[Proliferation of the rat myocardium injured in the early stages of postnatal ontogeny].
Focal myocardial necrosis was induced in noninbred white rats aged 7, 14 and 30 days by injection of a small amount of 96% ethanol into the left ventricle. The animals were sacrificed days 2-30 after the operation. The mitotic index (MI) of muscle cell nuclei was determined in various parts of the heart: in the left and right atria and their auricles, trabecular, compact myocardium, in subepicardial zones of both ventricles and perinecrotic area. It was established that in the compact myocardium, myocyte proliferation is suppressed and does not renew after left ventricular injury. In the remaining zones where the control animals showed mitoses, MI of myocytes increased after heart injury. The later the injury was made the less marked was the increase of MI. in 7-day-old rats MI reached 320-500% of control on the 4th and 120-380% on the 7th postoperative days. MI rose in some parts of the heart only in "high mitotic" rats operated on the 14th and 30th postnatal days. The reparative activity of connective tissue progressed with heart growth.
D000818:Animals; D002455:Cell Division; D000431:Ethanol / Q000494:pharmacology; D006321:Heart / Q000254:growth & development*; D006335:Heart Injuries / Q000503:physiopathology*; D006352:Heart Ventricles / Q000187:drug effects; D008940:Mitotic Index; D009336:Necrosis; D010875:Pipecolic Acids / Q000494:pharmacology; D051381:Rats
D010875:Pipecolic Acids; C010927:dimecolin; D000431:Ethanol
Proliferatsiia miokarda, povrezhdennogo na rannikh stadiiakh postnatal'nogo ontogneza krys.