title: Randomised comparison of growth hormone versus IGF-1 on early post-myocardial infarction ventricular remodelling in rats.
abstract: OBJECTIVE
  Growth hormone and insulin-like growth factor-1 participate in post-myocardial infarction healing, but their relative importance is unclear. We compared the treatment effects of these agents on left ventricular remodelling.
  
  
  METHODS
  Wistar rats were randomised into a single dose of either growth hormone (0.5microg, n=29), or insulin-like growth factor-1 (0.5microg, n=27), delivered by direct intramyocardial punctures, and were compared with controls (n=30). Five minutes after treatment, myocardial infarction was generated by permanent ligation of the left coronary artery. Twenty-four hours post-ligation, serum levels of catecholamines were measured using radioimmunoassay and infarct size as well as infarct expansion index were calculated. The expression of genes related to extracellular matrix and angiogenesis was measured using polymerase chain reaction.
  
  
  RESULTS
  Infarct expansion index was lower in growth hormone-treated rats (0.28+/-0.03, p=0.007) and in insulin-like growth factor-1-treated rats (0.35+/-0.03, p=0.044) compared to controls (0.51+/-0.06). Infarct size was significantly (p=0.0076) lower in growth hormone-treated rats (32.2+/-2.0%) and marginally (p=0.094) lower in insulin-like growth factor-1-treated rats (36.2+/-2.3%) compared to controls (42.0+/-2.7%). Survival rates were comparable in the three groups. Epinephrine was lower in the growth hormone group (2.8+/-0.2microg/l) compared to either controls (5.0+/-0.6microg/l, p=0.007), or to insulin-like growth factor-1-treated rats (6.3+/-0.6microg/l, p=0.0001). Collagen I and III expression in the infarct zone was higher in the growth hormone group compared to either the insulin-like growth factor-1 group or to controls.
  
  
  CONCLUSIONS
  Both growth hormone and insulin-like-growth factor-1 decrease early infarct expansion, but growth hormone results in more favourable extracellular matrix remodelling and sympathetic activation.
authors: Department of Pathology, University of Ioannina, 1 Stavrou Niarxou Avenue, 45110 Ioannina, Greece.
authors: K E
authors: KE
authors: Hatzistergos
authors: A C
authors: AC
authors: Mitsi
authors: C
authors: C
authors: Zachariou
authors: A
authors: A
authors: Skyrlas
authors: E
authors: E
authors: Kapatou
authors: M G
authors: MG
authors: Agelaki
authors: A
authors: A
authors: Fotopoulos
authors: T M
authors: TM
authors: Kolettis
authors: V
authors: V
authors: Malamou-Mitsi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D002395:Catecholamines / Q000097:blood; D054059:Coronary Occlusion / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000187:drug effects; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D013006:Growth Hormone / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism / Q000401:mortality / Q000473:pathology*; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000235:genetics; D019014:fas Receptor / Q000378:metabolism
chemical_list: D002395:Catecholamines; D019014:fas Receptor; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone