We have previously shown that metabolic arrest induced with ATP-regulated potassium channel openers (PCOs) can improve lung preservation by adding Aprikalim (a PCO, Rhone-Poulene Roher) to modified Euro-Collins solution for pulmonary artery flush. Because the membrane hyperpolarizing effects of a PCO potentially competes with the depolarizing effects of a hyperkalemic solution, this study evaluated the effects of the potassium gradient on PCO-mediated lung protection.

Twenty rabbits underwent lung protection in four groups. Group 1 underwent harvest and reperfusion as a “no ischemia” control. Groups 2, 3, and 4 underwent harvest followed by 18 hours of cold ischemic storage before reperfusion. Groups 1 and 4 received Euro Collins as the pulmonary flush at induction of ischemia. Group 2 received Euro Collins plus Aprikalim (100 μM); and group 3 received lactated Ringer’s plus Aprikalim. After ischemic storage, the lungs were reperfused with autologous blood for 2 hours. Every 30 minutes, the lungs were given a 10-minute 100% fractional inspired oxygen (F_iO₂) challenge to measure maximal gas exchange as an indication of graft function.

Repeated measures ANOVA showed Aprikalim improved graft function after 18 hours of cold ischemia (p < 0.0001). No significant differences were found when Aprikalim was used in either Euro-Collins (group 2) or lactated Ringer’s (group 3) solution.

The ability of the PCO Aprikalim to preserve gas exchange in a model of hypothermic pulmonary ischemia-reperfusion injury was not affected by the plasmolemmal potassium gradient. This is consistent with recent findings in myocardial protection studies that the protective effects of PCOs may be intracellular.