生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2002年
1期
38-42
,共5页
丁学琴%刘贵明%王俊科%盛卓人
丁學琴%劉貴明%王俊科%盛卓人
정학금%류귀명%왕준과%성탁인
一氧化碳%一氧化氮%血红素氧化酶抑制剂%血管舒张反应
一氧化碳%一氧化氮%血紅素氧化酶抑製劑%血管舒張反應
일양화탄%일양화담%혈홍소양화매억제제%혈관서장반응
carbon monoxide%nitric oxide%heme oxygenase inhibitor%vasodilation
本研究观察了一氧化碳(CO)对离体大鼠肺动脉的舒张作用.制备Wistar大鼠肺动脉环,作出ACh浓度效应曲线之后,肺动脉环用一氧化氮合成酶抑制剂L-NAME 30 μmol/L (n=10)或血红素氧化酶抑制剂ZnPPIX 10 μmol/L+L-NAME 30 μmol/L (n=10) 孵育30 min,再制备一个ACh的浓度效应曲线,观察ZnPPIX对ACh的浓度效应曲线的影响.另取一组肺动脉环,分为内皮完整组和去内皮组,观察外源性CO对肺动脉环张力的影响.结果表明,用 L-NAME孵育后,ACh的血管舒张反应受抑,最大抑制率为50.4±9.2%;用ZnPPIX+L-NAME孵育后,ACh的血管舒张反应进一步受抑,最大抑制率为84.4±11.2%.外源性CO无论对内皮完整组还是去内皮组肺动脉都有舒张作用.本研究提示,ZnPPIX可抑制ACh的内皮依赖性肺动脉舒张反应,CO是一个内皮源性的血管舒张因子,外源性CO可舒张肺动脉.
本研究觀察瞭一氧化碳(CO)對離體大鼠肺動脈的舒張作用.製備Wistar大鼠肺動脈環,作齣ACh濃度效應麯線之後,肺動脈環用一氧化氮閤成酶抑製劑L-NAME 30 μmol/L (n=10)或血紅素氧化酶抑製劑ZnPPIX 10 μmol/L+L-NAME 30 μmol/L (n=10) 孵育30 min,再製備一箇ACh的濃度效應麯線,觀察ZnPPIX對ACh的濃度效應麯線的影響.另取一組肺動脈環,分為內皮完整組和去內皮組,觀察外源性CO對肺動脈環張力的影響.結果錶明,用 L-NAME孵育後,ACh的血管舒張反應受抑,最大抑製率為50.4±9.2%;用ZnPPIX+L-NAME孵育後,ACh的血管舒張反應進一步受抑,最大抑製率為84.4±11.2%.外源性CO無論對內皮完整組還是去內皮組肺動脈都有舒張作用.本研究提示,ZnPPIX可抑製ACh的內皮依賴性肺動脈舒張反應,CO是一箇內皮源性的血管舒張因子,外源性CO可舒張肺動脈.
본연구관찰료일양화탄(CO)대리체대서폐동맥적서장작용.제비Wistar대서폐동맥배,작출ACh농도효응곡선지후,폐동맥배용일양화담합성매억제제L-NAME 30 μmol/L (n=10)혹혈홍소양화매억제제ZnPPIX 10 μmol/L+L-NAME 30 μmol/L (n=10) 부육30 min,재제비일개ACh적농도효응곡선,관찰ZnPPIX대ACh적농도효응곡선적영향.령취일조폐동맥배,분위내피완정조화거내피조,관찰외원성CO대폐동맥배장력적영향.결과표명,용 L-NAME부육후,ACh적혈관서장반응수억,최대억제솔위50.4±9.2%;용ZnPPIX+L-NAME부육후,ACh적혈관서장반응진일보수억,최대억제솔위84.4±11.2%.외원성CO무론대내피완정조환시거내피조폐동맥도유서장작용.본연구제시,ZnPPIX가억제ACh적내피의뢰성폐동맥서장반응,CO시일개내피원성적혈관서장인자,외원성CO가서장폐동맥.
The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 μmol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 μmol/L)+L-NAME (30 μmol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 μmol/L L-NAME, and attenuated further after pretreatment with 10 μmol/L ZnPPIX+30 μmol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.
