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Korean Circ J. 1990 Sep;20(3):381-395. Korean. Original Article. https://doi.org/10.4070/kcj.1990.20.3.381
Kim MS , Yoo HJ , Chung MH , Lim JK , Lee YS .
Abstract

The present study was performed to investigate the role catecholamine in the genesis of reperfusion injury of ischemic heart. The possible involvement of catecholamine in the xanthine oxidase-linked production of oxygen free radicals was studied. langendorff preparations of rat hearts were made ischemic for 60 min followed by reperfusion. Upon reperfusion norepinephrine(NE) was significantly released into the coronary effluent regardless of oxygenation of the perfusion solution. Both the increased releases of creatine phosphokinase(CPK) and malondialdehyde(MDA) and the production of superoxide anion in the ischemic-reperfused hearts were significantly reduced by the treatment with either reserpine, a catecholamine depletor, or propranolol, a beta-adrenergic receptor blocker. In the reserpinized hearts, infusion of exogenous NE reversed the releases of CPK and MDA and the superoxide anion production to the original higher levels. The releases of CPK and MDA as well as the production of superoxide anion induced by NE in the reserpinized hearts were significantly depressed either by allopurinol, a specific competitive inhibior of xanthine oxidase(XOD), or by the calcium removal from the perfusion solution. Compared with the XOD activity of control ischemic hearts, that of the hearts treated with reserpine or propranolol showed lower activity in the oxygen radical producing 0-form and higher activity in D/0-form. In the reserpinized ischemic hearts, infusion of exogenous NE increased 0-form, but decreased D/0-form of XOD. The changes in XOD activities induced by exogenous NE was prevented by phenylmethylsulfonyl fluoride(a serine protease inhibitor) and pimoxide(a calmodulin inhibitor) as well as by calcium removal from the perfusion solution. It is suggested from the results that in the inchemic-reperfused heart of rat catecholamine participates in D/0 to 0-form conversion of XOD by promoting the calcium-calmodulin-dependent proteolysis and plays a contributing role in the production of oxygen free radical.

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