiological manifestations of heart failure. At this early phase of cardiomyopathy, significant reduction (P less than 0.05) in sarcoplasmic reticulum Ca2+, K+-ATPase was observed without any change in mitochondrial, lysosomal or sarcolemmal marker enzymes. Myocardial calcium (P less than 0.01) and glutathione (P less than 0.001) levels were increased significantly. Detailed analysis of myocardial phospholipid profiles failed to show any significant differences between control and treated dogs. In contrast, red cell membranes showed increased phosphatidylcholine (PC) and decreased phosphatidylserine (PS) contents, resulting in a significant increase in PC/PS ratio (P less than 0.05). No significant changes were detected in activities of catalase, superoxide dismutase or glutathione peroxidase in erythrocytes or myocardial tissue from control and adriamycin-treated animals. A significant (P less than 0.05) elevation in plasma sialic acid was observed following adriamycin treatment. Our results suggest that early adriamycin-induced damage is unlikely to result from alterations in cellular processes protecting tissues against oxidant injury. Regression analysis indicated that, of the various abnormalities observed, only the elevated myocardial calcium levels and the increases in plasma sialic acid correlated with the degree of myocardial functional impairment. Our findings suggest the presence of sarcolemmal alterations in Ca2+ handling in early adriamycin-induced myocardial injury and indicate that measurement of plasma sialic acid should be further investigated as a possible noninvasive indicator of impending adriamycin cardiotoxicity.
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PMID:Adriamycin cardiomyopathy: implications of cellular changes in a canine model with mild impairment of left ventricular function. 299 97

We examined the hypothesis that oxygen radicals may mediate the vasodilator effect of VIP on cerebral arterioles in cats equipped with cranial windows. The appearance of superoxide anion radical in cerebral extracellular space during VIP application was examined by measuring the rate of superoxide dismutase (SOD)-inhibitable reduction of nitroblue tetrazolium (NBT). Although VIP (1 and 10 micrograms/ml) caused substantial reduction of NBT, the rate of the SOD-inhibitable portion was not significantly different from zero. We also examined the effect of scavenging of superoxide and hydrogen peroxide by topical application of SOD plus catalase on the vasodilator effect of VIP (0.05-1.0 microgram/ml). The dilation in response to VIP was not significantly affected in either large or small arterioles by scavenging of superoxide and hydrogen peroxide. We conclude that VIP does not cause generation of superoxide and that superoxide or other reactive oxygen species derived from it, such as hydrogen peroxide and hydroxyl radical, are not mediators of the cerebral vasodilation caused by VIP.
Stroke
PMID:Superoxide anion radical does not mediate vasodilation of cerebral arterioles by vasoactive intestinal polypeptide. 302 25


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