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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01032.2001
Submitted on November 27, 2001
Accepted on February 11, 2002
1 Anesthesiology, The Medical College of Wisconsin, Milwaukee, WI, USA; Anesthesiology, Xuzhou Medical College, Xuzhou, WI, China
2 Anesthesiology, The Medical College of Wisconsin, Milwaukee, WI, USA
3 Anesthesiology, The Medical College of Wisconsin, Milwaukee, WI, USA; Physiology, The Medical College of Wisconsin, Milwaukee, WI, USA
4 Anesthesiology, The Medical College of Wisconsin, Milwaukee, WI, USA; Physiology, The Medical College of Wisconsin, Milwaukee, WI, USA; Research Service, Veterans Affairs Medical Center, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: qunchen{at}mcw.edu.
Brief ischemia prior to normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear if it protects against moderate long-term hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia prior to 4 hours 17°C hypothermic ischemia on cardiac cytosolic [Ca2+], mechanical and metabolic function, and infarct size, and 2) the potential role of KATP channels in eliciting cardioprotection. We found that IPC before 4 hours moderate hypothermia improved myocardial perfusion, contractility and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca2+] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36±2 (SEM)% to 15±1% with IPC. Bracketing ischemic pulses with 200 µM 5-hydroxydecanoic acid or 10 µM glibenclamide increased infarct size to 28±3% and 26±4%, respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia, and that this is associated with decreased cytosolic [Ca2+] loading and enhanced KATP channel opening.
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