GUT PHOSPHOLIPASE A(2) MEDIATES NEUTROPHIL PRIMING AND LUNG INJURY AFTER MESENTERIC ISCHEMIA-REPERFUSION
GUT PHOSPHOLIPASE A(2) MEDIATES NEUTROPHIL PRIMING AND LUNG INJURY AFTER MESENTERIC ISCHEMIA-REPERFUSION
复制标题
DOI：
10.1152/ajpgi.1995.268.3.g397
复制
发表时间：
1995-03-01
影响因子：
4.5
通讯作者：
BANERJEE, A
中科院分区：
文献类型：
--
作者：
KOIKE, K;MOORE, EE;BANERJEE, A
肠缺血再灌注(IIR)通过循环PMN启动、肺PMN隔离、肺微血管渗漏增加等过程，诱发中性粒细胞(PMN)介导的肺损伤。在大鼠肠I/R(缺血45min，再灌流6h)模型上，与假手术组相比，1)缺血时肠磷脂酶A(2)被激活，2)循环PMN被激活(用N-甲酰-Met-Leu-Phe产生超氧阴离子来评估)，3)与假手术组相比，再灌注2小时出现了I-125标记的过度白蛋白肺渗漏(P<；0.05)。在再灌流后15分钟内给予PLA2抑制剂奎纳克林，可逆转过度的肠道PLA2活性，并阻止随后的PMN预充和肺渗漏(P<；0.05)。然而，当再灌注2小时后给予奎纳克林时，循环中的PMN启动和肺渗漏继续发生，尽管肠道中的磷脂酶A(2)活性受到抑制。结论：肠内磷脂酶A(2)的激活可能是肠I/R后循环PMN预充和肺微血管渗漏后遗症的先决条件。
Intestinal ischemia-reperfusion (IIR) provokes polymorphonuclear neutrophil (PMN)-mediated lung injury via a process characterized by circulating PMN priming, pulmonary PMN sequestration, and increased microvascular leak in the lung. We found in rats subjected to intestinal I/R (ischemia 45 min and reperfusion 6 h) that 1) intestinal phospholipase A(2) (PLA(2)) was activated during ischemia, 2) circulating PMN priming (assessed by superoxide production with N-formyl-Met-Leu-Phe) occurred after 1 h reperfusion, and 3) exaggerated I-125-labeled albumin lung leak occurred after 2 h reperfusion, compared with sham-treated animals (P < 0.05). Treatment with a PLA(2) inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA(2) activity and abrogated subsequent PMN priming and lung leak (P < 0.05). However, when quinacrine was administered after 2 h of reperfusion, circulating PMN priming and lung leak continued to evolve despite suppression of intestinal PLA(2) activity. We conclude that intestinal PLA(2) activation may be a prerequisite for the sequelae of circulating PMN priming and pulmonary microvascular leak observed after intestinal I/R.