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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A recent study has indicated that the generation of an oxygen radical in freeze-clamped myocardium on reperfusion can be directly demonstrated using electron-spin resonance spectroscopy (ESR). However, the results need to be analyzed with caution, since artifactual radicals are misleading problems common to this method. To test whether that reported superoxide is truly the biologically existing radical or an artifactual radical, we performed experiments using isolated, perfused rat and rabbit hearts and open-chest canine hearts subjected to ischemia/reperfusion. Radicals were freeze trapped at 77 degrees K, and ESR measurements were made. The ESR spectra exhibited four free radicals. Among these, two radicals which had been previously claimed as superoxide and a nitrogen-centered radical were shown as mechanically yielded artifactual radicals. These were produced by pulverization of the frozen sample. In artifact-free samples, superoxide could not be detected. The radicals native to the myocardium were identified as coenzyme Q10-. and another radical the species of which remains unclear.
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PMID:Is superoxide demonstration by electron-spin resonance spectroscopy really superoxide? 283 95

In the first part of this study, oxygen derived radicals (O2-radical) were indirectly demonstrated as causative agents for ischemia/reperfusion injury by showing myocardial protection of radical scavengers. In 19 open chest dogs, the left anterior descending coronary artery was occluded for 90 min and subsequently reperfused for 60 min. Group A received SOD (15000 U/kg), catalase (5 mg/kg) and 20% mannitol (18 ml/kg) via the left atrium starting 15 min pre-occlusion and ending 15 min after reperfusion. Group B received infusion of saline and served as control. The severity of myocardial injury was evaluated by epicardial ECG, hemodynamics, echo cardiographical asynergy area and left ventricular wall thickness, histopathological findings and magnitude of necrotic area. Group A demonstrated less injury than group B in most of the parameters. In particular, ratios of necrotic to perfused areas determined by dual fluorescence methods were significantly limited in group A (34.1 +/- 12.0 vs 66.0 +/- 11.3%), indirectly verifying that the O2- radicals play an important role in the genesis of ischema/reperfusion injury. In the second part of the study, the direct measurement of radicals in freeze-clamped myocardium was reported using electron spin resonance (ESR) spectroscopy. With this method, it was not possible to demonstrate the generation of O2-radicals in ischemic/reperfused myocardium. However, the data suggested that coenzyme Q10 anion radical, which exists in the normal myocardium, might provide an index of tissue injury.
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PMID:The link between free radicals and myocardial injury. 284 5

This study was undertaken to determine whether pretreatment of the donor rat with coenzyme Q10 (CoQ10) would protect against hepatic ischemia induced for 30 minutes at normothermic body temperature. Fresh liver transplants were used as controls (minus warm ischemia of 30 minutes) and gave a 1-week survival rate of 84.6%. CoQ10 was administered intravenously (10 mg/kg body weight) to the donor rat 1 hour before induction of warm ischemia (group A). In another group (B), the same dose was given intravenously not only to the donor rat but also to the recipient rat 1 hour before grafting. None of the placebo group survived more than 2 days. The 1-week survival rates of the groups pretreated with CoQ10 were 45.5% for group A and 50% for group B. There was no significant difference between groups A and B. A statistically significant difference was demonstrated between the placebo group and both CoQ10-treated groups (p less than 0.05). It was therefore assumed that CoQ10, accumulated in the donor liver, was a primary factor in improving survival. Serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), serum alkaline phosphatase (SALP), total bilirubin, and total protein were measured by means of light and electron microscopic examination of the liver 6 months after transplantation. Long-term-surviving rats with transplanted, ischemically damaged liver that was pretreated with CoQ10 showed a decrease in the activity of SGOT and SGPT and an increase in levels of total protein to the normal range (as well as to those levels exhibited by fresh-liver-transplanted rats) with practically no change in levels of SALP, total bilirubin, or in histologic findings. These results indicate that donor pretreatment with CoQ10 is useful for increasing survival after warm ischemic damage of rat liver grafts.
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PMID:Ischemic damage prevention by coenzyme Q10 treatment of the donor before orthotopic liver transplantation: biochemical and histologic findings. 331 78

This study tests the hypothesis that the oxygen radical scavenger coenzyme Q10 can be given both intravenously and in the cardioplegic solution and can improve muscle salvage following surgical revascularization. Pilot studies were carried out in dogs undergoing 40 minutes of coronary artery ligation with reperfusion with normal blood, with the heart in the beating, working state. Intravenous infusions of coenzyme Q10 (10 mg/kg) 5 minutes before reperfusion resulted in improved recovery of creatine phosphate, adenosine triphosphate, total adenine nucleotide, and myocardial function reverse estimated by postextrasystolic potentiation, in comparison with the degree of recovery in untreated dogs. Experimental studies were done on 27 dogs undergoing 2 hours of left anterior descending coronary artery occlusion and subsequent reperfusion with and without total vented bypass. Thirteen dogs received intravenous coenzyme Q10 10 minutes before extracorporeal circulation, six received substrate-enriched blood cardioplegic solution with added coenzyme Q10, and six received normal blood reperfusate. Six others had cardioplegic reperfusion without coenzyme Q10. The systolic bulging that occurred during ischemia (ultrasonic crystals) persisted after reperfusion with normal blood (-25% systolic shortening, p less than 0.05), and 44% transmural triphenyltetrazolium chloride nonstaining occurred in the area at risk. Conversely, hearts receiving substrate-enriched blood cardioplegic solution recovered 37% contractility (p less than 0.05), with the least, and only, subendocardial triphenyltetrazolium chloride nonstaining (25% of area at risk) occurring with intravenous coenzyme Q10 before bypass and coenzyme Q10 supplementation of the cardioplegic solution. Intravenous coenzyme Q10, given just before reperfusion (possibly in transit to the operating room), enhances the role of substrate-enriched blood cardioplegic solution (especially when added to the cardioplegic solution) in salvaging ischemic myocardium and allowing immediate functional recovery.
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PMID:Reperfusate composition: supplemental role of intravenous and intracoronary coenzyme Q10 in avoiding reperfusion damage. 374 85

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

To evaluate effects of coenzyme Q10 added to a potassium cardioplegic solution for myocardial protection, 17 mongrel dogs underwent 60 minutes of ischemic cardiac arrest under cardiopulmonary bypass. Cardiac arrest was induced by infusing the cardioplegic solution into the aortic root every 20 minutes. Experimental animals were divided into three groups according to the cardioplegic solution used. In Group 1, we used our clinical potassium cardioplegic solution (K+, 22.31 mEq/L); in Group 2, potassium cardioplegic solution with coenzyme Q10 added (coenzyme Q10, 30 mg/500 ml of solution); and in Group 3, cardioplegic solution with coenzyme Q10 solvent. Exogenous coenzyme Q10 in the cardioplegic solution provided significantly high myocardial stores of adenosine triphosphate and creatine phosphate and a low level of lactate during induced ischemia and reperfusion. Furthermore, percent recovery of the aortic flow in Group 2 was significantly higher than that in the other two groups. Ultrastructures of the ischemic myocardium in Group 2 were better preserved than those in Group 1. Addition of coenzyme Q10 to potassium cardioplegia resulted in improved myocardial oxygen utilization and accelerated recovery of myocardial energy metabolism after reestablishment of circulation.
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PMID:Effects of coenzyme Q10 added to a potassium cardioplegic solution for myocardial protection during ischemic cardiac arrest. 396 34

The present study was performed to clarify oxygen-induced damage following myocardial reperfusion, using three mitochondrial preparations from isolated rabbit hearts (nonischemic hearts and those subjected to 40 and 90 minutes of normothermic global ischemia). The viability of mitochondria was evaluated by adenosine triphosphate generation. The extent of mitochondrial injury produced by reactive oxygen metabolism was assessed by the intensity of hydroxyl radical signal detected with electron spin resonance spectroscopy and the reduction of coenzyme Q10 level. The greatest oxygen-induced injury was observed in 40-minute ischemic mitochondria exposed to pure oxygen. The use of superoxide dismutase and catalase satisfactorily prevented the oxygen-induced injury. Moreover, the net adenosine triphosphate generation of the 40-minute ischemic mitochondria was comparable to that of the nonischemic mitochondria without the enzymes. These results suggest that reperfusion of the ischemic myocardium with viable mitochondria is deleterious, because mitochondria are susceptible to injury resulting from oxidative metabolism, and that the use of superoxide dismutase, together with catalase, is beneficial for the restoration of cardiac function after ischemia.
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PMID:In vitro study on contribution of oxidative metabolism of isolated rabbit heart mitochondria to myocardial reperfusion injury. 608 77

In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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PMID:Effect of coenzyme Q10 on hypertrophied ischemic myocardium during aortic cross clamping for 2 hr, from the aspect of energy metabolism. 622 44

The present study was undertaken to determine whether hepatic ischemia and the subsequent reflow of blood had any effect on the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione, and whether coenzyme Q10 (6 mg/kg of body weight) altered these levels. Ischemia of the rat liver for 90 min resulted in decreases of 19.1 and 19.6% of endogenous alpha-tocopherol and total glutathione (GSH + GSSG) without significant changes in the levels of endogenous total coenzyme Q homologs (oxidized and reduced). Restoration of the blood flow resulted in marked decreases in endogenous coenzyme Q homologs, alpha-tocopherol, and total glutathione in the control group. In coenzyme Q10-treated animals, however, there were no changes in the levels of endogenous total coenzyme Q9, alpha-tocopherol, or total glutathione as well as in the level of the enhanced total coenzyme Q10 during the reperfusion period. On the other hand, decreases in alpha-tocopherol and total glutathione during the period of ischemia remained unchanged. 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 exogenous coenzyme Q10 functions as an antioxidant with endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in lipid peroxidation during reperfusion.
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PMID:Changes in the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in rat liver after hepatic ischemia and reperfusion, and the effect of pretreatment with coenzyme Q10. 669 4

A protective effect of coenzyme Q10 on the ischemic and reperfused myocardium was investigated in the isolated working rat heart preparation. Rats were treated intraperitoneally with 30 mg/kg coenzyme Q10, daily for 7 days. The controls were given the same dose of the vehicle. After 25 min of equilibration the hearts were made totally ischemic at 35.5 degrees C for 30 min, arrested with high potassium cardioplegic solution immediately after aortic cross clamping. The recovery of cardiac power in the coenzyme Q10 pretreated group was significantly (P less than 0.05) better than that in vehicle pretreated group. Creatine phosphokinase (CPK) release during reperfusion was significantly (P less than 0.05) reduced by the pretreatment of coenzyme Q10. Tissue analysis for high energy phosphate compounds revealed no significant difference between the two groups. Tissue lactate content at 30 min of ischemia was significantly (P less than 0.001) lower in the coenzyme Q10 pretreated group. These results suggest that pretreatment with coenzyme Q10 is effective for reducing ischemic injury caused by aortic cross clamping.
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PMID:Effects of pretreatment with coenzyme Q10 on myocardial preservation during aortic cross clamping. 682 5


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