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Titolo:
Cardiomyocyte apoptosis and ventricular remodeling after myocardial infarction in rats
Autore:
Palojoki, E; Saraste, A; Eriksson, A; Pulkki, K; Kallajoki, M; Voipio-Pulkki, LM; Tikkanen, I;
Indirizzi:
Univ Helsinki, Cent Hosp, Minerva Inst Med Res, Dept Med, FIN-00029 HUS, Finland Univ Helsinki HUS Finland FIN-00029 es, Dept Med, FIN-00029 HUS, Finland Univ Helsinki, Cent Hosp, Dept Clin Chem, FIN-00029 HUS, Finland Univ Helsinki HUS Finland FIN-00029 pt Clin Chem, FIN-00029 HUS, Finland Univ Turku, Dept Med, FIN-20520 Turku, Finland Univ Turku Turku Finland FIN-20520 u, Dept Med, FIN-20520 Turku, Finland Univ Turku, Dept Anat, FIN-20520 Turku, Finland Univ Turku Turku FinlandFIN-20520 , Dept Anat, FIN-20520 Turku, Finland Univ Turku, Dept Pathol, FIN-20520 Turku, Finland Univ Turku Turku Finland FIN-20520 Dept Pathol, FIN-20520 Turku, Finland
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: H2726 - H2731
SICI:
0363-6135(200106)280:6<H2726:CAAVRA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-CONVERTING ENZYME; NECROSIS-FACTOR-ALPHA; HEART-FAILURE; DNA FRAGMENTATION; CELL-DEATH; MYOCYTES; REPERFUSION; INVOLVEMENT; ACTIVATION; EXPRESSION;
Keywords:
ischemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Voipio-Pulkki, LM Univ Helsinki, Cent Hosp, Minerva Inst Med Res, Dept Med, POB340, FIN-00029 HUS, Finland Univ Helsinki POB340 HUS Finland FIN-00029 HUS, Finland
Citazione:
E. Palojoki et al., "Cardiomyocyte apoptosis and ventricular remodeling after myocardial infarction in rats", AM J P-HEAR, 280(6), 2001, pp. H2726-H2731

Abstract

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 by4 wk.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 22:03:21