Ri. Ogilvie et D. Zborowskasluis, ACUTE EFFECT OF L-ARGININE ON HEMODYNAMICS AND VASCULAR CAPACITANCE IN THE CANINE PACING MODEL OF HEART-FAILURE, Journal of cardiovascular pharmacology, 26(3), 1995, pp. 407-413
The effect of L-arginine, 250 mg/kg over 10 min, on hemodynamics and v
enous function was studied in nine splenectomized dogs under light pen
tobarbital anesthesia before and after 17 +/- 1 days of rapid right ve
ntricular pacing (RRVP) at 250 beats/min. Chronic RRVP induced mild co
ngestive heart failure with increased mean circulatory filling (Pmcf),
right atrial (Pra) and pulmonary capillary wedge pressures (Ppcw), an
d reduced cardiac output (CO). During the development of heart failure
, total vascular compliance assessed from Pmcf-blood volume relationsh
ips during circulatory arrest was unchanged, but total vascular capaci
tance was markedly reduced, with an increase in stressed and reduction
in unstressed blood volumes. At baseline but not after RRVP, L-argini
ne increased CO and reduced pulmonary vascular resistance. There were
no significant changes in Pra, Ppcw, or total peripheral resistance. L
-Arginine failed to alter total vascular compliance and capacitance or
central blood volume in the baseline or failure state. These results
do not support the hypothesis that increased Pmcf and reduced total va
scular capacitance in the early stages of pacing-induced heart failure
are caused by reduced substrate availability for or an endogenous com
petitive antagonist of NO synthase in venous endothelial cells.