Cardiomyocyte apoptosis and ventricular remodeling after myocardial infarction in rats.
We investigated the role of cardiomyocyte apoptosis in the remodeling of the left ventricle from 24 h to 12 wk after myocardial infarction in the rat. Infarct size planimetry, quantification of cardiomyocyte apoptosis, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) methodology, and echocardiography (left ventricular diastolic diameter and ejection fraction) were performed. Sham-operated animals showed low rates of cardiomyocyte apoptosis (0.03%) and no change in diastolic diameter or ejection fraction during the study. Twenty-four hours after infarction, TUNEL positivity was high in the infarct areas (1.4%) and border zones (4.9%). It declined to 0.34% (P < 0.01 vs. sham) at 4 wk and 0.10% at 12 wk in the border zones. In the remote myocardium, cardiomyocyte apoptosis increased to 0.07% (P = 0.03 vs. sham) on day 1 and remained on the same level up to 4 wk. The increase in diastolic diameter 1-4 wk after infarction correlated (r = 0.60, P < 0.01) with cardiomyocyte apoptosis in the noninfarcted myocardium, which quantitatively contributed most (>50%) to the apoptotic cell loss by 4 wk.
Palojoki
E
E
Minerva Institute for Medical Research, Helsinki University Central Hospital, Helsinki FIN-00029, Finland.
Saraste
A
A
Eriksson
A
A
Pulkki
K
K
Kallajoki
M
M
Voipio-Pulkki
L M
LM
Tikkanen
I
I
D000818:Animals; D017209:Apoptosis; D002452:Cell Count; D004562:Electrocardiography; D020287:In Situ Nick-End Labeling; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume; D016276:Ventricular Function; D020257:Ventricular Remodeling