Endoh K, Kao J, Domek M J, Leung F W
Research and Medical Services, Sepulveda Veterans Administration Medical Center, California.
Gastroenterology. 1993 Jan;104(1):114-21. doi: 10.1016/0016-5085(93)90842-z.
Intragastric hypertonic (2 mol/L) saline produces injury in the gastric mucosa and a significant increase in gastric blood flow (hyperemia) in anesthetized rats. We studied the mechanism of this hyperemia.
Rats were treated with intravenous boluses of NG-nitro-L-arginine methyl ester (3 mg/kg) to block synthesis of endogenous nitric oxide, pyrilamine (1 mg/kg) to inhibit H1 receptors, or indomethacin (5 mg/kg) to block synthesis of endogenous prostaglandins during blood flow studies or with subcutaneous capsaicin (125 mg/kg) 10-14 days before blood flow studies to ablate capsaicin-sensitive afferent nerves. Gastric mucosal blood flow was measured by hydrogen gas clearance before and during intragastric administration of 2 mol/L saline.
The gastric hyperemia induced by intragastric 2 mol/L saline was completely blocked only by indomethacin. The associated gastric mucosal damage was increased significantly.
In the rat stomach, the gastric hyperemia induced by intragastric 2 mol/L saline is mediated by endogenous prostaglandins and plays a protective role. Endogenous nitric oxide, H1 receptors, and capsaicin-sensitive afferent nerves are not involved in this protective hyperemia.
胃内高渗（2摩尔/升）盐水可导致麻醉大鼠胃黏膜损伤，并使胃血流量显著增加（充血）。我们研究了这种充血的机制。
在血流量研究期间，给大鼠静脉注射大剂量NG-硝基-L-精氨酸甲酯（3毫克/千克）以阻断内源性一氧化氮的合成，注射吡拉明（1毫克/千克）以抑制H1受体，或注射吲哚美辛（5毫克/千克）以阻断内源性前列腺素的合成；或者在血流量研究前10 - 14天给大鼠皮下注射辣椒素（125毫克/千克）以消除辣椒素敏感传入神经。在胃内给予2摩尔/升盐水之前和期间，通过氢气清除法测量胃黏膜血流量。
胃内2摩尔/升盐水诱导的胃充血仅被吲哚美辛完全阻断。相关的胃黏膜损伤显著增加。
在大鼠胃中，胃内2摩尔/升盐水诱导的胃充血由内源性前列腺素介导，并起保护作用。内源性一氧化氮、H1受体和辣椒素敏感传入神经不参与这种保护性充血。
