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Archivos de cardiología de México
versión On-line ISSN 1665-1731versión impresa ISSN 1405-9940
Resumen
RENDON, Dairo A. y LOPEZ, Luis F.. Activation of mitochondrial oxidative phosphorylation during (+/-)-isoproterenol-induced cell injury of myocardium. Arch. Cardiol. Méx. [online]. 2001, vol.71, n.1, pp.13-19. ISSN 1665-1731.
Hydrolytic and synthetic activities of mitochondrial ATPase were studied during (+/-)-isoproterenol-induced cell injury of the myocardium (67 mg/kg body weight). This research was a long-term study (72 h) in which rat heart homogenates, and a potentiometric method were used. Hydrolytic activities in homogenates from (+/-)-isoproterenol-treated rats were not statistically different, during the whole long-term study, from the hydrolytic activity in normal homogenates. The synthetic activity (mitochondrial oxidative phosphorylation) of mitochondrial ATPase increased at 3, 6, and 18 h (35, 48 and 23% respectively) after (+/-)-isoproterenol administration with regard to the control group. At 12 h and 21-72 h after drug administration, the data revealed no differences between synthetic activity of mitochondrial ATPase in control vs (+/-)-isoproterenol treated homogenates. The facts that synthetic and hydrolytic activities in homogenates from (+/-)-isoproterenol treated rats were never lower than the synthetic and hydrolytic activities in normal homogenates, and that activation of mitochondrial oxidative phosphorylation occurred at some times after (+/-)-isoproterenol treatment, suggest that no considerable and "negative" modifications occur in the active configuration of mitochondrial ATPase during (+/-)-isoproterenol-induced injury of the myocardium (67 mg/kg body weight).
Palabras llave : Isoproterenol; Oxidative phosphorylation; Mitochondrial ATPase.