DEGREE OF EXTERNAL FORCE TO THE LEFT-VENTRICLE DETERMINES HEMODYNAMIC-RESPONSE TO NITROPRUSSIDE IN FAILING HEARTS - COMPARISON WITH THE RESPONSE TO DOBUTAMINE

Vasodilators frequently, although not always, increase cardiac output (GO) in patients with congestive heart failure (CHF) despite a decreas e in left ventricular (LV) diastolic pressure. In patients with CHF, v asodilator-induced decrease in LV diastolic pressure without decrease in ''preload'' plays an important role in the vasodilator-induced incr ease in CO failure that may be caused by a vasodilator-induced reducti on in external force to the LV. To clarify the hypothesis that a hemod ynamic response to vasodilators depends on the degree of external forc e to the LV in failing hearts before drug administration and to examin e whether the degree of the external force also affects a hemodynamic response to positive inotropic agents, we produced in 17 dogs two diff erent conditions of LV dysfunction with high LV end-diastolic pressure (EDP: greater than or equal to 15 mm Hg), i.e., 1 with high right ven tricular (RV) EDP (condition 1) and the other with lower RVEDP than co ndition 1 (condition 2), and compared hemodynamic effects of nitroprus side or dobutamine between these two conditions. Condition 1 was produ ced by the injection of a small dose of microspheres into the left cor onary artery and intravenous infusion of dextran. Condition 2 was prod uced only by the injection of a large dose of microspheres. The nitrop russide-induced decrease in LVEDP was associated with a greater decrea se in RVEDP and lesser decreases in mean left atrial pressure and LV e nd-diastolic diameter in condition 1 than in condition 2. CO increased in condition 1; however, CO then decreased in condition 2. The nitrop russide-induced changes in CO inversely correlated with those in RVEDP (r = 0.65, p < 0.05). Dobutamine increased CO in both conditions. The refore, a hemodynamic response to vasodilators, in contrast to respons e to positive inotropic agents, depends on the degree of external forc e to the left ventricle before drug administration in failing hearts.