Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute myocardial ischemia and reperfusion injury of rats were produced by ligating the left coronary artery for 15 min and reopening. The myocardial calcium contents were increased from 3.53 +/- 0.58 mumol/g dry wt in sham operation group to 6.02 +/- 1.19 mumol/g dry wt with reducing SOD/MDA ratio and showing ventricular extrasystole (VE), ventricular tachycardia (VT), and ventricular fibrillation (VF). Sinomenine (Sin) and verapamil (Ver) infusion 15 min before ischemia attenuated the elevated calcium contents to the level of the sham operation group, increased SOD/MDA ratio, and produced antagonistic effects on VE, VT, VF. These improvements indicated that Sin, similar to Ver, prevented myocardial injury by lowering intracellular Ca2+ accumulation.
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PMID:[Prevention of sinomenine on isolated rat myocardial reperfusion injury]. 801 64

The implication of eicosanoid metabolism and its relationship with oxygen free radical production in the process of ischemia-reperfusion associated with rat pancreas transplantation has been explored in this study. For this purpose male Sprague-Dawley rats were classified as follows: group I, control animals not surgically manipulated; group II, pancreas transplantation, after 30 min preservation in UW solution; group III, pancreas transplantation after 12 h preservation under the same conditions; group IV, same as group III but with administration of SOD 5 min prior to organ revascularization. The results show post-transplantation increases in 6-keto-PGF1 alpha, TXB2, LTB4 and 12-HETE in pancreatic tissue independent of preservation time. The fact that SOD administration could reverse these increases even though an efficient xanthine oxidase irreversible inhibitor such as allopurinol was present in the preservation solution suggests that eicosanoid generation in the recipient rat would be mediated by an oxygen free radical dependent mechanism not exclusively dependent on endothelial xanthine oxidase activity.
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PMID:Arachidonate metabolism in ischemia-reperfusion associated with pancreas transplantation. 801 60

Oxygen free radicals have been widely implicated in the pathogenesis of brain injury due to ischemia followed by reperfusion. The success of making transgenic animals overexpressing human CuZn-superoxide dismutase (CuZn-SOD) in brain cells allows researchers to discern the specific role of superoxide radicals in reperfusion injury after focal ischemia. It has been shown that increased brain levels of CuZn-SOD in transgenic mice protect neurons from ischemia/reperfusion injury. However, overexpression of CuZn-SOD does not provide neuronal protection in permanent focal ischemia in mice, when compared with non-transgenic mouse littermates. It is proposed that molecular genetic approaches of modifying antioxidant levels in the brain offer a unique tool for studying oxidative mechanisms in focal cerebral ischemia.
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PMID:Oxygen radicals in focal cerebral ischemia. 802 3

Paeonol 60 mg.kg-1 ip, was given to rats for 15 days. On the 16th day myocardial ischemia reperfusion injury was produced in the rat heart by occlusion of the left coronary artery and the release of the occlusion. The results showed that paeonol significantly improved myocardial SOD activity (5.8 +/- 0.6.mg-1 compared with reperfusion control 3.4 +/- 0.9, P < 0.01), reduced the MDA content (11.4 +/- 1.7 nmol.mg-1 versus 17 +/- 1.3, P < 0.01) and cardiac CPK release (1523 +/- 478.5 U.L-1 versus 2355 +/- 626.5, P < 0.01). The myocardial ultrastructure was also protected keeping them from the oxygen free radical damage. It appears that paeonol is an efficient protective agent against ischemia reperfusion damage in the rat heart.
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PMID:[Anti-ischemia reperfusion damage and anti-lipid peroxidation effects of paeonol in rat heart]. 804 13

We investigated immunohistochemically the localization and changes of copper/zinc superoxide dismutase (CuZn-SOD) and manganese superoxide dismutase (Mn-SOD) in the rat brain following 1 h of middle cerebral artery (MCA) occlusion. In normal brain, immunoreactivity to both SODs was observed in medium-sized neurons in the striatum and in many neurons in the neocortex. Mn-SOD was predominantly stained in cortical interneurons. The immunostaining of both SODs rapidly decreased or disappeared in neurons in the lateral segment of the striatum (ischemic center) 4 h after MCA occlusion, when the neurons were degenerating. Most neurons in the neocortex (ischemic penumbra) decreased their CuZn-SOD immunoreactivity but not Mn-SOD immunoreactivity 4 h after ischemia, when only a few neurons showed histopathological changes. CuZn-SOD immunoreactivity in almost all cortical neurons disappeared 1 day after ischemia, but Mn-SOD immunoreactivity was still preserved in interneurons, when cortical neurons showed typical pathological changes. Some cortical neurons in the boundary zone between normal and infarcted areas showed intense immunostaining to both SODs and glial SOD immunoreactivity appeared after 3 and 7 days. These results suggest that early loss of the scavenging system of free radicals may lead to neuronal damage after ischemic insult, and that induced SODs in the boundary zone between the normal and infarcted areas may act as a defense mechanism against damage.
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PMID:An immunohistochemical study of copper/zinc superoxide dismutase and manganese superoxide dismutase following focal cerebral ischemia in the rat. 805 37

Kidney preservation under mild hypothermic conditions (24 degrees C) was performed to preserve organs for a long time, to determine the viability of damaged organs, and to evaluate the viability of organs that have previously been stored in cold solution. Rabbit kidneys were perfused via the renal arteries. The perfusate was composed of glucose, allopurinol, PEG-SOD, adenosine, dexamethasone, insulin, HES and FC-43. This solution was an attempt to simulate the electrolyte constitution of extracellular fluid (pH 7.40 delta pH). The functions of all groups of kidneys were evaluated by measuring urine output, urine pH and urine electrolytes. The suitable perfusion pressure was 80 mmHg. The kidneys without a warm ischemic period were well stored and functioned for over 12 hours under 24 degrees C perfusion. In the warm ischemic groups, the viability and histological structure of the kidneys were well maintained and conditioned for 12 hours at up to 35 min of warm ischemia. The kidneys which were stored in 4 degrees C UW-solution for 24 hours had a good urination using mild hypothermic perfusion for 12 hours. This suggest that mild hypothermic perfusion will become a useful method for preserving the condition of organs and for determining and evaluating the viability of organs that have previously been stored in cold solution.
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PMID:[Experimental studies on functional preservation, conditioning and evaluation of the viability of rabbit kidneys utilizing mild hypothermic perfusion]. 805 26

Superoxide radicals formed during reperfusion of ischemic tissues have been identified as a key mediator in the microvascular manifestations of postischemic tissue damage. This understanding is based on studies in laboratory animals in which high doses of superoxide dismutase (SOD; 2.0-25.0 mg/kg body wt iv) were found to inhibit postischemic leukocyte adhesion and the leakage of fluid and macromolecules. Using a dorsal skinfold chamber model in hamsters, we demonstrate now that protection from reperfusion-induced leukocyte adhesion to venular endothelium after 4 h of ischemia to striated muscle can be attained by pretreatment of the animals with a significantly lower dose of exogenous CuZn-SOD (0.25 mg/kg body wt) or with heparin (2,000 IU/kg body wt), which induces a comparable increase in SOD plasma activity through the release of endogenous extracellular SOD from endothelial cell binding sites. This protective effect was maintained until 24 h after reperfusion. In contrast, CuZn-SOD or heparin failed to attenuate the postischemic shutdown of nutritional capillary perfusion, a phenomenon that is due to ischemia-induced endothelial cell swelling, rather than due to reperfusion-associated events, and hence is not susceptible to strategies directed against oxygen radicals generated during the reperfusion phase. The results of this study 1) imply that postischemic leukocyte/endothelium interaction can be attenuated by a low and clinically more relevant dose of SOD, and 2) caveat the administration of heparin in laboratory animals (i.e., to keep catheters patent) in studies of experimental ischemia/reperfusion injury or other oxygen radical-dependent pathomechanisms.
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PMID:Heparin-released superoxide dismutase inhibits postischemic leukocyte adhesion to venular endothelium. 809 97

The effect of Rhizoma Ligustici Chuanxiong and allopurinol on ischemia-reperfusion damage of rabbit ear flap was studied. The results showed that MDA level was higher and SOD activity lower distinctly at 0.5 hour after reperfusion than that at 16 hours of postischemia and preischemia, Rhizoma Ligustici Chuanxiong and allopurinol changed the result markedly with a decrease of necrosis rate. The effect of Rhizoma Ligustici Chuanxiong was more significant than that of allopurinol in promoting microcirculation, preventing clot formation, reducing exudation and hemorrhage.
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PMID:[Effects of Rhizoma Ligustici chuanxiong and allopurinol on ischemia-reperfusion damage of rabbit ear flap]. 811 66

The distribution of heat shock protein hsp70 mRNA after 10 min of middle cerebral artery (MCA) occlusion was investigated through in situ hybridization in transgenic (Tg) mice overexpressing CuZn-superoxide dismutase (CuZn-SOD) and in control nontransgenic (nTg) littermates. In the ischemic cortex of nTg mice, hsp70 mRNA was detected 1 h after reperfusion and was observed for up to 6 h. In Tg mice, however, it was still detectable within the cortex even at 24 h. In the caudate putamen, hsp70 mRNA appeared at 1 h and was present for up to 6 h in both nTg and Tg mice. Although hsp70 mRNA was detected in the thalamus only at 1 h in nTg mice, it was observed for up to 6 h in Tg mice. Similarly, hsp70 mRNA was detected in the hippocampus of nTg mice only at 1 h, whereas it was detected in Tg mice at 1 h and continued up to 24 h, with high intensity in the CA1 subfield. Despite the significant amounts of hsp70 mRNA in both Tg and nTg mice following ischemia, there was no observable neuronal necrosis (as assessed using hematoxylin and eosin staining) for up to 7 days. Cortical cerebral blood flow (CBF), measured by laser-Doppler flowmetry, did not differ between nTg and Tg mice during ischemia and reperfusion, despite exhibiting hyperemia following hypoperfusion. These results suggest that oxidative stress affects the expression of hsp70 following temporary focal ischemia. An alteration in oxidation stress, which resulted from reduced levels of superoxide radicals in the presence of the CuZn-SOD transgenes, may permit the prolonged expression of hsp70.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged expression of hsp70 mRNA following transient focal cerebral ischemia in transgenic mice overexpressing CuZn-superoxide dismutase. 816 90

Open chest dogs undergoing 30-min occlusion of the left anterior descending coronary artery (LAD), followed by 20-min reperfusion, received silibinin (2 mg/kg body weight), allopurinol (100 mg for two days as pretreatment, 20 mg/kg body weight during ischemia and reperfusion), superoxide dismutase (SOD, 5 and 0.5 mg/kg body weight, starting from the last minute of ischemia over 6 min). Control and treated dogs were comparable with respect to myocardial regional contractile force (strain gauge), malondialdehyde (MDA) and creatinine kinase (CK) levels of sinus coronarius blood samples, heart rate, and blood pressure. Allopurinol and large doses of SOD produced significant improvement in contractility and decreased MDA levels, which might suggest free radical mediated reactions during reperfusion.
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PMID:Effect of antioxidant treatment on the myocardium during reperfusion in dogs. 819 77


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