Early rather than delayed administration of lisinopril protects the heart after myocardial infarction in rats

被引:33
作者
Zornoff, LAM [1 ]
Matsubara, BB [1 ]
Matsubara, LS [1 ]
Paiva, SAR [1 ]
Spadaro, J [1 ]
机构
[1] UNESP, Fac Med Botucatu, Dept Clin Med, BR-18618000 Botucatu, SP, Brazil
关键词
myocardial infarction; ventricular remodeling; angiotensin-converting enzyme inhibitor; lisinopril; rat;
D O I
10.1007/s003950050183
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: ACE inhibitors have shown beneficial results in several studies after myocardial infarction (MI). However, these studies have shown conflicting results about the ideal starting time of the ACE inhibitors administration after MI and the importance of infarct size. Objectives: This study was designed to assess the long-term effects of lisinopril on mortality, cardiac function, and ventricular fibrosis after MI, in rats. Methods: Lisinopril (20 mg/kg/day) was given on day 1 or 21 days after coronary occlusion in small or large infarctions. Results: The mortality rate was reduced by 39% in early treatment and 30% in delayed treatment in comparison to the untreated rats. Early treatment reduced cardiac dysfunction in small MIs; however, delayed treatment did not. No statistical difference was observed among the groups for large MIs. No statistical difference was observed among the groups with large or small MIs on myocardial hydroxyproline concentration. Conclusions: Both early and delayed treatments with lisinopril increased survival. Treatment exerts no marked effects on fibrosis; early treatment has exerted beneficial influences on cardiac function whereas delayed treatment had no consistent effects. The protective effect of lisinopril is detectable only in small (< 40% of LV) MIs.
引用
收藏
页码:208 / 214
页数:7
相关论文
共 29 条
[1]   LEFT-VENTRICULAR FAILURE INDUCED BY MYOCARDIAL-INFARCTION .1. MYOCYTE HYPERTROPHY [J].
ANVERSA, P ;
LOUD, AV ;
LEVICKY, V ;
GUIDERI, G .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 248 (06) :H876-H882
[2]   IMPAIRED BETA-ADRENERGIC STIMULATION IN THE UNINVOLVED VENTRICLE POST-ACUTE MYOCARDIAL-INFARCTION - REVERSIBLE DEFECT DUE TO EXCESSIVE CIRCULATING CATECHOLAMINE-INDUCED DECLINE IN NUMBER AND AFFINITY OF BETA-RECEPTORS [J].
BAUMANN, G ;
RIESS, G ;
ERHARDT, WD ;
FELIX, SB ;
LUDWIG, L ;
BLUMEL, G ;
BLOMER, H .
AMERICAN HEART JOURNAL, 1981, 101 (05) :569-581
[3]   COLLAGEN-METABOLISM IN CULTURED ADULT-RAT CARDIAC FIBROBLASTS - RESPONSE TO ANGIOTENSIN-II AND ALDOSTERONE [J].
BRILLA, CG ;
ZHOU, GP ;
MATSUBARA, L ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1994, 26 (07) :809-820
[4]   CHRONIC INFARCTION DECREASES MAXIMUM CARDIAC WORK AND SENSITIVITY OF HEART TO EXTRACELLULAR CALCIUM [J].
FELLENIUS, E ;
HANSEN, CA ;
MJOS, O ;
NEELY, JR .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 249 (01) :H80-H87
[5]   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
[6]   CALCIUM-DEPENDENT AND LENGTH-DEPENDENT FORCE PRODUCTION IN RAT VENTRICULAR MUSCLE [J].
HIBBERD, MG ;
JEWELL, BR .
JOURNAL OF PHYSIOLOGY-LONDON, 1982, 329 (AUG) :527-+
[7]   EFFECT OF LONG-TERM CAPTOPRIL THERAPY ON LEFT-VENTRICULAR REMODELING AND FUNCTION DURING HEALING OF CANINE MYOCARDIAL-INFARCTION [J].
JUGDUTT, BI ;
SCHWARZMICHOROWSKI, BL ;
KHAN, MI .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1992, 19 (03) :713-721
[8]  
KLEBER FX, 1991, AM J CARDIOL, V68, pD121
[9]   CONVERTING ENZYME-INHIBITION SPECIFICALLY PREVENTS THE DEVELOPMENT AND INDUCES REGRESSION OF CARDIAC-HYPERTROPHY IN RATS [J].
LINZ, W ;
SCHOLKENS, BA ;
GANTEN, D .
CLINICAL AND EXPERIMENTAL HYPERTENSION PART A-THEORY AND PRACTICE, 1989, 11 (07) :1325-1350
[10]  
Litwin S. E., 1995, HEART FAILURE, V11, P182