BASAL RELEASE OF ENDOTHELIUM-DERIVED NITRIC-OXIDE PLAYS AN IMPORTANT ROLE IN THE PREVENTION OF AFTERLOAD MISMATCH IN ACUTE LEFT-VENTRICULARDYSFUNCTION

The basal release of endothelium-derived nitric oxide (EDNO) is consid ered to play an important role in regulating the vascular tone in norm al subjects; however, its role in the presence of acute heart failure is unknown. This study was designed to clarify the role of a basal rel ease of EDNO in the presence of acute heart failure. Acute ischemic le ft ventricular (LV) dysfunction was produced in 22 dogs by coronary mi croembolization. After the embolization, only saline solution was intr avenously infused for sixty minutes in 10 dogs. In another 12 dogs, N- G-monomethyl-L-arginine (L-NMMA), which is known to inhibit the format ion of EDNO in the vascular endothelium, was intravenously infused at a rate of 20 mu g/kg/minute for sixty minutes. Infusion of saline solu tion did not produce any changes in hemodynamic variables. Infusion of L-NMMA caused increases in mean aortic pressure, systemic vascular re sistance, and LV end-diastolic pressure without changes in the LV peak + and - dP/dt (time constant) of LV pressure fall, and these changes were associated with a giant ''v'' wave in the tracing of left atrial pressure and a decrease in cardiac output. The basal release of EDNO m ay play an important role in the prevention of afterload elevation, su bsequent cardiac output reduction, and afterload mismatch in the prese nce of acute heart failure.