Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts.
We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') before ischemia. Preconditioning accelerated, whereas cardioplegia delayed, ischemic contracture (time to peak contracture: PC = 8.1 +/- 0.3 and CP = 25.1 +/- 0.2 min vs. C = 15.6 +/- 0.3 min, P < 0.05). The ischemia-induced decline in ATP was delayed by cardioplegia but accelerated by preconditioning (P < 0.05). In a parallel study, preconditioning and cardioplegia protected postischemic contractile function to a similar extent. Thus, in the blood-perfused rat heart, preconditioning accelerated ischemic contracture and depletion of ATP. In contrast, cardioplegia slowed ischemic contracture and ATP depletion.
D000255:Adenosine Triphosphate / Q000172:deficiency* / Q000378:metabolism; D000818:Animals; D001769:Blood; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D010710:Phosphates; D000255:Adenosine Triphosphate