Effects of growth hormone supplementation on left ventricular morphology and myocyte function with the development of congestive heart failure

被引:44
作者
Houck, WV
Pan, LC
Kribbs, SB
Clair, MJ
McDaniel, GM
Krombach, RS
Merritt, WM
Pirie, C
Iannini, JP
Mukherjee, R
Spinale, FG
机构
[1] Med Univ S Carolina, Div Cardiothorac Surg, Charleston, SC 29403 USA
[2] Pfizer Inc, Pfizer Cent Res, Dept Cardiovasc & Metab Dis, Groton, CT 06340 USA
关键词
ventricles; contractility; hormones; growth substances;
D O I
10.1161/01.CIR.100.19.2003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Release of growth hormone (GH), putatively through alterations in insulin growth factor-1 (IGF-1) levels, has been implicated to influence left ventricular (LV) myocardial structure and function. The objective of this study was to determine contributory mechanisms by which GH supplementation may influence LV function with the development of congestive heart failure (CHF). Methods and Results-Pigs were assigned to the following groups: (1) chronic pacing at 240 bpm for 3 weeks (n = 10), (2) chronic pacing and GH supplementation (200 mu g.kg(-1).d(-1), n = 10), and (3) controls (n = 8). GH treatment increased ICF-1 plasma levels by nearly 2.5-fold throughout the pacing protocol. In the untreated pacing CHF group, LV fractional shortening was reduced and peak wall stress increased. In the pacing CHF and GH groups, LV fractional shortening was higher and LV wall stress lower than untreated CHF values. Steady-state myocyte velocity of shortening was reduced with pacing CHF and was unchanged from CHF values with GH treatment. In the presence of 25 nmol/L isoproterenol, the change in myocyte shortening velocity was reduced in the untreated CHF group and increased in the GH-treated group. LV sarcoplasmic reticulum Ca2+-ATPase abundance was reduced with pacing CHF but was normalized with GH treatment. Conclusions-Short-term GH supplementation improved LV pump function in pacing CHF as a result of favorable effects on LV remodeling and contractile processes. Thus, GH supplementation may serve as a novel therapeutic modality in developing CHF.
引用
收藏
页码:2003 / 2009
页数:7
相关论文
共 28 条
[1]   Myosin heavy chain synthesis is increased in a rabbit model of heart failure [J].
Eble, DM ;
Walker, JD ;
Mukherjee, R ;
Samarel, AM ;
Spinale, FG .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (02) :H969-H978
[2]   A preliminary study of growth hormone in the treatment of dilated cardiomyopathy [J].
Fazio, S ;
Sabatini, D ;
Capaldo, B ;
Vigorito, C ;
Giordano, A ;
Guida, R ;
Pardo, F ;
Biondi, B ;
Sacca, L .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (13) :809-814
[3]  
GAASCH WH, 1995, HEART FAILURE, P14
[4]  
GERDES AM, 1994, CARDIOSCIENCE, V5, P31
[5]  
HU Y, 1996, HORM METAB RES, V29, P211
[6]   INSULIN-LIKE GROWTH FACTOR-I INDUCES HYPERTROPHY WITH ENHANCED EXPRESSION OF MUSCLE-SPECIFIC GENES IN CULTURED RAT CARDIOMYOCYTES [J].
ITO, H ;
HIROE, M ;
HIRATA, Y ;
TSUJINO, M ;
ADACHI, S ;
SHICHIRI, M ;
KOIKE, A ;
NOGAMI, A ;
MARUMO, F .
CIRCULATION, 1993, 87 (05) :1715-1721
[7]   Long-term cardiovascular effects of growth hormone treatment in GH-deficient adults - Preliminary data in a small group of patients [J].
Johannsson, G ;
Bengtsson, BA ;
Andersson, B ;
Isgaard, J ;
Caidahl, K .
CLINICAL ENDOCRINOLOGY, 1996, 45 (03) :305-314
[8]   THE CELLULAR BASIS OF PACING-INDUCED DILATED CARDIOMYOPATHY - MYOCYTE CELL LOSS AND MYOCYTE CELLULAR REACTIVE HYPERTROPHY [J].
KAJSTURA, J ;
ZHANG, X ;
LIU, Y ;
SZOKE, E ;
CHENG, W ;
OLIVETTI, G ;
HINTZE, TH ;
ANVERSA, P .
CIRCULATION, 1995, 92 (08) :2306-2317
[9]  
Klindt J, 1998, J ANIM SCI, V76, P2368
[10]   MECHANICAL-PROPERTIES OF RAT CARDIAC SKINNED FIBERS ARE ALTERED BY CHRONIC GROWTH-HORMONE HYPERSECRETION [J].
MAYOUX, E ;
VENTURACLAPIER, R ;
TIMSIT, J ;
BEHARCOHEN, F ;
HOFFMANN, C ;
MERCADIER, JJ .
CIRCULATION RESEARCH, 1993, 72 (01) :57-64