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Titolo:
Adenosine A(3) pretreatment before cardioplegic arrest attenuates postischemic cardiac dysfunction
Autore:
Thourani, VH; Ronson, RS; Jordan, JE; Guyton, RA; Vinten-Johansen, J;
Indirizzi:
Emory Univ, Sch Med, Div Cardiothorac Surg,Dept Surg, Carlyle Fraser HeartCtr,Cardiothorac Res Lab, Atlanta, GA 30322 USA Emory Univ Atlanta GA USA 30322 rdiothorac Res Lab, Atlanta, GA 30322 USA
Titolo Testata:
ANNALS OF THORACIC SURGERY
fascicolo: 6, volume: 67, anno: 1999,
pagine: 1732 - 1737
SICI:
0003-4975(199906)67:6<1732:AAPBCA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFARCT SIZE-REDUCTION; ISOLATED RABBIT HEART; POTASSIUM CARDIOPLEGIA; RECEPTOR STIMULATION; MOLECULAR-CLONING; ACTIVATION; PROTECTS; INJURY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Vinten-Johansen, J Crawford Long Hosp, Cardiothorac Res Lab, 550 PeachtreeNE, Atlanta, GA 30365 USA Crawford Long Hosp 550 Peachtree NE Atlanta GA USA 30365
Citazione:
V.H. Thourani et al., "Adenosine A(3) pretreatment before cardioplegic arrest attenuates postischemic cardiac dysfunction", ANN THORAC, 67(6), 1999, pp. 1732-1737

Abstract

Background. The cardioprotective effects of the adenosine A(3) receptor ina cardioplegia model have not been described. We tested the hypothesis that infusion of the A(3) receptor agonist, Cl-IB-MECA (100 nM), as a pretreatment (PTx) and/or as a cardioplegic (CP) additive reduces postischemic myocardial injury. Methods. Isolated perfused rat hearts underwent 30 minutes of normothermicischemia, 60 minutes of intermittent hypothermic cardioplegia (10 degrees C), followed by 2 hours of reperfusion. Hearts were divided into four groups: (1) no pretreatment (PTx) and unsupplemented cardioplegia (CP) (control), (2) Cl-IB-MECA PTx and unsupplemented CP (A(3)-PTx), (3) no PTx and Cl-IB-MECA CP (A(3)-CP), or (4) Cl-IB-MECA PTx and Cl-IB-MECA CP (A(3)-[PTx+CP]). Results. Coronary now was not increased after A(3) pretreatment when compared to baseline values. After 2 hours of reperfusion, left ventricular developed pressure in control and A(3)-CP groups was depressed to 43% +/- 3% and 47% +/- 2% of baseline; while A(3)-PTx and A(3)-[PTx+CP] significantly increased left ventricular developed pressure (65% +/- 3% and 61% +/- 5%) from baseline relative to control and A(3)-CP. Effluent creatine kinase activity was significantly decreased by A(3)-PTx (1520 +/- 32 IU/L), A(3)-[PTx+CP] (1481 +/- 41 IU/L) from control (1734 +/- 54 IU/L) and A(3)-CP (1750 +/- 43 IU/L). Myocardial edema (% tissue water) was significantly less in A(3)-PTx (78 +/- 0.6%) and A(3)-[PTx+CP] (76% +/- 2%) compared with control (85%+/- 0.4%) and A(3)-CP (83% +/- 2%). Conclusions. Adenosine A(3) receptor stimulation as a pretreatment attenuates postischemic cardiodynamic dysfunction and creatine kinase release but has no cardioprotection as an adjunct to cold cardioplegia. (C) 1999 by TheSociety of Thoracic Surgeons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:16:38