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Ann Thorac Surg 2004;77:651-657
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Sodium-hydrogen exchange inhibition attenuates in vivo porcine myocardial stunning

Randy M. Stevens, MDa, M. Salik Jahania, MDa, Robert M. Mentzer, Jr, MDa, Robert D. Lasley, PhDa*

a Department of Surgery, University of Kentucky College of Medicine, Lexington, Kentucky, USA

Accepted for publication June 6, 2003.

* Address reprint requests to Dr Lasley, Department of Surgery, University of Kentucky College of Medicine, MN276, Chandler Medical Center, 800 Rose St, Lexington, KY 40536-0298, USA
e-mail: rlasley{at}uky.edu

BACKGROUND: Inhibition of the sodium-hydrogen exchanger isoform 1 with HOE-642 (cariporide) has been shown to protect against ischemia-reperfusion injury and to decrease myocardial cell death in numerous animal preparations; however the effects of cariporide in stunned myocardium are not as well understood. We sought to determine whether cariporide attenuated myocardial stunning in vivo.

METHODS: Open chest anesthetized pigs (22–33 kg) were subjected to 15 min of left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Regional ventricular function was assessed by segment shortening. Contractility was measured by stroke work and by load-insensitive preload recruitable stroke work and preload recruitable stroke work area. Vehicle or HOE-642 (1 mg/kg, IV) was administered 10 min before LAD occlusion.

RESULTS: Cariporide treatment significantly improved postischemic segment shortening, stroke work, preload recruitable stroke work, and preload recruitable stroke work area and had no systemic hemodynamic effects. After 3 h of reperfusion, control animals recovered 33% ± 4% and 33% ± 3% of preischemic LAD segment shortening and preload recruitable stroke work area values, respectively, whereas animals treated with HOE-642 recovered 59% ± 6% and 57% ± 6%, respectively (p < 0.05). Seven (39%) of 17 control animals exhibited ventricular fibrillation during reperfusion; none of the cariporide-treated pigs fibrillated.

CONCLUSIONS: Sodium–hydrogen exchange inhibition can attenuate postischemic myocardial stunning in addition to its well-described anti-infarct properties. Inhibition of the sodium–hydrogen exchanger may be beneficial in patients susceptible to postischemic myocardial dysfunction associated with cardiac surgery.




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