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)

Evidence for in vivo antioxidative activity of reduced CoQ homologs has been presented. This came from studies with experimental endotoxemia in mice, reoxygenation of rat liver following ischemia, and reoxygenation of canine heart following 24-hour cold preservation. In radical-induced injury of hepatocytes, it has been first shown that reduced CoQ9 acts as a potential antioxidant regardless of its cellular concentration, whereas reduced CoQ10 acts in cells containing CoQ10 as the predominant homolog. The antioxidant activity of reduced CoQ homologs appears to be independent of that of alpha-tocopherol under the conditions employed.
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PMID:Antioxidant function of coenzyme Q. 129 10

Metabolic disturbances in the canine liver during warm ischemia by Pringle's method for 60 minutes and the role of Coenzyme Q10 (CoQ10), Prostaglandin E1 (PGE1) and ONO-3708, TXA2 receptor antagonist, were studied. Mongrel dogs were divided into five groups; control group, group of liver ischemia without drugs, groups of liver ischemia with CoQ10, PGE1 and ONO-3708 pretreatment. Metabolic rates of PGI2, TXA2, insulin, glucagon and glucose and production of lipid peroxides in the five groups were measured at the points before Pringle's procedure, 5 minutes, 60 minutes and 120 minutes after declamping. In the group of ischemia without drug administration, the hepatic metabolism of PGI2, TXA2, insulin and glucose were decreased after declamping. The metabolism of glucagon, however, was not disturbed by warm ischemia. The production of lipid peroxides increased at 5 minutes after declamping. In the groups of CoQ10, PGE1 and ONO-3708 pretreatment, changes of PGI2, TXA2 and insulin metabolism in the liver were improved, and an increased production of lipid peroxides by warm ischemia was normalized. This study suggests that CoQ10, PGE1 and ONO-3708 protect liver damage by warm ischemia as results of improvement of metabolic disturbances of PGI2, TXA2, insulin and suppression of lipid peroxides production.
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PMID:[Assessment for protective effects of CoQ10, PGE1 and TXA2 receptor antagonist (ONO-3708) on warm ischemic liver]. 138 60

This study was made in a canine isolated gracilis muscle model to measure directly the free radicals, to predict the severity of ischemia and reperfusion injury of the skeletal muscle by measuring its surface pH (mspH), and to determine the effect of Coenzyme Q10 (CoQ10) in reducing the extent of muscle injury. Animals were divided into three groups: group A (control, n = 10), group B (untreated, n = 10), and group C (CoQ10 treated, n = 10). In both groups B and C, 5 hr ischemia followed by 40 min of reperfusion was made. Free radicals were measured directly by electron spin resonance spectrometer (ESR) and mspH was measured using a pH microprobe. Serum creatine phosphokinase (CPK) was estimated before ischemia, 5 and 30 min after reperfusion. The extent of muscle injury was evaluated morphologically by Evan's blue dye exclusion test. ESR intensity in group B was 0.55 +/- 0.19 and decreased to 0.30 +/- 0.04 in group C (P less than 0.01). Rate of recovery of mspH was higher in group C (7.16 +/- 0.06) compared to group B (6.88 +/- 0.11, P less than 0.01) and CPK in group C was less (847 +/- 381 IU/liter) than in group B (1356 +/- 519 IU/liter, P less than 0.05) after 30 min of reperfusion. In group C the morphological muscle injury was less (37.8 +/- 5%) compared to group B (56.7 +/- 3.6%, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radical injury in skeletal muscle ischemia and reperfusion. 166 96

Gastric mucosal blood flow and its regulating factors were studied in normal and stressed rats. In addition, vascular regulating factors and the role of CoQ10 anion radical and SOD (superoxide dismutase) level in gastric mucosa were also investigated as well as the influence of 5-HT (5-hydroxytryptamine) on gastric mucosal blood flow. Gastric mucosal blood flow was measured by the hydrogen gas clearance method. The vascular pattern of the stomach was investigated by the infusion method with two-colored silicon rubber. CoQ10 anion radical and SOD levels in gastric tissue were assayed by electron spin resonance (ESR) and radioimmunoassay. The gastric mucosal blood flow decreased significantly early after the induction of stress. Impairment of gastric mucosal blood flow was highly correlated with 5-HT and CoQ10 anion radical and SOD levels. Reduction in gastric mucosal blood flow was consequently due to opening of arteriovenular shunt and hyperpermeability of true capillaries influenced by 5-HT. These results demonstrate that ischemia and reperfusion after reduction of the gastric mucosal blood flow resulted in the sequence of events that led to formation of acute gastric mucosal lesions.
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PMID:Gastric microcirculation and its regulating factors in stress. 194 Feb 4

The present study was undertaken to determine whether alpha-tocopherol pretreatment could modify cellular free radical metabolism during hepatic ischemia and subsequent reperfusion and prolong the viability of the liver. Although ischemia of the liver for 90 minutes did not permit survival of the animals, alpha-tocopherol administration (10 mg/kg of body weight) for 3 days increased the survival rate to 45.5%. The period of ischemia was accompanied by decreases in the hepatic adenosine triphosphate (ATP) level, endogenous alpha-tocopherol, and total glutathione (reduced and oxidized) without any significant increase in endogenous coenzyme Q (CoQ) homologs (CoQ9 and CoQ10) and lipid peroxide formation. The subsequent restoration of blood flow resulted in a low recovery of ATP and marked decreases in endogenous alpha-tocopherol, total glutathione, and CoQ homologs and, on the contrary, a marked increase in lipid peroxide levels. In alpha-tocopherol-treated animals, however, resynthesis of ATP was accelerated even after 90 minutes of ischemia, and there were no changes in the levels of total glutathione or CoQ homologs or in the level of the enhanced alpha-tocopherol during the reperfusion period. The pretreatment also completely suppressed the elevation of lipid peroxide levels. These results are compatible with the assumption that cellular damage caused by hepatic ischemia can be explained by free radical reaction processes during ischemia and especially reperfusion and suggest that administration of a free radical scavenger and antioxidant, alpha-tocopherol, is effective in ischemic liver cell injury.
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PMID:Role of free radicals in ischemic rat liver cell injury: prevention of damage by alpha-tocopherol administration. 394 24

The present study was undertaken to determine whether CoQ10 administration to rats can protect hepatic mitochondrial functions, improve energy metabolism during hepatic ischemia and subsequent reperfusion, and prolong the viability of the organ. Although ischemia of the liver for 90 minutes did not permit survival of the animals, CoQ10 administration (6 mg/kg of body weight) increased the survival rate to 60%. The period of ischemia was accompanied by decreases in hepatic adenosine triphosphate (ATP) level and respiratory control index without significant increases in mitochondrial calcium content and lipid peroxide formation. The subsequent restoration of blood flow resulted in a low recovery of ATP level, recovery of respiratory control and ADP:O ratio to levels significantly lower than normal, and on the contrary, marked increases in mitochondrial calcium and lipid peroxide levels. However, in CoQ10-treated animals mitochondrial functions were all completely reversible, and resynthesis of ATP was accelerated even after 90 minutes of ischemia. The pretreatment also completely suppressed the elevation of mitochondrial calcium and lipid peroxide levels. These results suggest that preservation with CoQ10 of cellular damages caused by hepatic ischemia is probably due to protection of cellular and subcellular membranes from lipid peroxidation, so that mitochondrial functions are restored and cellular calcium homeostasis is maintained.
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PMID:Preservation of ischemic rat liver mitochondrial functions and liver viability with CoQ10. 707 62

It has been reported that CoQ10, ubiquionone, may have a protective effect on the mitochondrial injury induced by myocardial ischemia and reperfusion during open heart surgery. The purpose of this study was to investigate whether CoQ10 may enhance myocardial protection when given before ischemia, during ischemia or during reperfusion in the isolated working rat heart. Hearts (n = 6-9/group) from male Wistar rats were aerobically (37 degrees C) perfused (20 min) with bicarbonate buffer. In the first series of studies, this was followed by a 3 min infusion of St. Thomas' Hospital cardioplegic solution containing various concentrations of CoQ10. Hearts were then subjected to 39 min of normothermic (37 degrees C) global ischemia and 35 min of reperfusion (15 min Langendorff, 20 min working). The percent recovery of aortic flow (%AF) was 50.5 +/- 3.3% in the CoQ10 free controls versus 55.9 +/- 4.4, 62.1 +/- 3.1*% (*p < 0.05) in the 29, 44 and 58 mumol/L CoQ10 groups, respectively. Creatine kinase (CK) leakage during Langendorff reperfusion had a tendency to decrease in the 58 mumol/L group. In the second series of studies, 3 min of cardioplegia without CoQ10 and 38 min of ischemia (37 degrees C) were followed by a 15 min Langendorff reperfusion with 0 or 58 mumol/L of CoQ10 and 20 min working reperfusion. %AF was 53.2 +/- 2.7 and 39.2 +/- 7.1% in the 0 and 58 mumol/L CoQ10 groups, respectively. CK leakage had a tendency to increase in the 58 mumol/L group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of CoQ10 on myocardial ischemia/reperfusion injury in the isolated rat heart]. 760 95

Sixteen dogs, divided randomly into a control group and coenzyme Q10 group (10mg/kg, intraperitoneally before the operation), underwent deep hypothermic circulatory arrest with cardiopulmonary bypass, as is done clinically. At four time points cerebral cortex and cerebrospinal fluid specimens were collected to study free radical formation, energy metabolism, and ultrastructure. During cardiopulmonary bypass cerebral electron spin resonance spectra and malondialdehyde contents were progressively higher than before bypass, especially at the 60 minutes of circulatory arrest and 30 minutes of reperfusion (p1 < 0.01, p2 < 0.05). In the coenzyme Q10 group at the latter two time points, they had increased less than in the control group at same time points (p1 < 0.02, p2 < 0.005). Adenosine triphosphate content in the cortex during bypass decreased gradually from the prebypass level (p1 < 0.02, p2 = p3 < 0.001), while lactate in cerebrospinal fluid increased (p1 < 0.05, p2 = p3 < 0.001). In the coenzyme Q10 group, adenosine triphosphate at the latter two time points was greater than that in the control group (p1 = p2 < 0.05), while the lactate changes were not significantly different from control at each time point (all p > 0.05). Ultrastructure of the cortex was normal before bypass and almost normal during bypass, but it was obviously abnormal at 60 minutes of circulatory arrest and more seriously abnormal at 30 minutes of reperfusion. In the coenzyme Q10 group the abnormality was obviously reduced. The results suggest that oxygen-derived free radicals and abnormal energy metabolism might play critical roles in brain ischemia/reperfusion injury. Coenzyme Q10 could protect the brain by improving cerebral metabolism.
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PMID:Mechanisms of brain injury with deep hypothermic circulatory arrest and protective effects of coenzyme Q10. 802 55

Myocardial stunning, defined as a reversible decrease in contractility after ischemia and reperfusion, may be a manifestation of reperfusion injury caused by free oxygen radical damage. The aim of this study was to test the hypothesis that pretreatment with coenzyme Q10 (ubiquinone), believed to act as a free radical scavenger, reduces myocardial stunning in a porcine model. Twelve swine were randomized to receive either oral supplementation with coenzyme Q10 or placebo for 20 days. A normothermic open-chest model was used with short occlusion (8 min) of the distal left descending coronary artery followed by reperfusion. Regional contractile function was measured with epicardial Doppler crystals in ischemic and nonischemic segments by measuring thickening fraction of the left ventricular wall during systole. Stunning time was defined as the elapsed time of reduced contractility until return to baseline. Coenzyme Q10 concentrations were measured in blood and homogenized myocardial tissue by high performance liquid chromatography. Plasma levels of reduced coenzyme Q10 (ubiquinol) were higher in swine pretreated with the experimental medication as compared to placebo (mean 0.45 mg/l versus 0.11 mg/l, respectively). Myocardial tissue concentrations, however, did not show any changes (mean 0.79 micrograms/mg dry weight versus 0.74 micrograms/mg). Stunning time was significantly reduced in coenzyme Q10 pretreated animals (13.7 +/- 7.7 min versus 32.8 +/- 3.1 min, P < 0.01). In conclusion, chronic pretreatment with coenzyme Q10 protects ischemic myocardium in an open-chest swine model. The beneficial effect of coenzyme Q10 on myocardial stunning may be due to protection from free radical mediated reperfusion injury. This protective effect seems to be generated by a humoral rather than intracellular mechanism.
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PMID:Coenzyme Q10 protects ischemic myocardium in an open-chest swine model. 824 92

EPR spectroscopy was used to measure paramagnetic species in rat hearts freeze-clamped during control perfusion by the Neely procedure, after 25 min of normothermic global ischemia or 20 min of total reperfusion with oxygenated perfusate. The analysis of spectral and relaxation parameters measured at -40 degrees C showed that in all three cases free radicals in heart tissue were semiquinones of CoQ10 and flavins. Ischemia increased the amount of free radical species (mostly flavosemiquinones) in myocardium about two times, the beginning of reflow of perfusate resulted in decrease of the intensity of the EPR signal to an initial level. The saturation curves were different for control, ischemic and reoxygenated postischemic samples, and they demonstrated the heterogeneity of free radical centers in cardiac mitochondria.
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PMID:[Free radical centers in isolated rat heart tissue in a normal state, in ischemia, and reperfusion]. 838 1


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