摘要
目的 观察低浓度一氧化碳 (CO)对大鼠肺动脉平滑肌细胞 (PASMC)的作用。方法 应用细胞培养 ,Lowry法测量蛋白质含量 ,Fura 2荧光指示剂测PASMC的胞内钙浓度 ([Ca2 + ] ) ,放射免疫cAMP、cGMP药盒测cAMP、cGMP浓度。结果 ①缺氧组PASMC内质网扩张 ,胞浆内出现髓鞘样结构 ,线粒体肿胀、空泡化。低浓度CO组PASMC的损害减轻、仅线粒体稍肿大 ,部分内质网有扩张。②缺氧组PASMC[Ca2 + ]明显升高 (P <0 .0 1) ,低浓度CO组PASMC[Ca2 + ]接近常氧组。③缺氧组PASMC的cAMP均有升高趋势 ,cAMP先降后升 ,cGMP缓慢升高。低浓度CO组PASMC的cGMP虽比常氧组有所升高 ,但无明显差异 (P >0 .0 5 )。缺氧及复合CO作用下cAMP均呈上升趋势 ,和常氧组比差异显著 (P <0 .0 1)。结论 缺氧可能通过第二信使系统促进PASMC的增生 ,而低浓度CO可以抑制缺氧的作用 ,至少部分可能是通过 [Ca2 + ]
Objective To study the effects of carbon monoxide (CO) on pulmonary arterial smooth muscle cells (PASMCs) of rats in vitro . Methods The PASMCs of rats were cultured in hypoxia, combined hypoxia and CO and in normal O 2 condition. Protein content was measured with Lowry′s method, intracellular [Ca 2+ ] with Fura 2 fluorescent marker and the level of cAMP and cGMP with radioimmunoassay. Results In the PASMCs of the hypoxia group, there were dilatation of endoplasmic reticulum, swelling of mitochondria, myelin figures in the cells and vacuolization. When PASMCs were exposed to hypoxia and low concentration of CO, the damages were ameliorated showing only mild swelling of mitochondria and partial dilatation of endoplasmic reticulum.Intracellular [Ca 2+ ] was significantly elevated in the PASMCs of the hypoxia group but was nearly normal in cells exposed to hypoxia and low cencentration of CO. The changes of cAMP and cGMP were different in the hypoxia group, cAMP showed a decrease in the beginning and increased later but cGMP kept on increasing gradually. After exposure to hypoxia and CO, cGMP showed a little increase but its level was not significantly different from the normal (P> 0.05); cAMP was markedly increased as compared with the normal (P>0.05). Conclusion Hypoxia can promote the proliferation of PASMCs through the second messenger system and CO in low concentration antagonizes the action of hypoxia partly through the mediation of [Ca 2+ ] cGMP system.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2000年第5期417-419,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目!(39700057)
