Inhibitory effect of Sialyl Lewis-X oligosaccharide on reperfusion injury -Optimal timing and temperature during cardioplegia-

目的：在血液灌流的大鼠离体心上观察选择素家族3个成员的主要配体唾液酸化Lewis-X类似物在温血停搏液中的作用。然后再灌流60min。根据停搏液中添加的补充药物，将心脏分为以下两组。对照组(n=6)采用标准温血停搏液。SLX组(n=6)：温血停搏液中加入唾液酸路易斯-X类似物(60μg/ml)。结果：再灌注期SLX组左室发展压和dp/dt显著高于对照组(p<0.05)，-dp/dt显著低于对照组(p&lt；0.05)。加入氯化乙酰胆碱后，SLX组再灌流15min的冠脉流量和NO生成量均显著高于对照组(P<0.05)。SLX组髓过氧化物酶活性显著低于对照组(p&lt；0.05)。结论：选择素介导的内皮-白细胞相互作用在心肌缺血再灌注损伤中可能起重要作用。在温血停搏液中补充唾液酸路易斯-X类似物可能通过抑制再灌注早期白细胞与内皮细胞的相互作用来提供更好的心肌保护。

Objective: Effects of supplemental Sialyl Lewis-X analogue, a major ligand for all three selectin family members, during warm blood cardioplegia were expressed in the blood perfused isolated rat heart.Methods: 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 SLX group (n=6) received warm blood cardioplegia supplemented with Sialyl Lewis-X analogue (60μg/ml). Cardiac function, endothelial function, myocardial metabolism and myocardial myeroperoxidase activity were assessed before and after cardioplegic arrest.Results: Left ventricular developed pressure and dp/dt were significantly (p<0.05) greater and -dp/dt was significantly (p<0.05) lower in the SLX 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 SLX group than the control group. Myeloperoxidase activity was significantly (p<0.05) lower in the SLX than the control group.Conclusions: 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.