脂肪乳剂诱导的胃松弛是通过一氧化氮介导的。

Intralipid-induced gastric relaxation is mediated via NO.

作者信息

Meulemans A, Schuurkes J

机构信息

Department of Gastrointestinal Pharmacology, Janssen Research Foundation, Beerse, Belgium.

出版信息

Neurogastroenterol Motil. 1995 Sep;7(3):151-5. doi: 10.1111/j.1365-2982.1995.tb00220.x.

DOI:10.1111/j.1365-2982.1995.tb00220.x

PMID:8536159

Abstract

UNLABELLED

In vitro, nitric oxide (NO) has been shown to be the neurotransmitter responsible for gastric relaxation. In vivo gastric relaxations can be controlled via reflex pathways originating in the duodenum. The aim of this study was to determine whether NO was involved in gastric relaxation in vivo in conscious dogs induced by intraduodenal administration of intralipid. Gastric tone was monitored with a flaccid bag introduced into the stomach via a gastric cannula and connected to a barostat. Intralipid administration into the duodenum caused a gastric relaxation (420 +/- 11 ml, n = 6) sensitive to inhibition by nitro-L-arginine (L-NNA) (5 mg kg-1 i.v.). This inhibitory effect of L-NNA was reversed by L-arginine (100 mg kg-1 i.v.).

IN CONCLUSION

intraduodenal administration of intralipid induces a gastric relaxation via a NO-dependent mechanism.

摘要

未标记

在体外实验中，一氧化氮（NO）已被证明是负责胃舒张的神经递质。在体内，胃舒张可通过起源于十二指肠的反射途径进行控制。本研究的目的是确定在清醒犬体内，十二指肠内给予脂肪乳剂诱导的胃舒张是否涉及NO。通过经胃插管将松弛袋引入胃内并连接至压力调节器来监测胃张力。向十二指肠内注射脂肪乳剂可引起胃舒张（420±11 ml，n = 6），该舒张对硝基-L-精氨酸（L-NNA）（5 mg kg-1静脉注射）的抑制敏感。L-精氨酸（100 mg kg-1静脉注射）可逆转L-NNA的这种抑制作用。