Effects of supplemental Sialyl Lewis
x analogue, a major ligand for all three selectin family members, during warm blood Cardioplegia were assessed in the blood perfused isolated rat heart. The isolated hearts were arrested for 60 min with warm blood cardioplegia given at 20-min intervals. This was followed by 60 min of reperfusion. The hearts were divided into the following two groups according to the supplemental drugs added to the cardioplegic solution. The control group (n=6) received standard warm blood cardioplegia. The Sialyl Lewis
x analogue group (n=6) received warm blood cardioplegia supplemented with Sialyl Lewis
x analogue (60 μg/ml). Cardiac function, endothelial function, myocardial metabolism and myocardial myeloperoxidase activity were assessed before and after cardioplegic arrest. Left ventricular developed pressure and dp/dt were significantly (p<0.05) greater and -dp/dt was significantly (p<0.05) lower in the Sialyl Lewis
x analogue group than the control group during reperfusion. Coronary flow at 15 min of reperfusion and NO production, when acetylcholine chloride was added were significantly (p<0.05) greater in the Sialyl Lewis
x analogue group than the control group. Myeloperoxidase activity was significantly (p<0.05) lower in the Sialyl Lewis
x analogue group than the control group. The results suggest that selectin-mediated endothelial-leukocyte interactions may play an important role in myocardial ischemia and reperfusion injury. Supplementation of Sialyl Lewis
x analogue during warm blood cardioplegia may provide superior myocardial protection by suppressing leukocyte-endothelial interaction during early reperfusion period.
抄録全体を表示