Zanotti A M, Gaffin S L
J Surg Res. 1985 Feb;38(2):113-5. doi: 10.1016/0022-4804(85)90015-0.
Occlusion of the superior mesenteric artery (SMA) is known to produce lethal shock in experimental animals, probably due to the presence of endotoxins released from the gut. A 60-min SMA occlusion shock was produced in 20 rabbits. Eight were pretreated with equine antilipopolysaccharide (anti-LPS) hyperimmune plasma, and seven survived (87.5%) for 10 days. However, only 2 out of 12 (16.6% chi 2 = 9.73, P less than 0.001) control rabbits survived. These results support the concept that endotoxins are involved in the etiology of SMA occlusion shock and that anti-LPS therapy may therefore be useful in the prevention of endotoxic shock.
已知肠系膜上动脉（SMA）闭塞会在实验动物中引发致命性休克，这可能是由于肠道释放的内毒素所致。对20只兔子造成了60分钟的SMA闭塞性休克。其中8只预先接受了马抗脂多糖（抗LPS）超免疫血浆治疗，7只存活（87.5%）达10天。然而，12只对照兔子中只有2只存活（16.6%，卡方 = 9.73，P < 0.001）。这些结果支持了内毒素参与SMA闭塞性休克病因的观点，因此抗LPS治疗可能有助于预防内毒素性休克。
