title: Growth hormone improves cardiac function in rats with experimental myocardial infarction.
abstract: Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although concomitant cardiac hypertrophy, generally considered to be a cardiovascular risk factor, has also been reported. In the present study, we combine a rat model with impaired cardiac performance after myocardial infarction (MI) with echocardiographic evaluation of GH effects on cardiac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in subsequent impaired cardiac performance. After 6 weeks' recovery, blind transthoracic echocardiography was performed to determine infarction size, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rats were treated with daily s.c. injections of saline (n = 8) or recombinant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg-1 body weight for 1 week. A new blind echocardiography examination was performed after treatment demonstrating a 13% increase in ejection fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a significant decrease in end-systolic volume. There were no significant changes in left ventricular (LV) or interventricular wall thickness, LV dimensions, heart rate or diastolic function. No effects were seen on LV weight, cardiac insulin-like growth factor (IGF) I, IGF-I receptor and GH receptor mRNA content. GH in a physiological dose improves systolic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in the treatment of heart failure and merits further investigation.
authors.affiliation: Research Centre for Endocrinology and Metabolism, Sahlgrenska University Hospital, Gothenburg, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Isgaard
authors.forename: V
authors.initials: V
authors.lastname: Kujacic
authors.forename: E
authors.initials: E
authors.lastname: Jennische
authors.forename: A
authors.initials: A
authors.lastname: Holmäng
authors.forename: X Y
authors.initials: XY
authors.lastname: Sun
authors.forename: T
authors.initials: T
authors.lastname: Hedner
authors.forename: A
authors.initials: A
authors.lastname: Hjalmarson
authors.forename: B A
authors.initials: BA
authors.lastname: Bengtsson
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004452:Echocardiography; D006333:Heart Failure / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D019382:Human Growth Hormone / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017526:Receptor, IGF Type 1 / Q000235:genetics; D011986:Receptors, Somatotropin / Q000235:genetics
chemical_list: D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D017526:Receptor, IGF Type 1