title: The effects of dopamine, dobutamine and amrinone on mitochondrial function in cardiogenic shock.
abstract: The impairment of mitochondrial in non-infarcted myocardium under cardiogenic shock complicated by acute myocardial infarction was studied. We induced acute myocardial infarction in dogs by ligating the circumflex branch of the left coronary artery (LCX). On basis of left ventricular systolic pressure (LVPs) after 60 minutes, we divided the dogs into two groups: a group in which LVPs fell to below 70% of the pre-LCX ligation 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 minutes. 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 Dopamine and Dobutamine groups, hemodynamics became restored to the preligation 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 functioned at a lower level of activity than that of the Control group. However, in the Dopamine, Dobutamine, and Amrinone groups, the mitochondria functioned at a higher level. Electron microscopy revealed mitochondrial damage in the Saline group only. The results indicate that an energy production disorder in the non-infarcted myocardium may have pathogenetic implications in cardiogenic shock associated with acute myocardial infarction, while dopamine, dobutamine, and amrinone improve mitochondrial function, and ultimately improve cardiac function.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Mukae
authors.forename: T
authors.initials: T
authors.lastname: Yanagishita
authors.forename: E
authors.initials: E
authors.lastname: Geshi
authors.forename: K
authors.initials: K
authors.lastname: Umetsu
authors.forename: M
authors.initials: M
authors.lastname: Tomita
authors.forename: S
authors.initials: S
authors.lastname: Itoh
authors.forename: N
authors.initials: N
authors.lastname: Konno
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000676:Amrinone / Q000494:pharmacology*; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002352:Carrier Proteins; D004280:Dobutamine / Q000494:pharmacology*; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology*; D042967:Electron Transport Complex I; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism; D008565:Membrane Proteins / Q000378:metabolism; D008929:Mitochondria, Heart / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D025261:Mitochondrial Proton-Translocating ATPases; D009203:Myocardial Infarction / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D012770:Shock, Cardiogenic / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D016277:Ventricular Function, Left
chemical_list: D002316:Cardiotonic Agents; D002352:Carrier Proteins; D008565:Membrane Proteins; D004280:Dobutamine; D009247:NADH, NADPH Oxidoreductases; D003576:Electron Transport Complex IV; D000251:Adenosine Triphosphatases; D025261:Mitochondrial Proton-Translocating ATPases; D042967:Electron Transport Complex I; C020439:oligomycin sensitivity-conferring protein; D000676:Amrinone; D004298:Dopamine