Inotropic agents and functional recovery from ischemic cardiac arrest.
Short periods of ischemic arrest may cause myocardial cell damage so that reperfusion does not result in an immediate return to normal metabolic and contractile activity. Studies have been carried out using a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest in order to determine whether the use of inotropic agents (isoprenaline and dobutamine) to augment contractile activity during the early phase of post-ischemic reperfusion extends pre-existing damage and results in ultimate impairment of contractile activity. The results indicated the existance of a substantial metabolic reserve, capable of providing sufficient energy for a marked increase in dP/dt and heart rate, without inducing tissue damage. However, in this isolated rat heart preparation the use of these agents had relatively little effect upon cardiac output and could be shown to induce a dose-dependent reduction in stroke volume.
D000818:Animals; D002315:Cardiopulmonary Bypass; D002395:Catecholamines / Q000494:pharmacology*; D004195:Disease Models, Animal; D004280:Dobutamine / Q000494:pharmacology*; D006321:Heart / Q000503:physiopathology; D006323:Heart Arrest / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects*; D051381:Rats; D012038:Regeneration / Q000187:drug effects
D002395:Catecholamines; D004280:Dobutamine; D007545:Isoproterenol