Singh G, Chaudry K I, Morrison M H, Chaudry I H
Department of Surgery, Michigan State University, East Lansing 48824.
Circ Shock. 1993 Apr;39(4):279-84.
Although recent studies have shown that gut absorptive function is significantly depressed even in the early hyperdynamic phase of sepsis, the mechanism responsible for this is unknown. Tumor necrosis factor (TNF-alpha) is a potent mediator of shock resulting in a marked inflammatory response leading to mucosal erosions of the gut and multiple organ failure. Although TNF is elevated in early sepsis, it remains unknown whether TNF plays any role in the depression of gut absorptive function under these conditions. To study this, we used the 1 hr D-xylose absorption test. C3H/HeN mice (n = 12) were lightly anesthetized, and a femoral artery and the portal vein were cannulated. After recovery from anesthesia, 125 micrograms recombinant murine TNF-alpha (rMuTNF-alpha)/kg body weight was given via the tail vein to one group of animals, while another group received an equivalent volume of saline (sham). One hour later, D-xylose was given orally. The systemic blood pressure was recorded 1 hr thereafter and D-xylose concentration in a sample of portal blood was determined colorimetrically. Results show that, while the systemic pressure was elevated 2 hr after administration of rMuTNF-alpha, D-xylose absorption was severely depressed. Thus the depressed gut absorptive function seen in the early stage of sepsis may be mediated directly or indirectly by TNF-alpha.
尽管最近的研究表明，即使在脓毒症的早期高动力阶段，肠道吸收功能也会显著降低，但其背后的机制尚不清楚。肿瘤坏死因子（TNF-α）是休克的一种强效介质，会引发明显的炎症反应，导致肠道黏膜糜烂和多器官功能衰竭。虽然在脓毒症早期TNF水平会升高，但在这些情况下TNF是否在肠道吸收功能降低中起任何作用仍不清楚。为了研究这一点，我们使用了1小时D-木糖吸收试验。将C3H/HeN小鼠（n = 12）轻度麻醉，插入股动脉和门静脉。麻醉恢复后，一组动物通过尾静脉给予125微克重组小鼠TNF-α（rMuTNF-α）/千克体重，而另一组接受等量的生理盐水（假手术组）。1小时后，口服D-木糖。此后1小时记录全身血压，并通过比色法测定门静脉血样本中的D-木糖浓度。结果表明，虽然给予rMuTNF-α后2小时全身血压升高，但D-木糖吸收严重降低。因此，脓毒症早期出现的肠道吸收功能降低可能直接或间接由TNF-α介导。
