Fluosol cardioplegia--a method of optimizing aerobic metabolism during arrest.

Fluosol-DA cardioplegia was compared with crystalloid cardioplegia as a method of myocardial preservation during ischemic arrest. Two groups of 12 pigs each were studied using the in situ pig heart model. Each group was subjected to 2-hour hypothermic (temperature 10-15 degrees C), hyperkalemic (35 mEq/l potassium) cardioplegic arrest. One group received the standard crystalloid cardioplegic solution (PO2 142-164 mm Hg) and the other received an oxygenated Fluosol cardioplegic solution (PO2 420-510 mm Hg). Myocardial contractility (max Vce) compliance, coronary blood flow (six pigs), and adenosine triphosphate and creatine phosphate (six pigs) were measured before and after cardioplegic arrest; high-energy phosphate (adenosine triphosphate and creatine phosphate) levels were also measured during the 2-hour arrest interval. All pigs had 1 hour of normothermic reperfusion, with measurements performed every 15 minutes. The results documented significantly better high-energy phosphate levels in the Fluosol than in the crystalloid group during arrest. During reperfusion, high-energy phosphate levels were equal in both groups. Contractility and compliance were depressed equally during reperfusion in both groups and coronary blood flow showed no significant difference from control in either group. We conclude that Fluosol can support aerobic metabolism during ischemic cardioplegic arrest and preserve high-energy phosphates, but it has no metabolic or hemodynamic advantage during reperfusion.