Effects of afterload reduction on global left ventricular and regional myocardial functions in the isolated canine heart with stenosis of a coronary arterial branch.
We examined the effects of graded reduction of afterload on the global left ventricular and regional myocardial functions as well as coronary hemodynamics in hearts with regional ischemia. We used isolated, paced canine hearts that were loaded with a hydraulic system that simulated the aortic input impedance of the dog's arterial tree. The loading conditions could be quantitatively and sequentially changed by the reduction of the systemic vascular resistance of the hydraulic system, while the preload was kept constant using a variable-height reservoir connected to the left atrium. The heart was perfused with arterial blood from a support dog. Mean coronary perfusion pressure was maintained equal to mean aortic pressure (AoP) by a servo-controlled pump. Then, the left circumflex branch was constricted to an approximate 50% flow reduction of the preischemic control condition. The myocardial lengths at ischemic and nonischemic regions were measured with two pairs of ultrasonic crystals. In the hearts without ischemia, cardiac output continued to increase, from 535 +/- 14 to 1181 +/- 74 ml/min (p less than 0.01), as mean AoP decreased fom 111 +/- 4 to 52 +/- 3 mm Hg (p less than 0.01), although mean coronary blood flow decreased by approximately 50%. During regional ischemia, at control pressures, performance of the ischemic region diminished from 0.94 +/- 0.15 to 0.77 +/- 0.15 mm (p less than 0.05). With a small decrease in afterload, from 98 +/- 6 to 86 +/- 3 mm Hg, performance improved slightly as in the normal region. With a larger reduction in afterload, from 86 +/- 3 to 55 +/- 6 mm Hg, performance of the ischemic region decreased from 0.77 +/- 0.15 to 0.61 +/- 0.15 mm (p less than 0.05) while cardiac output increased. Thus, there appears to be a bimodal change in performance: a baseline performance, perfusion pressure-mediated decrease and a second, afterload-modulated change.
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure; D002302:Cardiac Output; D002304:Cardiac Pacing, Artificial; D003250:Constriction; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology; D004285:Dogs; D006352:Heart Ventricles / Q000503:physiopathology; D009200:Myocardial Contraction; D010477:Perfusion; D014655:Vascular Resistance