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Am J Physiol Heart Circ Physiol 280: H830-H834, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H830-H834, February 2001

HOE-642 (cariporide) alters pHi and diastolic function after ischemia during reperfusion in pig hearts in situ

Michael A. Portman1, Anthony L. Panos2, Yun Xiao1, David L. Anderson2, and Xue-Han Ning1

1 Division of Cardiology, Department of Pediatrics, and 2 Division of Cardiothoracic Surgery, Department of Surgery, University of Washington and Children's Hospital and Regional Medical Center, Seattle, Washington 98105

The specific Na+/H+ exchange inhibitor HOE-642 prevents ischemic and reperfusion injury in the myocardium. Although this inhibitor alters H+ ion flux during reperfusion in vitro, this action has not been confirmed during complex conditions in situ. Myocardial intracellular pH (pHi) and high-energy phosphates were monitored using 31P magnetic resonance spectroscopy in open-chest pigs supported by cardiopulmonary bypass during 10 min of ischemia and reperfusion. Intravenous HOE-642 (2 mg/kg; n = 8) administered before ischemia prevented the increases in diastolic stiffness noted in control pigs (n = 8), although it did not alter the postischemic peak-elastance or pressure-rate product measured using a distensible balloon within the left ventricle. HOE-642 induced no change in pHi during ischemia but caused significant delays in intracellular realkalinization during reperfusion. HOE-642 did not alter phosphocreatine depletion and repletion but did improve ATP preservation. Na+/H+ exchange inhibition through HOE-642 delays intracellular alkalinization in the myocardium in situ during reperfusion in association with improved diastolic function and high-energy phosphate preservation.

magnetic resonance spectroscopy; metabolism; phosphates; intracellular pH


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