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

从尸体解剖材料中分离培养人肺动脉平滑肌细胞（HPASMC），检测一氧化氮（NO）对HPASMC生成PG12的影响，并检测IL-6对HPASMC生成NO的影响，以阐明HPASMC生成NO与proslaglandins的关系。il -1 β和TNF_2增强了HPASMC的NO生成。2)LPS和il -1 β处理的HPASMC对PGI_2生成的促进作用在LPS或il -1 β联合硝普钠处理的HPASMC中进一步增强。3) LPS或il -1 - β联合L-NMMA处理HPASMC时，LPS和il -1 - β对PGI_2生成的促进作用减弱。4)亚甲基蓝（MeB）抑制了HPASMC对PGI_2的生成，并减弱了LPS和il -1 β处理的HPASMC对PGI_2生成的增强作用。5)虽然IL-6没有改变HPASMC的基础NO生成，但它减弱了LPS或il -1 β处理的HPASMC增强的NO生成。6)LPS、il -1 β、TNF_2和SNP均未增加HPASMC的LDH释放量。这些实验结果表明：(1)NO能促进人肺动脉平滑肌细胞PGI_2的生成。(2)IL-6不仅抑制人肺动脉平滑肌细胞分泌前列腺素，而且抑制NO分泌。这一结果显示了IL-6在体内的抗炎作用。(3)肺动脉平滑肌可通过NO与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。需要进一步的检查来阐明。通过对COX-2和iNOS蛋白和基因的诱导，研究NO介导的PGl_2生成增强和il -6介导的NO生成抑制的机制。

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.