STEARE, SE; YELLON, DM; (1994) INCREASED ENDOGENOUS CATALASE ACTIVITY CAUSED BY HEAT-STRESS DOES NOT PROTECT THE ISOLATED RAT-HEART AGAINST EXOGENOUS HYDROGEN-PEROXIDE. CARDIOVASC RES , 28 (7) 1096 - 1101.
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Objective: The aim was to investigate the potential for the enhancement of endogenous catalase activity after heat stress to protect the isolated rat myocardium from the injurious effects of exogenous hydrogen peroxide. Methods: Male Sprague-Dawley rats were randomised to either heat stress or sham treatment. At 24 and 48 h after treatment hearts were retrogradely perfused at a constant flow rate of 10 ml.min(-1). After a 15 min stabilisation period hearts were perfused with 75 mu M hydrogen peroxide for 85 min. Mechanical function was measured by an intraventricular isovolumic latex balloon while coronary perfusate was collected for measurement of lactate dehydrogenase activity. At the end of the perfusion period the glutathione status of the hearts was determined. In separate experiments baseline cardiac catalase activity and glutathione state were measured 24 and 48 h after heat stress or sham treatment. Results: Cardiac catalase activity was increased by 49% at both 24 and 48 h after heat stress in comparison with sham controls. Glutathione concentrations were reduced by 12% 24 h after heat stress but had recovered by 48 h. Perfusion of sham hearts with 75 mu M hydrogen peroxide resulted in a progressive decline in mechanical function as evident by a fall in developed pressure and rise in diastolic pressure. Coronary resistance also rose during the perfusion period as shown by a progressive increase of coronary perfusion pressure. Coronary effluent lactate dehydrogenase release was only increased above basal concentrations at the end of the perfusion period, whereas cardiac glutathione concentrations were severely depleted. Hearts taken 24 h after heat stress showed a reduced resistance to the effect of 75 mu M hydrogen peroxide on mechanical activity, although there was no difference in the pattern of lactate dehydrogenase release or depletion of glutathione. Perfusion of hearts taken 48 h after heat stress with 75 mu M hydrogen peroxide resulted in the same effect on mechanical dysfunction, coronary resistance, lactate dehydrogenase release, and cardiac glutathione depletion as sham controls. Conclusion: The increase in endogenous cardiac catalase activity caused by prior heat stress is insufficient to protect the isolated rat heart from injury induced by exogenous hydrogen peroxide.
|Title:||INCREASED ENDOGENOUS CATALASE ACTIVITY CAUSED BY HEAT-STRESS DOES NOT PROTECT THE ISOLATED RAT-HEART AGAINST EXOGENOUS HYDROGEN-PEROXIDE|
|Keywords:||HEAT STRESS, OXIDANT STRESS, HYDROGEN PEROXIDE, CATALASE, MYOCARDIAL PROTECTION, POSTISCHEMIC VENTRICULAR RECOVERY, SHOCK RESPONSE, INJURY, REPERFUSION, ISCHEMIA|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science|
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