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J Thorac Cardiovasc Surg 2002;123:959-966
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Sodium/hydrogen-exchanger inhibition during cardioplegic arrest and cardiopulmonary bypass: An experimental study

From the Departments of Surgery and Anesthesiology-Center for Microvascular and Lymphatic Studies, and Pathology and Laboratory Medicine at the University of Texas-Houston, Medical School, and the Michael E. DeBakey Institute, Texas A&M University, Houston, Tex.

Supported in part by National Heart, Lung, and Blood Institute grant No. HL-36115 and National Institute of General Medical Sciences grant No. GM-00675. Dr Sauer is the recipient of a scholarship from Dr F. Kohler Chemie GmbH, Germany.

Received for publication July 11, 2001. Revisions requested Aug 13, 2001; revisions received Aug 29, 2001. Accepted for publication Oct 2, 2001. Address for reprints: Charles S. Cox, Jr, MD, 6431 Fannin, Suite 5.246. Houston, TX 77030 (E-mail: Charles.S.Cox{at}uth.tmc.edu).

Objective: We sought to determine whether pretreatment with a sodium/hydrogen-exchange inhibitor (EMD 96 785) improves myocardial performance and reduces myocardial edema after cardioplegic arrest and cardiopulmonary bypass.
Methods: Anesthetized dogs (n = 13) were instrumented with vascular catheters, myocardial ultrasonic crystals, and left ventricular micromanometers to measure preload recruitable stroke work, maximum rate of pressure rise (positive and negative), and left ventricular end-diastolic volume and pressure. Cardiac output was measured by means of thermodilution. Myocardial tissue water content was determined from sequential biopsy. After baseline measurements, hypothermic (28°C) cardiopulmonary bypass was initiated. Cardioplegic arrest (4°C Bretschneider crystalloid cardioplegic solution) was maintained for 2 hours, followed by reperfusion-rewarming and separation from cardiopulmonary bypass. Preload recruitable stroke work and myocardial tissue water content were measured at 30, 60, and 120 minutes after bypass. EMD 96 785 (3 mg/kg) was given 15 minutes before bypass, and 2 µmol was given in the cardioplegic solution. Control animals received the same volume of saline vehicle. Arterial-coronary sinus lactate difference was similar in both animals receiving EMD 96 785 and control animals, suggesting equivalent myocardial ischemia in each group.
Results: Myocardial tissue water content increased from baseline in both animals receiving EMD 96 785 and control animals with cardiopulmonary bypass and cardioplegic arrest but was statistically lower in animals receiving EMD 96 785 compared with control animals (range, 1.0%-1.5% lower in animals receiving EMD 96 785). Preload recruitable stroke work decreased from baseline (97 ± 2 mm Hg) at 30 (59 ± 6 mm Hg) and 60 (72 ± 9 mm Hg) minutes after cardiopulmonary bypass and cardioplegic arrest in control animals; preload recruitable stroke work did not decrease from baseline (98 ± 2 mm Hg) in animals receiving EMD 96 785 and was statistically greater at 30 (88 ± 5 mm Hg) and 60 (99 ± 4 mm Hg) minutes after bypass and arrest compared with control animals.
Conclusions: Sodium/hydrogen-exchanger inhibition decreases myocardial edema immediately after cardiopulmonary bypass and cardioplegic arrest and improves preload recruitable stroke work. Sodium/hydrogen-exchange inhibition during cardiac procedures with cardiopulmonary bypass and cardioplegic arrest may be a useful adjunct to improve myocardial performance in the immediate postbypass or arrest period.

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