PLATELET-ACTIVATING-FACTOR - AN ENDOGENOUS MEDIATOR FOR BOWEL NECROSIS IN ENDOTOXEMIA
PLATELET-ACTIVATING-FACTOR - AN ENDOGENOUS MEDIATOR FOR BOWEL NECROSIS IN ENDOTOXEMIA
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DOI：
10.1096/fasebj.1.5.3678700
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发表时间：
1987-11-01
期刊：
影响因子：
4.8
通讯作者：
ARROYAVE, JL
中科院分区：
文献类型：
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作者：
HSUEH, W;GONZALEZCRUSSI, F;ARROYAVE, JL
我们通过注射血小板活化因子（PAF）或PAF联合细菌内毒素建立了大鼠缺血性肠坏死模型。PAF引起严重的低血压，并且已经表明它在内毒素休克期间被释放。由于缺血性肠坏死常与休克或感染有关，因此PAF可能是脓毒症时引起休克和肠坏死的内源性药物。本研究证实：（1）正常小肠内含有少量PAF;（2）内毒素可引起小肠坏死;（3）内毒素可使动物肠内PAF生成明显增加;（4）PAF拮抗剂预处理可防止内毒素引起的肠坏死; 5）离体缓冲液灌注小肠对内毒素注射产生少量PAF。因此，我们认为PAF可能是内毒素血症的内源性介质，而内毒素血症导致肠坏死和休克。
We have developed a model of isochemic bowel necrosis in the rat by injecting platelet-activating factor (PAF) or PAF in combinaiton with bacterial endotoxin. PAF causes profound hypotension, and it has been suggested that it is released during endotoxin shock. Because ischemic bowel necrosis is often associated with shock or infection, it is possible that PAF is the endogenous medicator that causes shock and bowel necrosis during sepsis. In this study, we have demonstratd that: 1) normal intestine contained a small amount of PAF; 2) necrotic lesions of the intestine could be induced by endotoxin injection; 3) PAF production in the bowel is markedly increased in animals treated with endotoxin; 4) pretreatment of the animal with PAF antagonists prevent endotoxin-induced necrosis; 5) isolated, buffer-perfused small intestine produced a small quantity of PAF in response to endotoxin injection. Therefore, we conclude that PAF is likely endogenous mediator in endotoxemia, which causes bowel necrosis and shock.