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)

A randomized, prospective study of the effectiveness of preoperative administration of coenzyme Q10 on the prophylaxis of postoperative low cardiac output state was performed in 50 patients with acquired valvular diseases necessitating valve replacement. There were 25 patients in the treatment group and 25 in the control group. Patients in the treatment group received 30 to 60 mg of coenzyme Q10 orally for six days before operation. Preoperative clinical variables, operative procedures, total cardiopulmonary bypass time, and aortic cross-clamping time were similar for the two groups. Postoperatively, mild to severe low cardiac output state developed in 28 of 50 patients (56%) and necessitated the administration of considerable amounts of inotropic agent. The treatment group showed a significantly lower incidence of low cardiac output state during the recovery period than the control group (p less than 0.05). These results suggest that preoperative administration of coenzyme Q10 will increase the tolerance of human hearts to ischemia during aortic cross-clamping.
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PMID:Coenzyme Q10: the prophylactic effect on low cardiac output following cardiac valve replacement. 703 33

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

Studies were done on the protective effects of alpha-tocopherol and coenzyme Q10 (CoQ10) on warm ischemic damage to the rat kidney. Administration of alpha-tocopherol (10 mg/kg body wt/day) for 7 days or a single i.p. injection of CoQ10 (6 mg/kg body wt) increased the survival rate from 0 to 46.7% of the rats subjected to warm ischemia for 120 min. The administration of alpha-tocopherol and CoQ10 increased adenosine triphosphate (ATP) in the renal tissue from 0.53 +/- 0.18 to 0.92 +/- 0.29, and from 0.64 +/- 0.26 to 1.00 +/- 0.54 mumol/g wet weight, respectively, 4-hr reperfusion after 120 min of warm ischemia. Serum creatinine levels of the surviving rats after 120 min of warm ischemia was 9.98 +/- 0.19 mg/100 ml in the control group and 5.84 +/- 0.95 and 7.27 +/- 1.62 mg/100 ml, respectively, in alpha-tocopherol and CoQ10 administered group, when determined 2 days after the operation. These results indicate that alpha-tocopherol and CoQ10 have a protective effect on warm ischemic damage to the rat kidney, demonstrated by an increase in ATP resynthesis after reflow following warm ischemia and by the maintenance of a lower serum creatinine level. This effect was accompanied by an increase in the survival rate of ischemic rats.
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PMID:Protective effects of alpha-tocopherol and coenzyme Q10 on warm ischemic damages of the rat kidney. 729 91

The heart is the most susceptible of all the organs to premature aging and free radical oxidative stress. Clinical research has clearly documented the role of free radical damage and the progression of numerous degenerative diseases, particularly cardiovascular disease. This may be the result of acute ischemia-reperfusion injury, endothelial damage of hyperhomocysteinemia, as well as chronic oxidative damage secondary to lipid peroxidation. Fortunately, although highly responsive, and therefore vulnerable to the effects of oxidative stress, the heart is also receptive to the benefits of targeted phytonutrients, antioxidants, and nutritionals. The effects of antioxidant nutrients have been extensively evaluated in epidemiological, population, and clinical studies. Phytonutrients such as the natural flavonoids and carotenoids found in fresh fruits and vegetables or vitamins C, E, and beta-carotene have powerful antioxidant effects. In addition, minerals like selenium and nutrients such as coenzyme Q10 will minimize free radical risk and optimize a favorable outcome from the ubiquitous presence of oxidative stress on the cardiovascular system. The B complex, particularly folic acid, B12, and B6 are also essential in the prevention of hyperhomocysteinemia, another major risk factor for the circulatory system. Measures to minimize accumulation of heavy metals in the body, especially iron and copper, which are capable of initiating adverse free radical reactions, will also help to assuage oxidative stress. Thus, the combination of a healthy diet supplemented with antioxidants and phytonutrients may be useful in the prevention and promotion of optimum cardiovascular health.
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PMID:Free radicals, oxidative stress, oxidized low density lipoprotein (LDL), and the heart: antioxidants and other strategies to limit cardiovascular damage. 758 73

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

The authors prepared an experimental animal model of ischemia and reperfusion of the limbs to evaluate in vivo the reactive oxygen species involvement and protective role of coenzyme Q10 in reperfusion injury. A group of male rabbits (untreated group) underwent clamping of abdominal aorta for 3 hr and then declamping; at intervals blood sampling was drawn for coenzyme Q10, vitamin E, lactic acid and creatine kinase assays. Another group of male rabbits (treated group) underwent the same ischemia period but before declamping coenzyme Q10 was administered intra aorta. In untreated group, coenzyme Q10 and vitamin E plasma levels decreased while lactic acid and creatine kinase plasma levels increased during reperfusion. These data demonstrate that, after only 3 hr of ischemia, the extremities show a biochemical reperfusion injury, and this involves an increased consumption of antioxidants such as coenzyme Q10 and vitamin E. In the treated group, the increase of creatine kinase plasma levels during reperfusion was not significant, while the decrease in vitamin E was more marked.
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PMID:Protective role in vivo of coenzyme Q10 during reperfusion of ischemic limbs. 775 29

This study investigated the biosynthesis of ubiquinone in isolated and perfused hearts of young and aged rats exposed to ischemia and reperfusion. A first group of hearts was used to determine the changes in coenzyme Q9 (CoQ9) and coenzyme Q10 (CoQ10) concentrations at mitochondrial and microsomal level after 30 min of ischemia (98% reduction of the preischemic flow) and 60 min of reperfusion. A second group was utilized to evaluate the rate of CoQ9 and CoQ10 biosynthesis in the membranes by dissolving two ubiquinone precursors, p-OH-[U-14C]benzoate and mevalonolactone, in the perfusion buffer. The hearts were aerobically perfused for 60 min in the presence of the precursors either immediately after the equilibration period or following 30 min ischemia. The young rat hearts showed a 30% reduction in the mitochondrial levels of CoQ9 after ischemia and reperfusion with respect to the preischemic values (P < 0.05 and P < 0.01, respectively). On the contrary, the mitochondrial CoQ9 content was not modified under these conditions in the aged hearts. At the end of reperfusion, the biosynthesis of mitochondrial CoQ9 and CoQ10 was higher in the young rats (P < 0.05), and lower in the aged rats (P < 0.05), with respect to the aerobic perfusion. In both young and aged rats minor changes in CoQ9 concentrations and biosynthesis were observed at microsomal level. These results indicate that myocardial reperfusion decreases the mitochondrial content of ubiquinone and stimulates CoQ9 biosynthesis in young rats but not in aged rats.
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PMID:Adaptive changes in coenzyme Q biosynthesis to myocardial reperfusion in young and aged rats. 776 Mar 52

To evaluate the effect of coenzyme Q10 in reducing postoperative cardiac complications after ischemia and reperfusion, we randomly divided 40 patients undergoing elective coronary artery bypass into two groups: patients in group 1 received coenzyme Q10 (150 mg/day) for 7 days before operation, and those in group 2 were the control group. Concentrations of thiobarbituric acid-reactive substances (malondialdehyde), conjugated dienes, and cardiac isoenzymes of creatine kinase were measured in samples from both arterial and coronary sinus sites. Serial sampling was performed 5 minutes after heparin administration, at 10 and 30 minutes during cardiopulmonary bypass, 15 and 30 minutes after aortic cross-clamp removal, and 5 minutes after protamine administration. The concentrations of malondialdehyde, conjugated dienes, and creatine kinase in group 1 were significantly lower than those in group 2. The decrease in plasma malondialdehyde concentrations correlated positively with the decrease in creatine kinase levels in the coronary sinus. The treatment group showed a significantly lower incidence of ventricular arrhythmias during the recovery period than did the control group (p < 0.05). Although the percentage of patients requiring inotropic agents was not significantly different between the two groups, the mean dosage of dopamine required to maintain stable hemodynamics was significantly lower in patients of group 1 than in those of group 2 (p < 0.01). Our findings suggest that pretreatment with coenzyme Q10 may play a protective role during routine bypass grafting by attenuating the degree of peroxidative damage.
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PMID:Protection by coenzyme Q10 from myocardial reperfusion injury during coronary artery bypass grafting. 797 70

The effects of coenzyme Q10 (CoQ) were studied in isolated, isovolumic rat hearts during a 30-min period of global ischemia followed by 40 min of reperfusion. After reperfusion 1) the relative recovery of developed pressure (DP) was increased by CoQ (75 vs. 40% of the preischemic value for 20 microM CoQ and control hearts, respectively, P < 0.001); 2) diastolic pressure elevation was decreased by CoQ (20 vs. 50 mmHg in CoQ vs. control hearts, respectively, P < 0.001); and 3) recovery of high-energy phosphates and reduction of inorganic phosphate were approximately twofold greater in CoQ vs. control hearts (P < 0.001 for each parameter). The beneficial effects of CoQ were not observed when CoQ was added at the onset of reperfusion. The total free generation during reperfusion was not affected by CoQ. In unpaced hearts, in the presence of verapamil to prevent spontaneous beating, spontaneous Ca2+ oscillations were measured as scattered laser light intensity fluctuations (SLIF). The transient rise in SLIF in the postischemic reperfused myocardium, which previously has been shown to predict the extent of Ca2+ overload, was suppressed by CoQ (P < 0.001). These results suggest that while early CoQ treatment does not scavenge the primary burst of superoxide or hydroxy radical generation, which occurs on reperfusion, it markedly improves the functional recovery during reperfusion by enhancing the recovery of high-energy phosphates and preventing Ca2+ overload.
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PMID:Coenzyme Q10 enhances cardiac functional and metabolic recovery and reduces Ca2+ overload during postischemic reperfusion. 802 79

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


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