title: [Apoptosis in pressure overload-induced heart hypertrophy].
abstract: Pressure overload can result in heart hypertrophy, and induce apoptosis, but the phenomenon of apoptosis during the forepart of cardiomyocyte hypertrophy remains unclear. The aim of this study was to inquire into the process of cardiomyocyte apoptosis during the forepart of cardiomyocyte hypertrophy. We constructed the hypertrophy model by transverse aortic constriction of male SD rat. The apoptosis ratio was detected by TUNEL method and FCM. The result demonstrated that hypertrophy indexes increased with the time of constriction, reached the highest level at day 7, maintained that level, and then decreased at day 91. The apoptosis ratio of cardiomyocyte at day 4 was higher than that at day 0 detected by FCM method, and the ratio at day 7 was markedly lower than that at day 4. After day 28, the apoptosis ratio of cardiomyocyte went up again with the time of constriction after surgery. TUNEL method revealed that positive nuclei were observed in cardiomyocytes exclusively in the left ventricle; the apoptosis ratio increased when constriction continued. TUNEL method confirmed the result of FCM. These data indicate that cardiac hypertrophy is initiated by apoptosis of cardiomyocyte, these two factors(hypertrophy and apoptosis) maintain the balance between growth and death during the early short period of aortic constriction, and when aortic constriction goes on they are involved in the pathogenesis of heart remodeling.
authors.affiliation: Institute of Biomedical Engineeting, West China University of Medical Sciences, Chengdu 610041.
authors.forename: J
authors.initials: J
authors.lastname: Lu
authors.forename: J
authors.initials: J
authors.lastname: Xiao
authors.forename: H
authors.initials: H
authors.lastname: Luo
authors.forename: H
authors.initials: H
authors.lastname: Chen
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications*; D017209:Apoptosis; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology*; D008297:Male; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley