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一氧化氮调节回肠中的水和电解质转运。

Nitric oxide modulates water and electrolyte transport in the ileum.

作者信息

Barry M K, Aloisi J D, Pickering S P, Yeo C J

机构信息

Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.

出版信息

Ann Surg. 1994 Apr;219(4):382-8. doi: 10.1097/00000658-199404000-00009.

Abstract

OBJECTIVE

To test the hypothesis that nitric oxide is a modulator of ileal water and ion transport.

SUMMARY BACKGROUND DATA

Nitric oxide is produced in the vascular endothelium and enteric neural plexuses of the intestine and is involved in gastrointestinal motility and smooth muscle contractility. Little is known about the role of nitric oxide in intestinal epithelial transport.

METHODS

Ten-centimeter rabbit ileal segments (n = 50) were vascularly perfused with an electrolyte solution containing red cells. The lumen was perfused with a solution containing 14C-PEG. Net fluxes of water and ions were calculated during three 20-minute periods: basal, drug infusion, and recovery. Perfusion pressure was recorded to document changes in vascular resistance. Agents infused included the nitric oxide synthase substrate L-arginine, the nitric oxide source sodium nitroprusside, the substrate control D-arginine, and the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester.

RESULTS

L-arginine and sodium nitroprusside caused absorption of water and ions. NG-nitro-L-arginine methyl ester caused secretion of water and ions, which was prevented by synchronous infusion of L-arginine. Infusion of D-arginine had no effect. Both L-arginine and sodium nitroprusside caused mild vasodilation.

CONCLUSIONS

Inhibition of endogenous nitric oxide synthesis by NG-nitro-L-arginine methyl ester causes secretion of water and ions. This secretion is reversed by administration of the nitric oxide synthase substrate L-arginine. These findings are consistent with the hypothesis that endogenous nitric oxide has a proabsorptive influence over the ileum in the basal state.

摘要

目的

验证一氧化氮是回肠水和离子转运调节因子这一假说。

总结背景资料

一氧化氮在血管内皮和肠道的肠神经丛中产生,参与胃肠蠕动和平滑肌收缩。一氧化氮在肠上皮转运中的作用鲜为人知。

方法

用含红细胞的电解质溶液对50段10厘米长的兔回肠段进行血管灌注。肠腔用含14C - 聚乙二醇的溶液灌注。在三个20分钟时间段计算水和离子的净通量:基础期、药物输注期和恢复期。记录灌注压力以记录血管阻力变化。输注的药物包括一氧化氮合酶底物L - 精氨酸、一氧化氮供体硝普钠、底物对照D - 精氨酸和一氧化氮合酶抑制剂NG - 硝基 - L - 精氨酸甲酯。

结果

L - 精氨酸和硝普钠引起水和离子的吸收。NG - 硝基 - L - 精氨酸甲酯引起水和离子的分泌,同时输注L - 精氨酸可阻止这种分泌。输注D - 精氨酸无作用。L - 精氨酸和硝普钠均引起轻度血管舒张。

结论

NG - 硝基 - L - 精氨酸甲酯抑制内源性一氧化氮合成导致水和离子分泌。给予一氧化氮合酶底物L - 精氨酸可逆转这种分泌。这些发现与内源性一氧化氮在基础状态下对回肠有促吸收作用的假说一致。

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