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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The short-circuit current of the ileum, but not the colon, is altered in the streptozotocin diabetic rat.
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The short-circuit current of the ileum, but not the colon, is altered in the streptozotocin diabetic rat.

机译：回肠的短路电流，而不是结肠的短路电流，在链脲佐菌素糖尿病大鼠中改变。

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摘要

Ion transport in control and streptozotocin-diabetic rat colon and ileum was studied using the Ussing chamber technique. No differences were observed between control and diabetic colonic mucosal short-circuit current under either basal or carbachol (100 nmol/L-1 micromol/L)-stimulated or prostaglandin E2 (100 nmol/L-1 micromol/L)-stimulated conditions. Similarly to colonic tissues, no differences in the short circuit current in either carbachol-stimulated or prostaglandin E2-stimulated tissues were observed between control and diabetic ileal mucosa. The basal diabetic ileal short circuit current (99.58 +/- 22.67 microA) was significantly greater than that of control ileal tissues (29.67 +/- 4.45 microA). This difference was abolished by the sodium-glucose-cotransporter inhibitor, phloridzin (50 micromol/L) (118.00 +/- 28.09 microA vs. 25.60 +/- 4.59 microA) and was also prevented by the replacement of glucose with mannitol in the buffer bathing the apical side of the tissue (control: 17.05 +/- 5.85 microA vs. 17.90 +/- 3.10 microA). Acetazolamide (450 micromol/L; a carbonic anhydrase inhibitor), amiloride, and bumetanide (100 micromol/L each; Na+-channel blockers), piroxicam (50 micromol/L; a COX1 cyclooxygenase inhibitor), and ouabain (1 mmol/L; a K+ transport inhibitor) had no effect on the basal short circuit current of either control or diabetic ileal tissues. This indicated that the alteration in the basal short circuit current of diabetic ileal tissues was due to a change in cellular glucose transport, whereas the evoked changes in short circuit current were unaffected by the diabetic state.
机译：使用Ussing chamber技术研究了对照和链脲佐菌素-糖尿病大鼠结肠和回肠中的离子迁移。在基础或卡巴胆碱（100 nmol / L-1 micromol / L）刺激或前列腺素E2（100 nmol / L-1 micromol / L）刺激的条件下，对照组和糖尿病结肠黏膜短路电流均未观察到差异。与结肠组织相似，在对照组和糖尿病性回肠粘膜之间，未观察到卡巴胆碱刺激或前列腺素E2刺激的组织的短路电流差异。糖尿病基础回肠短路电流（99.58 +/- 22.67 microA）显着大于对照回肠组织的电流（29.67 +/- 4.45 microA）。钠-葡萄糖-共转运蛋白抑制剂Phloridzin（50 micromol / L）（118.00 +/- 28.09 microA对25.60 +/- 4.59 microA）消除了这种差异，并且通过在缓冲液中用甘露醇替代葡萄糖也可以防止这种差异沐浴组织的顶端（对照：17.05 +/- 5.85 microA对17.90 +/- 3.10 microA）。乙酰唑胺（450 micromol / L;碳酸酐酶抑制剂），阿米洛利和布美他尼（每种100 micromol / L; Na +通道阻滞剂），吡罗昔康（50 micromol / L; COX1环氧合酶抑制剂）和哇巴因（1 mmol / L） ; K +转运抑制剂）对对照或糖尿病回肠组织的基础短路电流没有影响。这表明糖尿病性回肠组织的基础短路电流的改变是由于细胞葡萄糖转运的变化引起的，而短路电流的诱发变化不受糖尿病状态的影响。

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