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J Thorac Cardiovasc Surg 2003;125:1499-1509
© 2003 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Sodium-hydrogen exchange inhibition preserves ventricular function after ventricular fibrillation in the intact swine heart

From the Departments of Surgery,^a Pediatrics,^b and Biostatistics,^c Columbia College of Physicians and Surgeons, New York, NY.

Supported in part by Department of Surgery Attending-Resident Start-up Grant and in part by the National Heart Lung, and Blood Institute of the National Institutes of Health (NRSA F32 HL69641-01).

Received for publication June 3, 2002. Revisions requested July 11, 2002; revisions received Aug 6, 2002. Accepted for publication Aug 15, 2002. Address for reprints: Henry M. Spotnitz, MD, Department of Surgery, Columbia College of Physicians and Surgeons, 622 West 168th St, PH 1422, New York, NY 10032 (E-mail: hms2{at}Columbia.edu).

Background: We tested the hypothesis that sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after ischemia-reperfusion injury in the intact porcine heart.
Methods: Twelve pigs (weight, 30-45 kg) were evenly divided into 2 groups. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and left ventricular pressure. Animals were given vehicle (control) or benzamide-N-(aminoiminomethl)-4-(4-[2-furanylcarbonyl]-1-piperazinyl)-3-(methylsulfonyl)methanesulfonate (BIIB 513; 3 mg/kg administered intravenously). Ten minutes later, hearts were subjected to 75 seconds of ventricular fibrillation. After reperfusion for 40 minutes, function studies were repeated. Hearts were arrested and excised. Postmortem data included passive pressure-volume curves and myocardial water content.
Results: Preload recruitable stroke work was significantly decreased from baseline after ischemia and reperfusion in the control group (27.7 ± 2.5 vs 48.0 ± 5.6 mm Hg [± SEM], P = .001) but not in the BIIB 513 group (43.0 ± 5.8 vs 45.5 ± 4.1 mm Hg, P = not significant). In vivo diastolic and postmortem passive left ventricular compliance were reduced after ischemia and reperfusion for control animals but remained unchanged for animals receiving BIIB 513. Time required to recover baseline blood pressure after ventricular fibrillation was significantly longer for control animals (159 ± 15 vs 88 ± 14 seconds [± SEM], P = .008). Myocardial water content (78.97% ± 0.94% vs 77.86% ± 0.46% [± SEM]) and normalized left ventricular mass (137.24 ± 6.17 vs 128.41 ± 1.96 g [± SEM]) were insignificantly increased in control animals.
Conclusions: Sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after 75 seconds of ventricular fibrillation and 40 minutes of reperfusion. This family of agents might prove useful in patients with severe left ventricular dysfunction undergoing ventricular fibrillation for implantable cardioverter defibrillator testing.