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

In 70 patients with confirmed transmural myocardial infarction the sensitivity of creatine kinase and creatine kinase MB at different times after admission was investigated by 364 measurements. Beside the number of correctly positive results the optimized standard method hitherto used was compared with the new optimized standard method with N-acetylcystein as activator. During the first 12 hours after admission the percentage of correctly positive results was 64,4% for creatine kinase (GSH) and 86,7% for creatine kinase (NAC). The sensitivity of cretine kinase MB, however, was found to be 71,1% (GSH) and 86,7% (NAC). With respect to the poor specifity of creatine kinase the sensitivity of creatine kinase MB, especially when using the new optimized standard method is superior. Similar results were established 24 and 48 hours after admission. Creatine kinase MB only fails in detection of myocardial infarction if the stroke is older than 3 days or if the enzyme activity determination intervals are too long.
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PMID:[Sensitivity of creatine kinase and creatine kinase MB in myocardial infarction. Evaluation of a new optimized standard method (author's transl)]. 43 69

The levels of lipid peroxides, determined as thiobarbituric acid reactive substances (TBARS), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were examined in the blood from stroke-prone spontaneously hypertensive rats (SHRSP), with and without cerebral lesions, and normotensive Wistar Kyoto (WK) rats. The levels of TBARS in the blood from healthy SHRSP were not significantly different from those of WK rats, while the values of SHRSP (male) with stroke were more than twice as high as those of healthy SHRSP. The activities of SOD and GSH-Px in stroke SHRSP were also statistically different from those of healthy SHRSP.
Stroke
PMID:Fluctuation of lipid peroxides and related enzyme activities at time of stroke in stroke-prone spontaneously hypertensive rats. 46 20

In order to investigate the effect of dietary EPA on liver GSH peroxidase (GSH-Px) activity in rats, highly concentrated EPA (78% ethyl ester form) was administrated to SHRSP (Stroke-prone spontaneously hypertensive rat) that were fed a casein, SPI (soybean protein isolate) or SPI diet with methionine for 4 weeks. The content of liver GSH in rats fed SPI was lower than that of rats fed the casein diet. Although no significant difference of liver GSH-Px was observed in rats after EPA supplement, a decrease of liver GSH-Px activity was found in rats fed the SPI diet when compared with rats fed the casein diet. The changes of liver GSH content and GSH-Px activity in rats fed SPI were found to be associated with methionine supplement. Addition of methionine to the SPI diet resulted in an increase of liver GSH content and GSH-Px activity. In addition, liver lipid peroxide concentration was increased in rats fed the SPI diet after EPA treatment. In contrast, EPA administered rats fed the SPI diet containing methionine showed a lower liver lipid peroxide concentration. These results suggest that methionine may play an important role in regulation of the utilization of EPA in SHRSP when fed a SPI diet.
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PMID:Effect of dietary protein on the peroxidation of eicosapentaenoic acid in stroke-prone spontaneously hypertensive rats. 179 53

1. The activities of glutathione (GSH) transferases in male, spontaneously hypertensive rats (SHR) and stroke-prone rats (SHR-SP) were different from those of normotensive male Wistar Kyoto rats (WKY). 2. These alterations of the enzyme activities were partly due to the changes in the levels of subunits 2 and 4. 3. Subunit selective alterations were observed in pathophysiological conditions, namely spontaneous hypertension. 4. The sex-related difference of GSH transferases in these animals was also discussed.
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PMID:Subunit selective alteration of hepatic glutathione transferases in spontaneously hypertensive rats. 195 32

Clinicopathological studies were performed on 156 lenses of human senile cataract obtained by cataract operations between 1970 and 1988. It became clear that the aging influences the functional destruction of the equatorial region, the pathological changes of the bow area, and changes of the extralens environment. After operation for the atrophic type of the posterior subcapsular cataract, aftercataract easily develops on the intraocular lens and this requires treatment. Long-term observations were carried out in 180 Wistar male rats under the same laboratory condition and histological studies were performed. The similarities between the senile Wistar rat cataract and the human senile cataract indicate that the Wistar rat cataract is useful as a model for studying the human senile cataract. These rats were initially classified into six groups (control, vitamin E diet, EPC eye drops, catalin eye drops and reduced catalin eye drops). To study the effects of the agents (vitamin E, ARI, EPC, catalin, reduced catalin) on the cataract in senile Wistar rats the mean cell density of lens epithelia were measured at 2 or 3-month intervals. There were no statistically significant differences in treated groups and the control group. The results suggest that these agents affect another factor of lens apart from the proliferative activity of lens epithelial cell. Effects of anti-cataract agents were investigated using cultured lens epithelial cells. When cultured rat lens epithelial cells were incubated in medium containing selenite, super-oxide dismutase (SOD) activity and GSH in the cells markedly decreased, and GSSG was markedly increased. When cultured rabbit lens epithelial cells were incubated in medium contained selenite and glutathione, SOD activity was maintained normal level. When cultured lens epithelial cells were incubated in medium contained selenite and pirenoxin, SOD activity also maintained a normal level. These results suggest that both glutathione and pirenoxin are effective as anti-cataract agents. Cataracts in spontaneously hypertensive rats (SHR) was investigated on male of Wistar-Kyoto rats (WKY), stroke resistant SHR (SHRSR) and stroke-prone SHR (SHRSP) rats aged 3 to 9 months. Cataracts in these rats were classified as follows: Type 0: no opaciiy, Type 1: nuclear opacity, Type 2: posterior subcapsular opacity, Type 3: nuclear opacity associated posterior subcapsular opacity and Type 4: complete opacity in both lenses. Incidence of cataract in WKY was 2.6%, SHRSR, 76.8% ant SHRSP, 88.2%. Incidence of nuclear opacity was remarkably higher in SHRSP (48.5%). In SHR aged from 3 to 5 months, nuclear opacity was ahead of the appearance of posterior subcapsular opacity which was increased during aging.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cataract--clinic and pathology]. 227 35

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

Prostaglandin release from microvessels isolated from the rabbit cerebral cortex was determined under three different atmospheric conditions: 100% O2 ("O2") room air, and 95% N2:5% CO2 ("N2-CO2"). Initial studies with homogenates prepared from rabbit cerebral microvessels (RCMV) indicated two pathways of enzymatic PGH2 transformation, namely PGI2 synthase and GSH-dependent PGH-PGE isomerase. We measured the release of the principal products of these pathways, 6-keto PGF1 alpha and PGE2 from freshly prepared RCMV. The release of 6-keto PGF1 alpha exceeded that of PGE2 in all three protocols. RCMV incubated in "N2-CO2" exhibited a reduction in the release of 6-keto PGF1 alpha compared to room air or "O2" incubated RCMV, evident at 30-60 min of incubation. No significant differences in the release of PGE2 were observed among the three incubation protocols. In all three incubation protocols the ratio of 6-keto PGF1 alpha to PGE2 did not differ during the initial 10 minutes of each incubation. After 30 to 60 min of incubation, this ratio did not change from the "O2" or room air treated RCMV, but decreased significantly for the "N2-CO2" treated group. To determine the reversibility of the apparent "N2-CO2" induced decline in 6-keto PGF1 alpha release, microvessels were removed from the nitrogen atmosphere and incubated in room air. Release was measured during the initial 10 min following reintroduction to room air and was compared to room air pretreated controls treated in an identical manner.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:Prostaglandin release from isolated rabbit cerebral cortex micro-vessels--comparison of 6-keto PGF1 alpha and PGE2 release from micro-vessels incubated in 100% O2, room air and 95% N2:5% CO2. 643 53

The incipient timing of cerebral strokes in the stroke-prone spontaneously hypertensive rats (SHRSP) was biochemically determined by investigating the relationship between the glutathione peroxidase (GSH-Px) activity in erythrocytes and the extent of stroke lesions. When the blood pressure of SHRSPs was maintained at over 240 mmHg, the GSH-Px activity fell, and the body weight also decreased. In SHRSP whose GSH-Px activity in erythrocytes had dropped below 23 units/ml of blood, the incidence of cerebral strokes was 98% (n = 88/90). The hematocrit level did not change even after the GSH-Px activity had dropped to 23 units/ml of blood. The reduced GSH-Px activity in erythrocytes observed during continued hypertension was found to be due to a decrease in GSH-Px protein, and not to any inactivation of the enzyme, as evident from immunochemical titration. At the moment when the GSH-Px activity had dropped to 23 units/ml of blood, and the control diet was changed to one based on fish or a hydralazine treatment given, the activity recovered, and an increase in body weight and prolongation of the life-span were observed. It was deduced from these findings that tracing the GSH-Px activity in erythrocytes in SHRSP would serve as an indicator for predicting and prognosing stroke lesions.
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PMID:Prediction of stroke lesions in stroke-prone spontaneously hypertensive rats by glutathione peroxidase in erythrocytes. 754 98

The mechanisms underlying cell damage in stroke or during experimental brain ischemia are not fully understood. L-Cysteine, an excitotoxic amino acid that could contribute to tissue damage, is normally found in relatively low levels in brain (ca. 0.05 mumol/g), compared to the cysteine-containing tripeptide, glutathione (GSH, ca. 1.5 mumol/g). We have observed that during brain ischemia in gerbils, levels of cysteine rise 10-13-fold over an 8 h period to 0.66 and 0.62 mumol/g, respectively, in the ischemic hippocampus and striatum. At the same time, levels of GSH fall by 0.84 and 0.94 mumol/g, respectively. The elevated free cysteine may be derived largely from GSH. The levels of cysteine found in ischemic brain are similar to those reported after parenteral administration of neurotoxic doses of L-cysteine to perinatal rats. The remarkable increase in cysteine during brain ischemia, coupled to its neurotoxic properties, may play a role in aspects of brain damage during or following brain ischemia.
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PMID:Brain ischemia markedly elevates levels of the neurotoxic amino acid, cysteine. 849 46

Ischemic-reperfusion injury in humans occurs in conditions such as stroke, cardiac arrest, subarachnoid hemorrhage or head trauma. Maximal tissue damage is observed during reperfusion, which is primarily attributed to oxidative injury resulting from production of oxygen free radicals. One of the major consequences of such damage is the depletion of the cellular antioxidant, glutathione (GSH) leading to oxidation of protein thiols to disulfides and the loss of activity of critical enzymes having active thiol group(s). Thus, the maintenance of thiol homeostasis is an important factor in cell survival. The effect of thiol antioxidants like alpha-lipoic acid and the isopropyl ester of GSH was examined on the morbidity and mortality of rats subjected to reperfusion following cerebral ischemia induced by bilateral carotid artery occlusion and hypotension. While the GSH isopropyl ester had no significant protective effect; after pretreatment of rats, alpha-lipoic acid was detected in the rat brain and it dramatically reduced the mortality rate from 78% to 26% during 24 h of reperfusion. The natural thiol antioxidant, alpha-lipoic acid is effective in improving survival and protecting the rat brain against reperfusion injury following cerebral ischemia.
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PMID:alpha-Lipoic acid protects against reperfusion injury following cerebral ischemia in rats. 873 70


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