The role of nitric oxide in PGI_2 production by human pulmonary artery smooth muscle cells

从尸检材料中分离培养人肺平滑肌细胞(HPASMC)，观察一氧化氮(NO)对HPASMC产生PG12的影响，以及IL-6对HPASMC产生NO的影响，以阐明HPASMC产生NO与前列腺素的关系。IL-1β和肿瘤坏死因子_2促进HPASMC产生NO的作用2)内毒素或IL-1β联合硝普钠处理HPASMC对PGI_2的促进作用进一步增强。3)当LPS或IL-1β与L-NMA共同作用时，HPASMC对PGI_2的促进作用减弱。4)亚甲蓝(Meb)抑制HPASMC产生PGI_2。5)虽然IL-6不改变HPASMC产生NO的基础水平，但它减弱了LPS或IL-1β对HPASMC产生NO的促进作用。上述实验结果提示：(1)NO可促进人肺血管平滑肌细胞产生PGI_2，IL-6不仅抑制前列腺素S的产生，而且对人肺动脉平滑肌细胞产生NO也有抑制作用。这一结果显示了IL-6在体内的抗炎作用。(3)肺血管平滑肌可通过NO和前列腺素的相互作用，积极参与肺血流和肺动脉张力的调节，其机制有待进一步研究。通过检测COX-2和iNOS蛋白和基因的诱导，探讨NO促进PGL_2和IL-6抑制NO产生的机制。

Human pulmonary arlcry smooth musclc cclls(HPASMC) were isolated and culfured from autopsy materials, and the effect of nitric oxide(NO) on PG12 production by HPASMC was examined and the effect of IL-6 on NO production by HPASMC was also examined to elucidate the relationship of the production of NO and proslaglandins by H PASMC.1)LPS, IL-1beta and TNF_2 enhanced the production of NO by HPASMC.2)The enlhanced production of PGI_2 by LPS-and IL-1beta-treated HPASMC was further augmenter when HPASMC were treated with LPS or IL-1beta together with sodium nitroprusside.3)The enhanced production of PGI_2 by LPS- and IL-1beta-treated HPASMC was attenuated when HPASMC were treated with LPS or IL-1beta together with L-NMMA.4)Methylene blue(MeB) suppressed PGI_2 production by HPASM C, and attenuated the enhanced production of PGI_2 by HPASMC treated with LPS or IL-1beta.5)Although IL-6 did not changed the basal production of NO by HPASMC, it attenuated the enhanced production of NO by HPASMC treated with LPS or IL-1beta.6)LPS, IL-1beta, TNF_2 and SNP up to the maximum concentrations used in these experiments did not increase thc LDH release from HPASMC treated with these agents.From these experimental lindings it is suggested that(1)NO enhances PGI_2 production by human pulmonary arlery smooth muscle cells.(2)IL-6 suppresses not only the production of prostagland ins but NO by human pulmonary artery smooth muscle cells. this result could show antiinllammatory aspect of IL-6 in vivo.(3)Pulmonary artery smooth lb muscles could actively participate in the regulation of pumonary blood flow and tonus of pulmonary artery by the interaction of NO and prostaglandins.Further examinations are needed to elucidate the. mechanisms of NO-mediated enhancement of PGl_2 production and IL-6-mediated suppression of NO production by examining the induction of COX-2 and iNOS proteins and genes.