We tested the effects of
glucose and
oxygen in
cardioplegic solutions on myocardial protection in the isolated perfused working rat heart. Recovery from 2 hours' hypothermic (8 degrees C) cardioplegic arrest was examined in 93 hearts.
Cardioplegic solution, which was delivered every 15 minutes, was supplemented with
glucose 28 mmol/L as a substrate or
sucrose 28 mmol/L as a nonmetabolizable osmotic control; it was equilibrated with either 98%
oxygen or 98%
nitrogen, both with 2%
carbon dioxide. Four combinations of hyperkalemic
cardioplegic solution were studied:
nitrogen-
sucrose,
nitrogen-
glucose,
oxygen-
sucrose, and
oxygen-
glucose. During hypothermic arrest, oxygenation of
cardioplegic solution greatly reduced myocardial
lactate production and prevented
ischemic contracture as indicated by coronary vascular resistance.
Glucose increased
lactate production modestly but significantly only when the
cardioplegic solution was nitrogenated. Although end-arrest myocardial
adenosine triphosphate and
creatine phosphate were greatly increased by oxygenation of
cardioplegic solution (p less than 0.005), we could not detect improved preservation of these high-energy
phosphates by
glucose. Averaged over reperfusion, percent recovery of cardiac output for the
nitrogen-
sucrose,
nitrogen-
glucose,
oxygen-
sucrose, and
oxygen-
glucose solutions was 32.3% +/- 6.1%, 45.9% +/- 4.6%, 44.5% +/- 4.6%, and 62.2% +/- 4.5%, respectively. Oxygenation of the
glucose solution or addition of
glucose to the oxygenated
solution significantly improved recovery of cardiac output. The benefits of
glucose and
oxygen were additive, so that the
oxygen-
glucose cardioplegic solution provided the best functional recovery. We conclude that the addition of
glucose to the fully oxygenated multidose cold
cardioplegic solution improves functional recovery without increasing
lactate production during arrest.