K. Yamamoto et al., BASAL RELEASE OF ENDOTHELIUM-DERIVED NITRIC-OXIDE PLAYS AN IMPORTANT ROLE IN THE PREVENTION OF AFTERLOAD MISMATCH IN ACUTE LEFT-VENTRICULARDYSFUNCTION, Angiology, 46(9), 1995, pp. 767-777
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.