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

目的：补充Sialyl Lewis-X类似物的影响，一个主要的配体为所有三个选择素家族成员，在温血心脏停搏液中表达的血液灌注离体大鼠heart.Methods：离体心脏停搏60分钟，给予温血心脏停搏液在20分钟的时间间隔。然后再灌注60分钟。根据心脏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）给予标准温血停搏液。SLX组（n=6）给予含Sialyl Lewis-X类似物（60μg/ml）的温血停搏液。结果：与对照组比较，SLX组再灌注时左室发展压（VP）、dp/dt显著升高（P<0.05），-dp/dt显著降低（P<0.05）; SLX组再灌注15分钟时的冠脉流量和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<0.05）。结论：选择素介导的内皮细胞-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。在温血停搏液中加入唾液酸化Lewis-X类似物可能通过抑制再灌注早期白细胞-内皮细胞相互作用而提供上级心肌保护。

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.