TY - JOUR
T1 - Evaluation of the Vasodilator vs Inotropic Effect of Milrinone Using an Animal Model of Left Ventricular Failure
T2 - Reversal of Disopyramide Depression of the Myocardium with Milrinone
AU - Goldberg, Emanuel
AU - Berdoff, Russell
AU - Spivack, George
AU - Haimowitz, Azriel
AU - Tay, Steven
PY - 1987/9
Y1 - 1987/9
N2 - Milrinone M has been shown to improve left ventricular LV performance in animal and human studies. M has strong vasodilator action, and whether increased LV performance is due primarily to vasodilation or to a direct positive inotropic effect is unclear. Ten mongrel dogs were studied. Disopyramide caused a significant and sus tained decrease in LV function and was a good model for myocardial depres sion. At equal reduction in systemic vascular resistance SVR, M reversed this LV depression to a significantly greater degree than nitroprusside NP did. At equal levels of vasodilation, M produced significantly greater improve ment in indices of LV function than NP did in our model of disopyramide- induced LV failure. This suggests that its effect on LV function is not due entirely to afterload reduction, or to reflex sympathetic stimulation, but has a substantial component of direct inotropic stimulation. This study also demon strated a reversal of disopyramide-induced LV dysfunction by M, which may be clinically useful since, as in many antiarrhythmics, myocardial depression may be a limiting factor in its use.
AB - Milrinone M has been shown to improve left ventricular LV performance in animal and human studies. M has strong vasodilator action, and whether increased LV performance is due primarily to vasodilation or to a direct positive inotropic effect is unclear. Ten mongrel dogs were studied. Disopyramide caused a significant and sus tained decrease in LV function and was a good model for myocardial depres sion. At equal reduction in systemic vascular resistance SVR, M reversed this LV depression to a significantly greater degree than nitroprusside NP did. At equal levels of vasodilation, M produced significantly greater improve ment in indices of LV function than NP did in our model of disopyramide- induced LV failure. This suggests that its effect on LV function is not due entirely to afterload reduction, or to reflex sympathetic stimulation, but has a substantial component of direct inotropic stimulation. This study also demon strated a reversal of disopyramide-induced LV dysfunction by M, which may be clinically useful since, as in many antiarrhythmics, myocardial depression may be a limiting factor in its use.
UR - http://www.scopus.com/inward/record.url?scp=0023232129&partnerID=8YFLogxK
U2 - 10.1177/000331978703800902
DO - 10.1177/000331978703800902
M3 - Article
C2 - 3662108
AN - SCOPUS:0023232129
SN - 0003-3197
VL - 38
SP - 657
EP - 662
JO - Angiology
JF - Angiology
IS - 9
ER -