Peripheral artery structure and endothelial function in heart failure: Effect of ACE inhibition

被引:49
作者
Mulder, P
Elfertak, L
Richard, V
Compagnon, P
Devaux, B
Henry, JP
Scalbert, E
Desche, P
Mace, B
Thuillez, C
机构
[1] UNIV ROUEN, INST FEDERAT RECH,SCH MED, GRP RECH VAISSEAUX COEUR MEDICAMENTS, DEPT PHARMACOL, F-76031 ROUEN, FRANCE
[2] UNIV ROUEN, SCH MED, DEPT HISTOL, F-76031 ROUEN, FRANCE
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1996年 / 271卷 / 02期
关键词
endothelial dysfunction; cardiovascular structure;
D O I
10.1152/ajpheart.1996.271.2.H469
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic heart failure (CHF) induces peripheral vasoconstriction and impairs endothelium-dependent relaxation of large arteries. We investigated in a rat model of CHF (coronary artery ligation) I)whether endothelial dysfunction also exists in resistance arteries, 2) whether this is associated with vascular morphological changes, and 3) the effect of angiotensin-converting enzyme (ACE) inhibition on these parameters. After 1 mo or 1 yr, CHF reduced the vasodilatory response to acetylcholine of isolated, perfused femoral and mesenteric artery segments. This impairment was more marked in femoral than in mesenteric arteries. However, CHF did not induce any arterial remodeling. Chronic treatment with the ACE inhibitor perindopril improved the response to acetylcholine and reduced media cross-sectional area and collagen density. Thus at the level of small peripheral arteries, CHF induces an endothelial dysfunction but does not affect vascular structure. ACE inhibition prevents the CHF-induced endothelial dysfunction and induces vascular remodeling. These changes could contribute to the observed beneficial effects of ACE inhibitors on hemodynamics and survival in CHF.
引用
收藏
页码:H469 / H477
页数:9
相关论文
共 29 条
[1]   MYOCARDIAL-INFARCTION IN RATS - INFARCT SIZE, MYOCYTE HYPERTROPHY, AND CAPILLARY GROWTH [J].
ANVERSA, P ;
BEGHI, C ;
KIKKAWA, Y ;
OLIVETTI, G .
CIRCULATION RESEARCH, 1986, 58 (01) :26-37
[2]   VASCULAR RELAXATION AND CYCLIC GUANOSINE-MONOPHOSPHATE IN A RAT MODEL OF HIGH-OUTPUT HEART-FAILURE [J].
ARNAL, JF ;
SCHOTT, C ;
STOCLET, JC ;
MICHEL, JB .
CARDIOVASCULAR RESEARCH, 1993, 27 (09) :1651-1656
[3]   BENEFICIAL HEMODYNAMIC-EFFECTS OF MILRINONE AND ENALAPRIL IN CONSCIOUS RATS WITH HEALED MYOCARDIAL-INFARCTION [J].
DEFELICE, A ;
HARRIS, A ;
FRERING, R ;
HORAN, P .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1989, 167 (02) :211-220
[4]   ACTIVATION OF ENDOTHELIAL L-ARGININE PATHWAY IN RESISTANCE ARTERIES - EFFECT OF AGE AND HYPERTENSION [J].
DOHI, Y ;
THIEL, MA ;
BUHLER, FR ;
LUSCHER, TF .
HYPERTENSION, 1990, 16 (02) :170-179
[5]   ENDOTHELIAL DYSFUNCTION OF HINDQUARTER RESISTANCE VESSELS IN EXPERIMENTAL HEART-FAILURE [J].
DREXLER, H ;
LU, WY .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (06) :H1640-H1645
[6]  
DREXLER H, 1987, NEW ENGL J MED, V316, P1429
[7]   ATHEROSCLEROSIS OR LIPOPROTEIN-INDUCED ENDOTHELIAL DYSFUNCTION - POTENTIAL MECHANISMS UNDERLYING REDUCTION IN EDRF/NITRIC OXIDE ACTIVITY [J].
FLAVAHAN, NA .
CIRCULATION, 1992, 85 (05) :1927-1938
[8]   LEFT-VENTRICULAR DIASTOLIC PRESSURE-VOLUME RELATIONS IN RATS WITH HEALED MYOCARDIAL-INFARCTION - EFFECTS ON SYSTOLIC FUNCTION [J].
FLETCHER, PJ ;
PFEFFER, JM ;
PFEFFER, MA ;
BRAUNWALD, E .
CIRCULATION RESEARCH, 1981, 49 (03) :618-626
[9]   EARLY AND LATE EFFECTS OF CAPTOPRIL TREATMENT AFTER LARGE MYOCARDIAL-INFARCTION IN RATS [J].
GAY, RG .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1990, 16 (04) :967-977
[10]  
HALPERN W, 1991, BLOOD VESSELS, V28, P245