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Growth hormone improves bioenergetics and decreases catecholamines in postinfarct rat hearts.

Artikel i vetenskaplig tidskrift
Författare Elmir Omerovic
Entela Bollano
Reza Mobini
Vuk Kujacic
B Madhu
Bassam Soussi
Michael Fu
Åke Hjalmarson
Finn Waagstein
Jörgen Isgaard
Publicerad i Endocrinology
Volym 141
Nummer/häfte 12
Sidor 4592-9
ISSN 0013-7227
Publiceringsår 2000
Publicerad vid Wallenberglaboratoriet
Institutionen för invärtesmedicin
Institutionen för de kirurgiska disciplinerna, Avdelningen för kirurgi
Sidor 4592-9
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Body Weight, Catecholamines, metabolism, Dopamine, analysis, blood, Echocardiography, Doppler, Energy Metabolism, Epinephrine, analysis, blood, Hemodynamic Processes, Human Growth Hormone, blood, therapeutic use, Insulin-Like Growth Factor I, analysis, Male, Myocardial Infarction, drug therapy, metabolism, Myocardium, chemistry, metabolism, Natriuretic Peptide, Brain, blood, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, beta, analysis, Ventricular Function, Left
Ämneskategorier Fysiologi, Cell- och molekylärbiologi

Sammanfattning

The aims of this study were to examine, in vivo, the effects of GH treatment on myocardial energy metabolism, function, morphology, and neurohormonal status in rats during the early postinfarct remodeling phase. Myocardial infarction (MI) was induced in male Sprague Dawley rats. Three different groups were studied: MI rats treated with saline (n = 7), MI rats treated with GH (MI + GH; n = 11; 3 mg/kg x day), and sham-operated rats (sham; n = 8). All rats were investigated with 31P magnetic resonance spectroscopy and echocardiography at 3 days after MI and 3 weeks later. After 3 weeks treatment with GH, the phosphocreatine/ATP ratio increased significantly, compared with the control group (MI = 1.69 +/- 0.09 vs. MI + GH = 2.42 +/- 0.05, P < 0.001; sham = 2.34 +/- 0.08). Treatment with GH significantly attenuated an increase in left ventricular end systolic volume and end diastolic volume. A decrease in ejection fraction was prevented in GH-treated rats (P < 0.05 vs. MI). Myocardial and plasma noradrenaline levels were significantly lower in MI rats treated with GH. These effects were accompanied by normalization of plasma brain natriuretic peptide levels (sham = 124.1 +/- 8.4; MI = 203.9 +/- 34.7; MI + GH = 118.3 +/- 8.4 ng/ml; P < 0.05 vs. MI). In conclusion, GH improves myocardial energy reserve, preserves left ventricular function, and attenuates pathologic postinfarct remodeling in the absence of induction of left ventricular hypertrophy in postinfarct rats. The marked decrease in myocardial content of noradrenaline, after GH treatment, may protect myocardium from adverse effects of catecholamines during postinfarct remodeling.

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