Gaffin S L, Gathiram P, Wells M T, Brock-Utne J G
Crit Care Med. 1986 Oct;14(10):889-91. doi: 10.1097/00003246-198610000-00012.
Ischemia of the intestines damages the permeability of the intestinal wall, allowing lipopolysaccharide (LPS) (endotoxin) to leak from the gut lumen into the blood circulation, causing shock and death. We measured LPS levels associated with corticosteroid treatment vs. no treatment in cats whose superior mesenteric artery had been occluded for 60 min. In untreated cats, the preocclusion mean plasma LPS concentration remained stable at 0.069 +/- 0.015 ng/ml. Toward the end of the occlusion period, mean plasma LPS rose to 0.239 +/- 0.032 ng/ml (p less than .01). Release of the clamp and reperfusion with oxygenated blood was followed within 20 min by a large rise in plasma LPS concentration to 0.825 +/- 0.11 ng/ml (p less than .01), which had returned to preocclusion levels about 80 min later. Methylprednisolone (30 mg/kg) was infused into a second group of cats 1.5 h before SMA occlusion. In these cats there was a complete inhibition of the LPS rise both during and after occlusion. These data suggest that the reported beneficial effect of corticosteroids in the treatment of septic shock may be mediated, in part, by reducing LPS leakage from the gut.
肠道缺血会损害肠壁的通透性，使脂多糖（LPS）（内毒素）从肠腔漏入血液循环，导致休克和死亡。我们测量了肠系膜上动脉闭塞60分钟的猫在接受皮质类固醇治疗与未治疗情况下的LPS水平。在未治疗的猫中，闭塞前血浆LPS平均浓度稳定在0.069±0.015 ng/ml。在闭塞期快结束时，血浆LPS平均浓度升至0.239±0.032 ng/ml（p<0.01）。松开血管夹并用含氧血液进行再灌注后20分钟内，血浆LPS浓度大幅升至0.825±0.11 ng/ml（p<0.01），约80分钟后又恢复到闭塞前水平。在第二组猫中，在肠系膜上动脉闭塞前1.5小时注入甲泼尼龙（30 mg/kg）。在这些猫中，闭塞期间及之后LPS的升高均被完全抑制。这些数据表明，皮质类固醇在治疗感染性休克方面所报道的有益作用可能部分是通过减少肠道LPS泄漏来介导的。
