摘要
目的 :观察血小板激活因子拮抗剂对急性重症胰腺炎 (SAP)时肠粘膜损伤以及细菌和内毒素移位的影响。 方法 :采用胰管内注射牛磺胆酸钠 胰蛋白酶的方法诱导猪SAP ,对照组用等渗盐水代替牛磺胆酸钠 胰蛋白酶进行胰管内注射。为了解血小板激活因子 (PAF)的特异性拮抗剂BN5 0 739对SAP肠粘膜损伤的影响 ,在诱导SAP之前 30min静脉注射BN5 0 739。测定肠粘膜血流量、肠粘膜内髓过氧化酶 (MPO)和丙二醛 (MDA)含量 ,观察肠粘膜的病理改变 ,并测定门静脉血的内毒素含量和门静脉血、肠系膜淋巴结、胰腺的细菌数量。 结果 :诱导SAP以前给予BN5 0 739能够增加肠粘膜血流量 ,减少肠粘膜MPO和MDA含量 ,降低门静脉血的内毒素浓度和移位细菌数量。 结论 :SAP时合并有肠粘膜损伤 ,用BN5 0 739拮抗PAF能够增加肠粘膜血流量、改善肠粘膜微循环、减轻肠粘膜的炎性细胞浸润和降低MDA和MPO含量 ,减轻肠粘膜损伤的严重程度 。
Objectives:To study the roles of platelet activating factor (PAF) in the pathogenesis of intestinal mucosal injury and endotoxin/bacterial translocation in severe acute pancreatitis (SAP) in pigs. Methods:Severe acute pancreatitis was induced by intraductal injection of a mixture of sodium taurocholate and trypsin. In order to observe the effects of BN50739, a specific antagonist of PAF, it was given 30 min prior to the induction of SAP. Mucosal blood flow, mucosal myeloperoxidase (MPO) and malondialdehyde (MDA) was determined, intestinal injury was observed microscopically, portal blood endotoxin levels and the bacterial counts in the portal blood, intestinal lymph nodes and the pancreas were determined. Results: Prior antagonism of PAF by BN50739 could reduce intestinal injury, increase the intestinal mucosal blood flow, and reduce the blood levels of endotoxin and the bacterial count in the portal blood, mesenteric lymph nodes and the pancreas. Conclusions:Intestinal mucosal injury developed in SAP. Antagonism of PAF by BN50739 can improve intestinal microcirculation and reduce the severity of intestinal mucosal injury, which is beneficial to the prevention of endotoxin/bacterial translocation.
出处
《医学研究生学报》
CAS
2002年第5期408-410,426,T002,共5页
Journal of Medical Postgraduates