ENDOTOXIN AFTER GUT ISCHEMIA REPERFUSION CAUSES IRREVERSIBLE LUNG INJURY
ENDOTOXIN AFTER GUT ISCHEMIA REPERFUSION CAUSES IRREVERSIBLE LUNG INJURY
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DOI：
10.1016/0022-4804(92)90145-p
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发表时间：
1992-06-01
影响因子：
2.2
通讯作者：
BANERJEE, A
中科院分区：
文献类型：
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作者：
KOIKE, K;MOORE, FA;BANERJEE, A
我们最近报道，肠缺血45分钟，再灌注6小时可引起中度~（125）I-白蛋白肺渗漏，再灌注18小时可逆转。我们的目的是确定第二次损伤，低剂量内毒素的影响肠缺血/再灌注（I/R）后6小时给予LPS（2.5 mg/kg），通过125 I-白蛋白渗漏、中性粒细胞内流（髓过氧化物酶测定，MPO）、组织病理学和死亡率。将大鼠随机分为假剖腹术组（SHAM）或上级肠系膜动脉闭塞45分钟组，6小时后用LPS或生理盐水处理。再灌注18小时后取肺，测定125 I-白蛋白渗漏和MPO，常规H&E染色后由无偏见的观察者进行显微镜检查。我们观察到LPS增加了肺中性粒细胞水平，无论是否有肠I/R。而再灌注18小时时，只有联合损伤（I/R + LPS）增加了125 I-白蛋白漏出。肺组织学证实，I/R + LPS的顺序组合引起显著的间质水肿和中性粒细胞隔离，伴有肺泡水肿、出血和炎性渗出，而I/R或LPS + LPS则没有。I/R + LPS组的死亡率为39%，显著高于单纯肠I/R组（0%）、单纯肠I/R组（0%）和单纯肠I/R + LPS组（4%）。总之，延迟暴露于低剂量内毒素将中度肠道I/R诱导的肺功能障碍转化为晚期器官衰竭。
We have recently reported that 45 min of gut ischemia causes moderate125I-albumin lung leak at 6 hr of reperfusion which was reversed at 18 hr. Our purpose was to determine the effect of a second insult, low dose endotoxin (LPS, 2.5 mg/kg), given 6 hr after gut ischemia/reperfusion (I/R) on this lung injury as assessed by125I-albumin leak, neutrophil influx (myeloperoxidase assay, MPO), histopathology, and mortality. Rats were randomized to either sham laparotomy (LAP) or 45 min of superior mesenteric artery occlusion and 6 hr later were treated with LPS or saline. At 18 hr reperfusion the lungs were harvested, assayed for125I-albumin leak and MPO, and microscopically examined by an unbiased observer after routine H&E staining. We observed that LPS increased lung neutrophil levels both with or without gut I/R. However, only the combined insult (I/R + LPS) increased125I-albumin leak at 18 hr of reperfusion. Lung histology confirmed that the sequential combination of I/R + LPS caused marked interstitial edema and neutrophil sequestration accompanied by alveolar edema, hemorrhage, and fibrinous exudate, while I/R or LAP + LPS did not. The mortality rate of I/R + LPS was 39% which was significantly higher than LAP alone (0%), gut I/R alone (0%), or LAP + LPS (4%). In conclusion, a delayed exposure to low dose endotoxin converts moderate gut I/R-induced lung dysfunction into advanced organ failure.