Lucas M L, Thom M M M, Bradley J M, O'Reilly N F, McIlvenny T J, Nelson Y B
Laboratory of Gastrointestinal Physiology, Division of Neuroscience & Biomedical Systems, Institute of Biological & Medical Science, Glasgow University, Glasgow, G12 8QQ, Scotland, Great Britain.
J Membr Biol. 2005 Jul;206(1):29-42. doi: 10.1007/s00232-005-0771-6.
Heat stable (STa) enterotoxin from E. coli reduced fluid absorption in vivo in the perfused jejunum of the anaesthetized rat in Krebs-phosphate buffer containing lactate and glucose (nutrient buffer), in glucose saline and in glucose free saline. Bicarbonate ion enhanced fluid absorption of 98 +/- 7 (6) microl/cm/h was very significantly (P < 0.0001) reduced by STa to 19 +/- 4 (6) microl/cm/h, but net secretion was not found. When impermeant MES substituted for bicarbonate ion, net fluid absorption of 29 +/- 3 (6) microl/cm/h was less (P < 0.01) than the values for phosphate buffer and bicarbonate buffer. With STa in MES buffer, fluid absorption of 3 +/- 2 (6) microl/cm/h was less than (P < 0.001) that in the absence of STa and not significantly different from zero net fluid absorption. E. coli STa did not cause net fluid secretion in vivo under any of the above circumstances. Neither bumetanide nor NPPB when co-perfused with STa restored the rate of fluid absorption. In experiments with zero sodium ion-containing perfusates, STa further reduced fluid absorption modestly by 20 microl/cm/h. Perfusion of ethyl-isopropyl-amiloride (EIPA) with STa in zero sodium ion buffers prevented the small increment in fluid entry into the lumen caused by STa, indicating that the STa effect was attributable to residual sodium ion and fluid uptake that zero sodium-ion perfusates did not eradicate. These experiments, using a technique that directly measures mass transport of fluid into and out of the in vivo proximal jejunum, do not support the concept that E. coli STa acts by stimulating a secretory response.
来自大肠杆菌的热稳定（STa）肠毒素，在含有乳酸盐和葡萄糖的 Krebs - 磷酸盐缓冲液（营养缓冲液）、葡萄糖盐水以及无葡萄糖盐水中，降低了麻醉大鼠灌流空肠的体内液体吸收。碳酸氢根离子可增强液体吸收，98±7（6）微升/厘米/小时，STa 使其显著降低（P<0.0001）至 19±4（6）微升/厘米/小时，但未发现净分泌。当用不可渗透的 MES 替代碳酸氢根离子时，29±3（6）微升/厘米/小时的净液体吸收低于（P<0.01）磷酸盐缓冲液和碳酸氢盐缓冲液的值。在 MES 缓冲液中加入 STa 时，3±2（6）微升/厘米/小时的液体吸收低于（P<0.001）无 STa 时的值，且与零净液体吸收无显著差异。在上述任何情况下，大肠杆菌 STa 在体内均未引起净液体分泌。与 STa 共同灌流时，布美他尼和 NPPB 均未恢复液体吸收速率。在含零钠离子的灌流液实验中，STa 使液体吸收进一步适度降低 20 微升/厘米/小时。在零钠离子缓冲液中，将乙基 - 异丙基 - 阿米洛利（EIPA）与 STa 一起灌流，可防止 STa 引起的管腔内液体进入的小幅增加，表明 STa 的作用归因于零钠离子灌流液未消除的残留钠离子和液体摄取。这些实验采用直接测量体内空肠近端液体进出质量转运的技术，不支持大肠杆菌 STa 通过刺激分泌反应起作用的概念。
