ACUTE EFFECT OF L-ARGININE ON HEMODYNAMICS AND VASCULAR CAPACITANCE IN THE CANINE PACING MODEL OF HEART-FAILURE

Citation
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
Citations number
38
Categorie Soggetti
Cardiac & Cardiovascular System","Respiratory System","Pharmacology & Pharmacy
ISSN journal
01602446
Volume
26
Issue
3
Year of publication
1995
Pages
407 - 413
Database
ISI
SICI code
0160-2446(1995)26:3<407:AEOLOH>2.0.ZU;2-W
Abstract
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.