A differential effect of ouabain and beta-agonists on contractility and lactic acid production in the hypertrophied heart.
In response to norepinephrine or isoproterenol, dogs with pressure overload cardiac hypertrophy showed depressed contractility and myocardial lactic acid production when compared to normal dogs. In these dogs with hypertrophy the inotropic response to ouabain remained normal and myocardial lactate production was not induced. This finding is compatible with the idea that the increased oxygen demand induced by beta-agonists exceeds the limited coronary blood flow reserve of the hypertrophied heart leading to myocardial anaerobic metabolism and reduced inotropic responsiveness. Ouabain, on the other hand, did not induce anaerobic metabolism and the inotropic response was not depressed.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology; D007773:Lactates / Q000096:biosynthesis*; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology*
D000318:Adrenergic beta-Agonists; D007773:Lactates; D010042:Ouabain; D007545:Isoproterenol; D009638:Norepinephrine