Herman C M, Kraft A R, Smith K R, Artnak E J, Chisholm F C, Dickson L G, McKee A E, Homer L D, Levin J
Ann Surg. 1974 Jun;179(6):910-6. doi: 10.1097/00000658-197406000-00016.
Experiments were carried out to test the hypothesis that during hemorrhagic shock endotoxin enters the circulation from ischemic bowel by way of the portal venous system and is then associated with irreversibility of the hemorrhagic shock state. After placement of sampling catheters in the portal vein, right atrium, and aorta, 14 awake, restrained baboons were subjected to 1 hour of hemorrhagic shock at a mean arterial pressure (MAP) of 60 torr followed by a second hour at 40 torr MAP. Six animals were resuscitated with Ringers lactate and their shed blood; 8 were maintained hypotensive until death. Serial blood samples were analyzed for the presence of endotoxin. Endotoxemia was found infrequently, with no greater incidence (p > 0.6) in portal venous samples than in systemic blood, so these data were pooled for further analysis. Furthermore, endotoxemia was no more frequent (p > 0.6) late in shock than it was in early shock or during the baseline period. Autopsy showed no evidence of ischemic damage to the splanchnic viscera. It was concluded that spontaneous endogenous entotoxemia is not a common feature of hemorrhagic shock in baboons and is not related to the duration or degree of severity of hemorrhagic shock in this subhuman primate species.
在失血性休克期间,内毒素通过门静脉系统从缺血肠进入循环,然后与失血性休克状态的不可逆性相关。在门静脉、右心房和主动脉中放置采样导管后,对14只清醒、受限的狒狒进行了1小时平均动脉压(MAP)为60托的失血性休克,随后第二小时MAP为40托。6只动物用乳酸林格氏液和它们流失的血液进行复苏;8只动物维持低血压直至死亡。对系列血样进行内毒素检测。内毒素血症很少被发现,门静脉血样中的发生率并不高于全身血液(p>0.6),因此将这些数据合并进行进一步分析。此外,休克后期内毒素血症的发生率并不比休克早期或基线期更高(p>0.6)。尸检未发现内脏缺血损伤的证据。得出的结论是,自发性内源性内毒素血症不是狒狒失血性休克的常见特征,并且与该灵长类动物物种失血性休克的持续时间或严重程度无关。