EFFECT OF PERINDOPRIL IN PACING-INDUCED CANINE MODELS OF ACUTE AND CHRONIC HEART-FAILURE

Citation
Ri. Ogilvie et D. Zborowskasluis, EFFECT OF PERINDOPRIL IN PACING-INDUCED CANINE MODELS OF ACUTE AND CHRONIC HEART-FAILURE, Canadian journal of cardiology, 11(10), 1995, pp. 934-940
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
0828282X
Volume
11
Issue
10
Year of publication
1995
Pages
934 - 940
Database
ISI
SICI code
0828-282X(1995)11:10<934:EOPIPC>2.0.ZU;2-O
Abstract
OBJECTIVE: To examine the effects of perindopril, a nonsulfhydryl-cont aining angiotensin-converting enzyme inhibitor, on total vascular capa citance and hemodynamics in acute and chronic dog models of heart fail ure. METHODS: Acute heart failure was induced by anesthetized, splenec tomized dogs by a volume load (dextran 70; 20 mL/kg) during rapid righ t ventricular pacing (RRVP) at 250 beats/min. Pretreatment with perind opril (0.3 mg/kg daily for six days, n=7) was compared with no treatme nt (n=7). Total vascular capacitance and compliance were measured from plots of mean circulatory filling pressure during acetylcholine-induc ed circulatory arrests at different blood volumes. Chronic heart failu re was induced by continuous RRVP in splenectomized dogs treated with perindopril (0.3 mg/kg daily, n=8), which were compared with untreated dogs (n=8). Hemodynamics and total vascular capacitance and complianc e were measured at baseline and after 33 days of RRVP. RESULTS: Perind opril treatment did not significantly modify the increased pulmonary c apillary wedge and mean circulatory filling pressures, reduced total v ascular compliance or total vascular capacitance associated with the v olume load and acute RRVP. During chronic RRVP, pu rindopril reduced w eight gain and the development of ascites, reduced right atrial pressu re (6.3+/-1.3 versus 10.3+/1.2 mmHg), mean circulatory filling pressur e (9.3+/-1.0 versus 14.7+/-1.2 mmHg), stressed blood volume (22+/-3 ve rsus 33+/-4 mL/kg) and central blood volume (10+/-1 versus 14+/-1 mL/k g) while increasing cardiac output (122+/-9 versus 98+/-7 mL/kg). Howe ver, the reduction in total vascular capacitance was not attenuated an d pulmonary capillary wedge pressure was not lowered significantly (18 .5+/-1.5 versus 21.4+/-1.3 mmHg). CONCLUSION: Perindopril failed to mo dify hemodynamics in the pacing-induced canine model of acute heart fa ilure but had beneficial effects in the model of chronic heart failure .