Experimental myocardial infarction. VI. Efficacy and toxicity of digitalis in acute and healing phase in intact conscious dogs.
Use of digitalis in myocardial infarction is controversial. To determine the efficacy and toxic threshold, serial infusions of 3 mug/kg per min of acetyl-strophanthidin were given to six intact conscious dogs 24 hr before and 1 hr, 2 days, and 7 days after myocardial infarction induced by inflation of a balloon cuff implanted on the left anterior descending coronary artery. Within 1 hr after myocardial infarction, heart rate increased by 28%. Left ventricular end-diastolic pressure increased from 7 to 20 mm Hg, and stroke volume decreased by 25%. At this time acetylstrophanthidin caused no beneficial hemodynamic change, 1 wk later, the heart rate and left ventricular end-diastolic pressure had declined toward normal but remained elevated. At this time, acetylstrophanthidin lowered left ventricular end-diastolic pressure by 25%, and increased the stroke volume and cardiac output by 25% and 21% respectively, without any change in heart rate or aortic pressure. Tolerance to acetylstrophanthidin, defined as appearance of ventricular tachycardia, declined the 1st hr after myocardial infarction by 24% (P<0.05) from the control level of 43 +/-4 mug/kg (SEM), but subsequently returned to control.Thus, immediately after myocardial infarction, tolerance to acetylstrophanthidin was reduced, and left ventricular failure was not ameliorated. 1 wk later in the healing phase of myocardial infarction, tolerance to acetylstrophanthidin returned to normal and left ventricular performance was improved by this drug. The study suggests a limited therapeutic role for digitalis in the treatment of left ventricular failure in the acute phase immediately after myocardial infarction, but beneficial effects may occur in the healing phase 1 wk later.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D002712:Chlorides / Q000097:blood; D004071:Digitalis Glycosides / Q000494:pharmacology / Q000627:therapeutic use* / Q000633:toxicity*; D004195:Disease Models, Animal; D004285:Dogs; D004361:Drug Tolerance; D004562:Electrocardiography; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood
D002712:Chlorides; D004071:Digitalis Glycosides; D002245:Carbon Dioxide; D012964:Sodium; D011188:Potassium; D010100:Oxygen