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Titolo:
Adenosine A(3)-receptor stimulation attenuates postischemic dysfunction through K-ATP channels
Autore:
Thourani, VH; Nakamura, M; Ronson, RS; Jordan, JE; Zhao, ZQ; Levy, JH; Szlam, F; Guyton, RA; Vinten-Johansen, J;
Indirizzi:
Emory Univ, Crawford Long Hosp, Carlyle Fraser Heart Ctr,Cardiothorac Res Lab, Sch Med,Dept Surg,Div Cardiothorac Surg, Atlanta, GA 30365 USA Emory Univ Atlanta GA USA 30365 Cardiothorac Surg, Atlanta, GA 30365 USA Emory Univ, Crawford Long Hosp, Carlyle Fraser Heart Ctr,Cardiothorac Res Lab, Sch Med,Dept Anesthesiol, Atlanta, GA 30365 USA Emory Univ Atlanta GAUSA 30365 d,Dept Anesthesiol, Atlanta, GA 30365 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 1, volume: 46, anno: 1999,
pagine: H228 - H235
SICI:
0363-6135(199907)46:1<H228:AASAPD>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE POTASSIUM CHANNELS; A(3) RECEPTOR STIMULATION; INFARCT SIZE-REDUCTION; ENDOGENOUS ADENOSINE; REPERFUSION INJURY; MOLECULAR-CLONING; RABBIT HEART; RAT; ACTIVATION; PROTECTION;
Keywords:
myocardial protection; purinergic receptors; rat; adenosine 5 '-triphosphate-sensitive potassium channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Vinten-Johansen, J Emory Univ, Crawford Long Hosp, Carlyle Fraser Heart Ctr,Cardiothorac Res Lab, Sch Med,Dept Surg,Div Cardiothorac Surg, 550 Peachtree St NE, Atlanta,GA 30365 USA Emory Univ 550 Peachtree St NE Atlanta GA USA 30365 USA
Citazione:
V.H. Thourani et al., "Adenosine A(3)-receptor stimulation attenuates postischemic dysfunction through K-ATP channels", AM J P-HEAR, 46(1), 1999, pp. H228-H235

Abstract

We tested the hypothesis that selective adenosine A(3)-receptor stimulation reduces postischemic contractile dysfunction through activation of ATP-sensitive potassium (K-ATP) channels. Isolated, buffer-perfused rat hearts (n= 8/group) were not drug pretreated (control) or were pretreated with adenosine (20 mu M), 2-chloro-N-6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide(C1-IB-MECA; A(3) agonist, 100 nM), Cl-IB-MECA + 8-(3-noradamantyl)-1,3-dipropylxanthine (KW-3902; A(1) antagonist, 5 mu M), C1-IB-MECA + glibenclamide (Glib; K-ATP-channel blocker, 0.3 mu M), or Glib alone for 12 min before30 min of global normothermic ischemia followed by 2 h of reperfusion. After 2 h of reperfusion, left, ventricular developed pressure (LVDP,%baseline) in control hearts was depressed to 34 +/- 2%. In hearts pretreated with Cl-IB-MECA, there was a statistically significant increase in LVDP (50 +/- 6%), which was reversed with coadministration of Glib (37 +/- 1%). Control hearts also showed similar decreases in left ventricular peak positive rate of change in pressure (dP/dt). Therefore, the A(3) agonist significantly attenuated postischemic cardiodynamic injury compared with the control, whichwas reversed by Glib. Cumulative creatine kinase (CK in U/min) activity was most pronounced in the control group (10.4 +/- 0.6) and was significantlydecreased by Cl-IB-MECA(7.5 +/- 0.4), which was reversed by coadministration of Glib (9.4 +/- 0.2). Coronary flow was increased during adenosine infusion (160% of baseline) but not during C1-IB-MECA infusion. Effects of C1-IB-MECA were not reversed by the specific A(1) antagonist KW-3902. We conclude that cardioprotection afforded by As-receptor stimulation may be mediated in part by K-ATP channels. C1-IB-MECA may be an effective pretreatment agent that attenuates postischemic cardiodynamic dysfunction and CK release without the vasodilator liability of other adenosine agonists.

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Documento generato il 30/11/20 alle ore 23:35:42