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Titolo:
RELATIVE INDUCTION OF HEAT-SHOCK-PROTEIN IN CORONARY ENDOTHELIAL-CELLS AND CARDIOMYOCYTES - IMPLICATIONS FOR MYOCARDIAL PROTECTION
Autore:
AMRANI M; LATIF N; MORRISON K; GRAY CC; JAYAKUMAR J; CORBETT J; GOODWIN AT; DUNN MJ; YACOUB MH;
Indirizzi:
HAREFIELD HOSP,NATL HEART & LUNG INST,HEART SCI CTR,DEPT CARDIOTHORACSURG HAREFIELD UB9 6JH MIDDX ENGLAND HAREFIELD HOSP,NATL HEART & LUNG INST,HEART SCI CTR,DEPT CARDIOTHORACSURG HAREFIELD UB9 6JH MIDDX ENGLAND
Titolo Testata:
Journal of thoracic and cardiovascular surgery
fascicolo: 1, volume: 115, anno: 1998,
pagine: 200 - 209
SICI:
0022-5223(1998)115:1<200:RIOHIC>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISOLATED RAT-HEART; NITRIC-OXIDE; CARDIOPLEGIC ARREST; MECHANICAL FUNCTION; RECOVERY; ISCHEMIA; RELEASE; VASODILATATION; PERFORMANCE; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
M. Amrani et al., "RELATIVE INDUCTION OF HEAT-SHOCK-PROTEIN IN CORONARY ENDOTHELIAL-CELLS AND CARDIOMYOCYTES - IMPLICATIONS FOR MYOCARDIAL PROTECTION", Journal of thoracic and cardiovascular surgery, 115(1), 1998, pp. 200-209

Abstract

Objectives: Induction of the 70 kd heat shock protein in the heart isknown to exert a protective effect against postischemic mechanical and endothelial dysfunction. However, the exact site of induction and the mechanisms involved remain unknown. The aim of this study was to investigate the relative capacity of endothelial and myocardial cells to express the 70 kd heat shock protein in response to heat stress, as well as their significance. Methods: (1) Postischemic recovery of cardiac mechanical and endothelial function was studied in isolated rat hearts with and without endothelial denudation with saponin, (2) Semiquantitative determination of induction of 70 kd heat shock protein by Western immunoblotting was performed in the whole cardiac homogenate, in isolated cardiac myocytes, and in coronary endothelial cells. (3) Immunocytochemistry was used to visualize the distribution of induction of 70 kd heat shock protein in both cell types, Results: Postischemic recovery (percent preischemic value a standard error of the mean) of cardiac output in hearts from heat-stressed animals was significantly improved (66.7 +/- 6.9 vs 44.5 +/- 4.5 in the control group, p < 0.01), Inheat-stressed hearts treated with saponin no improvement in the recovery of cardiac output was noted (44.7 +/- 6.9 in heat-stressed hearts vs 38.0 +/- 4.0 in heat-stressed, saponin-treated hearts, p = not significant). Endothelial function (as assessed by the vasodilatory response to the endothelium-dependent vasodilator 5-hydroxytryptamine) improved from 31.0 +/- 5.2 in the control group to 65.8 +/- 7.1 in heat-stressed hearts (p < 0.02 vs control) and dropped to -1.9 +/- 3.8 in heat-stressed hearts treated with saponin. Immunocytochemistry showed thatonly sections of hearts from heat-treated rats showed a strong specific reaction with heat shock protein antibody, The positive staining was seen in endothelial cells. Induction of 70 kd heat shock protein content in the whole cardiac homogenate from heat-stressed rats as measured by Western immunoblotting was 5.2 +/- 1.9 (vs 0.0 in non-heat-stressed rats, p < 0.0001) and dropped to 0.0 in heat-stressed hearts treated with saponin, The tentative amount of 70 kd heat shock protein was 18.1 +/- 7.8 in isolated endothelial cells from heat-stressed hearts and 2.3 +/- 2.3 in isolated cardiac myocytes (p < 0.01 vs endothelial cells). Conclusions: Coronary endothelial cells are the main site of induction of 70 kd heat shock protein in the heart and appear to contribute to the protective effects of heat stress on the recovery of mechanical and endothelial function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 21:41:26