THE EFFECTS OF DOPAMINE, DOBUTAMINE AND AMRINONE ON MITOCHONDRIAL-FUNCTION IN CARDIOGENIC-SHOCK

The impairment of mitochondria in non-infarcted myocardium under cardi ogenic shock complicated by acute myocardial infarction was studied. W e induced acute myocardial infarction in dogs by ligating the circumfl ex branch of the left coronary artery (LCX). On basis of left ventricu lar systolic pressure (LVPs) after 60 minutes, we divided the dogs int o two groups: a group in which LVPs fell to below 70% of the pre-LCX l igation level, and a Control group in which LVPs remained more than 90 %. The former group was further divided into four subgroups, depending on infusion of dopamine, dobutamine, amrinone or saline after 90 minu tes. Mitochondria were prepared and mitochondrial respiratory activity determined. In the Saline group, hemodynamics became reduced to less than 70% of the preligation level after 120 minutes, however, in the D opamine and Dobutamine groups, hemodynamics became restored to the pre ligation level. In the Amrinone group, LVPs decreased slightly, while cardiac output, LV Max. dp/dt and myocardial blood flow increased. In the Saline group, mitochondria in the non-infarcted myocardium functio ned at a lower level of activity than that of the Control group. Howev er, in the Dopamine, Dobutamine, and Amrinone groups, the mitochondria functioned at a higher level. Electron microscopy revealed mitochondr ial damage in the Saline group only. The results indicate that an ener gy production disorder in the noninfarcted myocardium may have pathoge netic implications in cardiogenic shock associated with acute myocardi al infarction, while dopamine, dobutamine, and amrinone improve mitoch ondrial function, and ultimately improve cardiac function.