title: [Protective effect of peptide semax the rat heart in acute myocardial infarction].
abstract: Semax, a member of ACTH-derived peptides family, has been employed in the treatment of acute ischemic stroke in patients. It decreased neurological deficit and reduced NO hyperproduction in the rat brain, caused by acute cerebral hypoperfusion. We suggested that semax is also able to protect rat heart from ischemic damage in acute myocardial infaction (AMI). AMI was induced by left coronary artery occlusion, myocardial ischemic area averaged 30 % of left ventricle. In 2 hours after coronary occlusion, the AMI group developed 11 % reduced mean arterial blood pressure and 48 % increased diastolic blood pressure in left ventricle in comparison with sham-operated control group. However, infusion of either dobutamine, which directly stimulates myocardial contractility, or sodium nitroprusside and phenylephrine, that change vascular resistance and thus cardiac afterload, did not reveal distinctions in hemodynamic parameters between groups. These data indicate absense or only moderate cardiac dysfunction in rats with AMI and are consistent wih morphometrical and histochemical studies that did not detect any necrotic or apoptotic (TUNEL-test) changes in left ventricular cardiomyocytes in spite of development of distinct ischemic disturbances of mitochondria and nuclear in about 50 % of cardiomyocytes in 2 hours after AMI. Semax (150 microg/kg), given i. p. 15 min and 2 hours after coronary occlusion, caused no effect on cardiac function, but completely prevented ischemia-induced ultrastructural changes of cardiomyocytes. This protective effect was accompanied by the ability of peptide to blunt the increase in plasma concentrations of nitrates, observed in AMI group.
authors.forename: A V
authors.initials: AV
authors.lastname: Golubeva
authors.forename: S A
authors.initials: SA
authors.lastname: Gavrilova
authors.forename: T V
authors.initials: TV
authors.lastname: Lipina
authors.forename: M V
authors.initials: MV
authors.lastname: Shornikova
authors.forename: A B
authors.initials: AB
authors.lastname: Postnikov
authors.forename: L A
authors.initials: LA
authors.lastname: Andreeva
authors.forename: Iu S
authors.initials: IuS
authors.lastname: Chentsov
authors.forename: V B
authors.initials: VB
authors.lastname: Koshelev
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D004280:Dobutamine / Q000494:pharmacology; D006321:Heart / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects / Q000648:ultrastructure; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000648:ultrastructure; D009566:Nitrates / Q000097:blood; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D010446:Peptide Fragments / Q000627:therapeutic use*; D010656:Phenylephrine / Q000494:pharmacology; D020011:Protective Agents / Q000627:therapeutic use*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D002316:Cardiotonic Agents; D009566:Nitrates; D010446:Peptide Fragments; D020011:Protective Agents; D009599:Nitroprusside; D010656:Phenylephrine; D009569:Nitric Oxide; D004280:Dobutamine; C048487:ACTH (4-7), Pro-Gly-Pro-; D000324:Adrenocorticotropic Hormone