title: Ventricular loading is coupled with DNA synthesis in adult cardiac myocytes after acute and chronic myocardial infarction in rats.
abstract: To determine whether the overload associated with myocardial infarction and ventricular failure in rats is coupled with activation of DNA synthesis in the remaining left and right ventricular myocytes, flow cytometric analysis was performed on myocyte nuclei prepared from both ventricles 7 and 30 days after coronary occlusion. In addition, oral captopril was administered in separate groups of control and experimental rats to establish whether a relation existed between attenuation of ventricular loading and magnitude of DNA synthesis in myocytes. Results demonstrated that left ventricular failure and right ventricular dysfunction at 7 days after infarction were biventricularly associated with marked increases in the number of myocyte nuclei in the G2M phase of the cell cycle. In contrast, the fraction of nuclei in the G0+G1 phase decreased. In comparison with the earlier time point, the 30-day interval was characterized by a significant magnitude of cardiac hypertrophy, a moderate amelioration of ventricular pump function, and a decrease in the percentage of myocyte nuclei in the G2M phase in both ventricles. However, 30 days after infarction, the number of right ventricular myocyte nuclei in the S and G2M phases remained elevated with respect to control animals. Captopril therapy reduced the extent of ventricular loading and the population of myocyte nuclei in the cell cycle at 7 days. In conclusion, DNA synthesis in myocyte nuclei may represent an important adaptive component of the myocardial response to infarction.
authors.affiliation: Department of Medicine, New York Medical College, Valhalla 10595.
authors.forename: J M
authors.initials: JM
authors.lastname: Capasso
authors.forename: S
authors.initials: S
authors.lastname: Bruno
authors.forename: W
authors.initials: W
authors.lastname: Cheng
authors.forename: P
authors.initials: P
authors.lastname: Li
authors.forename: R
authors.initials: R
authors.lastname: Rodgers
authors.forename: Z
authors.initials: Z
authors.lastname: Darzynkiewicz
authors.forename: P
authors.initials: P
authors.lastname: Anversa
mesh_terms: D000818:Animals; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use; D002453:Cell Cycle; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D002469:Cell Separation; D004247:DNA / Q000096:biosynthesis*; D005434:Flow Cytometry; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology*; D006439:Hemodynamics; D006965:Hyperplasia; D008297:Male; D008938:Mitosis; D009203:Myocardial Infarction / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D004247:DNA; D002216:Captopril