Capitulo de libro
NON ISCHEMIC MYOCARDIAL PRECONDITIONING BY TACHYCARDIA AND EXERCISE
Fecha
2003Registro en:
978-1-4615-0355-2
978-1-4020-7195-9
978-1-4613-5036-1
1000642
Institución
Resumen
Myocardial preconditioning can be induced not only by ischemia but also by physiological stimuli like tachycardia and exercise. We studied in dogs the preconditioning effect of tachycardia. Five brief periods of tachycardia prior to occluding a coronary artery followed by reperfusion, reduced the infarct size by about 50%. This effect was prevented by blockade of adenosine receptors and also of mitochondrial ATP dependent potassium channels. Tachycardia did not produce ischemia and the results were not explained by changes in collateral flow to the ischemic region or in the hemodynamic variables. Since tachycardia produced preconditioning, we studied the possibility that exercise also induces preconditioning. In instrumented dogs the performance of brief periods of exercise on a treadmill a few minutes (early preconditioning) or 24 hours (late preconditioning) prior to a coronary occlusion and reperfusion, reduced the infarct size by about 77% and 46% respectively. Exercise did not produce ischemia and the results could not be explained by changes in collateral flow nor in the hemodynamic variables. This effect may partly explain the decrease in the incidence of coronary acute syndromes by regular exercise in humans. Because tachycardia and the intracoronary administration of Ca2+ induce preconditioning, we studied the changes in calcium transient induced by ischemia and the effect of tachycardia on these changes in myocardial sarcoplasmic reticulum vesicles. Ischemia increased Ca2+ release and decreased Ca2+ uptake by the sarcoplasmic reticulum. These effects were reverted in hearts preconditioned with tachycardia. These results suggest that the protective effect of tachycardia and probably that of exercise may be partly due to a decrease in the cytosolic Ca2+ overload produced by ischemia.