神経原性肺水腫における一酸化窒素(NO)の役割

一氧化氮（NO）在神经源性肺水肿中的作用

• 批准号: 11671491
• 负责人: 山下 明子
• 金额: $ 2.3万
• 依托单位: Nagoya University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671491/
• 关键词: 神経原性肺水腫; NOS

フィブリン肺水腫の発生にNOSが及ぼす影響について調べるために、まず、ラットの脳室内に生理食塩水、L-NAME、L-Arginineをあらかじめ投与し、迷走神経切断群と非切断群について、それぞれフィブリン肺水腫の発生率を調べた。結果は、L-NAME投与+迷走神経非切断群の14匹すべてが、Grade3の肺水腫となり、L-Arginine投与+迷走神経非切断群は、生理食塩水投与+迷走神経非切断群に比べ肺水腫の発生率に差はなかった。一方、生理食塩水投与+迷走神経切断群は、14匹すべてGrade2-3の肺水腫となり、L-NAME投与+迷走神経切断群およびL-Arginine投与+迷走神経切断群は、肺水腫発生率について、生理食塩水投与+迷走神経非切断群と差がなかった。また、肺水分量でみた場合、L-NAME投与+迷走神経非切断群で有意に肺水分量が増加し、L-Arginine投与は、生理食塩水投与+迷走神経切断群の肺水分量増加を有意に抑制した。以上の結果より脳室内へのL-NAME投与は、NOSを中枢で抑制し、肺水腫発生を増強させる効果があり、迷走神経が切断されるとこの効果がなくなることが明らかになった。次に、肺水腫ラットのFroth中の、NPY量を測定した。L-NAME投与+迷走神経非切断群で有意にFroth中NPYは減少し、L-Arginine投与+迷走神経切断群で有意にFroth中NPYは増加した。これらの結果より、中枢性にNOSを抑制した場合、迷走神経非切断群で、交感神経活動が抑制されることが示され、中枢性N0Sは、遠心性迷走神経作用が傷害されない状況において、神経原肺水腫発生に抑制的に作用していることが示唆された。

The impact of NOS and insulin on the development of pulmonary edema can be regulated. In addition, physiological water, L-NAME, and L-Arginine can be administered in the room, and the development rate of pulmonary edema can be regulated between the transected and non-transected groups of the brain. Results There were 14 differences in the incidence of pulmonary edema between L-NAME administration and + CPN, Grade 3 pulmonary edema, L-Arginine administration and + CPN, physiological water administration and + CPN. One side, physiological water administration and + mistrust nerve disconnection group, 14-level Grade 2 - 3 pulmonary edema, L-NAME administration and + mistrust nerve disconnection group, L-Arginine administration and + mistrust nerve disconnection group, pulmonary edema incidence rate, physiological water administration and + mistrust nerve disconnection group. L-NAME administration and L-arginine administration intentionally increased the lung water content in both groups. L-Arginine administration and L-Arginine administration intentionally inhibited the lung water content in both groups. The above results show that the L-NAME of the indoor brain is inhibited, NOS is inhibited, pulmonary edema is increased, and the effect of the brain is cut off. The amount of NPY in the middle of the lung edema was determined. NPY in Froth decreases when L-NAME is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth decreases when L-NAME is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and + NPY in Froth increases when L-Arginine is cast and + NPY in Froth decreases when L-Arginine is cast and NPY in Froth decreases when L-Arginine is cast and The result is that central NOS is inhibited, central NOS is not blocked, sympathetic nervous activity is inhibited, central NOS is inhibited, telecentric NOS is inhibited, and neurogenic pulmonary edema is inhibited.