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Ann Thorac Surg 1997;63:1107-1112
© 1997 The Society of Thoracic Surgeons

Original Article: Cardiovascular

The Contribution of Na+/H+ Exchange to Ischemia-Reperfusion Injury After Hypothermic Cardioplegic Arrest

Takashi Yamauchi, MD, Hajime Ichikawa, MD, Yoshiki Sawa, MD, Norihide Fukushima, MD, Koji Kagisaki, MD, Kazuhiro Maeda, PhD, Hikaru Matsuda, MD, Ryota Shirakura, MD

Department of Organ Transplantation and First Department of Surgery, Osaka University Medical School, Osaka, Japan

Accepted for publication November 5, 1996.

Background. Na+/H+ exchange has been reported to be one of the key mechanisms in myocardial ischemia-reperfusion injury. However, the effect of temperature on Na+/H+ exchange is not fully understood.

Methods. Sodium-propionate-induced cell swelling, an indicator of the function of the Na+/H+ exchanger, was measured in rat thymic lymphocytes. A Langendorff perfused rat heart model was also employed to investigate the effect of the pharmacologic inhibition of Na+/H+ exchange on the recovery of cardiac function after hypothermic ischemia. This was done using FR168888, an inhibitor of Na+/H+ exchange.

Results. In the in vitro study, rat lymphocytes were observed to swell at 17°, 22°, and 27°C, indicating that the Na+/H+ exchanger remains functional even under hypothermic conditions. FR168888 was found to significantly inhibit Na+/H+ exchange-induced cell swelling, even at 17°C. In the in vivo study, pretreatment with FR168888 was found to prevent the deterioration of ventricular function, even after 5 hours of hypothermic cardioplegic arrest. This was associated with a decrease in the reperfusion-induced elevation in resting tension.

Conclusions. These results suggest that Na+/H+ exchange in the heart still occurs, even under hypothermic conditions, and contributes to reperfusion injury, even after hypothermic cardioplegic arrest.




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