一氧化碳对大鼠离体肺动脉的舒张作用

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 3 0 μmol/L (n =10 )或血红素氧化酶抑制剂ZnPPIX 10μmol/L +L NAME 3 0 μmol/L (n =10 )孵育 3 0min ,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 5 0 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

Vasodilative action of carbon monoxide on rat pulmonary artery in vitro

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 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/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 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/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.