title: Worsening of ischemic damage in hearts from rats with selective growth hormone deficiency.
abstract: The effects of growth hormone (GH) deficiency on cardiac function were studied in young male rats administered an anti-GH-releasing hormone (GHRH) serum from postnatal day 20 to 40. Dependence of heart abnormalities on GH deficiency was ascertained by giving a group of anti-GHRH serum-treated rats GH replacement therapy. Heart preparations from anti-GHRH serum-treated rats, undergoing low-flow ischemia, showed a progressive increase in left ventricular end-diastolic pressure with poor recovery of mechanical activity and increased coronary perfusion pressure upon reperfusion. Hearts from anti-GHRH serum + GH-treated rats, undergoing global reduction to the flow, showed only a minimal increase of left ventricular end-diastolic pressure and, upon reperfusion, cardiac mechanical activity recovered almost completely. Similar findings were also observed in heart preparations from control (normal rabbit serum-treated) rats. Infusion of acetylcholine (10(-6) M) into heart preparations in the preischemic period increased coronary perfusion pressure values more markedly in hearts from normal rabbit serum- and anti-GHRH serum + GH-treated rats than in those from anti-GHRH serum-treated rats. These results indicate that selective GH deficiency in young male rats renders the heart more sensitive to ischemic damage and leads to an impairment of cardiac muscarinic receptor function.
authors.affiliation: Department of Pharmacology, Chemoterapy and Toxicology, University of Milano, Italy.
authors.forename: V
authors.initials: V
authors.lastname: De Gennaro Colonna
authors.forename: G
authors.initials: G
authors.lastname: Rossoni
authors.forename: D
authors.initials: D
authors.lastname: Bonacci
authors.forename: S
authors.initials: S
authors.lastname: Ciceri
authors.forename: L
authors.initials: L
authors.lastname: Cattaneo
authors.forename: E
authors.initials: E
authors.lastname: Müller
authors.forename: F
authors.initials: F
authors.lastname: Berti
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors*; D013006:Growth Hormone / Q000172:deficiency* / Q000235:genetics / Q000627:therapeutic use; D007106:Immune Sera; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D010902:Pituitary Gland / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007106:Immune Sera; D012333:RNA, Messenger; D007987:Gonadotropin-Releasing Hormone; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D000109:Acetylcholine