Microvascular changes after cardioplegia solution infusion and blood reperfusion. Effects of adenosine

The hypothesis that hyperkalemic, crystalloid cardioplegia solutions damage the microvasculature, leading to decreased microvascular flow and increased neutrophil accumulation during reperfusion, was tested in a model system. Intravital microscopic observations were performed during a 20 minute perfusion of the hamster cremaster with cardioplegia solutions (10°C) via the femoral artery with the iliac occluded, and during a subsequent 2 hour blood reperfusion period (iliac open). Arteriolar vasoconstriction (27% decrease in diameter, p<0.05) and a 25% decrease in the density of perfused capillaries (p<0.05) occurred during reperfusion in animals receiving crystalloid cardioplegia (16 mEq K⁺) compared to control animals (no cardioplegia solution given). Rolling neutrophils accumulated on venular endothelium in cardioplegia treated animals (250% increase, p<0.05) and extravascularly (myeloperoxidase levels 2.0±0.5 U/g vs. 1.3±0.3 U/g in control, p<0.05). The addition of adenosine (10^-4 M) and albumin (2% by volume) to the cardioplegia perfusate, accompanied by the administration of adenosine (10^-4 M) during reperfusion, produced arteriolar vasodilation (34% diameter increase, p<0.05) and inhibited extravascular neutrophil accumulation (myeloperoxidase level of 1.5±0.2 U/g, p<0.05 vs control), but capillary perfusion was still significantly diminished (28% decrease, p<0.05). We conclude that microvascular blood flow decreases and neutrophils accumulate in tissues during blood reperfusion following infusion of hyperkalemic crystalloid cardioplegia solutions. Adenosine partially reversed these changes by dilating arterioles and decreasing neutrophil accumulation. The microvascular changes seen were independent of perfusate temperature, and were most likely due to endothelial dysfunction induced by the high potassium content and crystalloid composition of the cardioplegia solution.