MYOCARDIAL PROTECTION WITH POTASSIUM-CHANNEL OPENERS IS AS EFFECTIVE AS ST THOMAS SOLUTION IN THE RABBIT HEART

Background. Previous work from our laboratory has demonstrated the adv antage of adenosine triphosphate-sensitive potassium-channel openers a s cardioplegic agents when compared with hyperkalemic (20 mmol/L KCl) Krebs-Henseleit solution. However, Krebs-Henseleit with 20 mmol/L KCl is not an ideal hyperkalemic cardioplegia. Therefore, we investigated the hypothesis that hyperpolarized arrest with pinacidil and aprikalim could provide equal or superior myocardial protection to hyperkalemic arrest with the widely accepted St. Thomas' solution. Methods. Myocar dial protection was compared in the blood-perfused isolated parabiotic rabbit heart Langendorff model. Twenty-four hearts were protected wit h a 50-mL infusion of cardioplegia for a 30-minute global normothermic ischemic period followed by 30 minutes of reperfusion. Systolic funct ion (percent recovery of developed pressure) and the diastolic propert ies of the left ventricle were measured. Coronary blood flow was measu red throughout each experiment. Results. The percent recovery of devel oped pressure (mean a standard error of the mean) for St. Thomas' solu tion, pinacidil, and aprikalim was 53.1% +/- 5.4%, 64.0% +/- 3.0%, and 62.4% +/- 3.2%, respectively. The time (minutes) until mechanical and electrical arrest was significantly longer in the pinacidil (4.82 +/- 0.10 and 12.06 +/- 1.07) and aprikalim (3.33 +/- 0.28 and 11.12 +/- 0 .94) groups when compared with the St. Thomas group (1.84 +/- 0.74, an d 3.17 +/- 1.44). Coronary blood flow upon reperfusion was significant ly greater in the pinacidil (16.4 +/- 2.1 mL/min) and aprikalim (19.4 +/- 2.8 mL/min) groups compared with the St. Thomas' solution group (8 .0 +/- 1.0 mL/min), and this returned to baseline after 15 minutes of reperfusion. Conclusions. Myocardial protection with pinacidil and apr ikalim is comparable with that of St. Thomas' solution in the blood-pe rfused isolated rabbit heart despite prolonged mechanical and electric al activity during ischemia.