Pulmonary and systemic hemodynamic effects of cardiac glycosides

Abstract

any physiological actions of digitalis glvcosides have been elucidated only recently although their effects in reversing congestive heart failure and slowing the heart rate have long been known.1-3 These drugs increase myocardial contractility and produce generalized vasoconstriction with consequent increase in systemic resistance. In some species, they also evoke constriction of the hepatic veins, with resultant splanchnic pooling. These actions are similar in normal subjects and those with congestive cardiac failure, but cardiac output varies with the way in which venous return is altered. In contrast to the extensive information on cardiac and systemic actions, little is known of the way in which digitalis glycosides affect the lung circulation.4-6 Because of the potential importance of digitalis-induced vasoconstriction on the pulmonary vasculature, this report concerns the effects of acetyl strophanthidin, strophanthidin (ouabain), and digoxin on the pulmonary as well as systemic circulation of the intact unanesthetized dog. In additional experiments, to eliminate the possible role of altered right or left heart dynamics, a preparation was devised in which a mechanical pump replaced the right heart and maintained pulmonary blood flow constant. Concurrently, left atria1 pressure was maintained at con-trol level after glycoside injection.