抽象
慢性缺氧最近已显示上调大鼠肺诱导型一氧化氮合酶(iNOS)基因的表达。在本研究中,我们提出质疑NO合成的诱导是否可以改变来自慢性低氧(CH)大鼠肺动脉(PA)的反应性。剂量 - 响应曲线,以苯肾上腺素(PE)10(-9),以5×10(-6)M)在PA检查环以及响应于L-精氨酸类似物,之后从CH或含氧量正常(N)大鼠分离的肺培养不同时间。虽然最大收缩到PE没有在PA从比较到N大鼠在时间0(361 +/- 53 506 VS +/- 52毫克,分别)CH大鼠不同,它被显着延长温育(149 +/- 28后下降VS 386 +/- 47毫克,分别在4小时; p <0.001)。这种现象持续内皮剥蚀后,但由N G - 甲基-L-精氨酸(L-NMMA)(5×10(-4)M)反转,由放线菌素d防止(2×10(-6)M)。与此相反,最大收缩到PE中从CH大鼠主动脉是在时间0和4小时相似。一个短的温育,PA收缩到L-NMMA后比在N-大鼠更大CH(96 +/- 17 33 VS +/- 9毫克,在90分钟; P <0.05),被内皮剥脱后废除,但在持续CH大鼠卡米达佐的存在下(5×10(-4)M)。 At 4 h, contraction to L-NMMA was abolished in endothelium-denuded PA from N rats but only attenuated in those from CH rats. In salt solution perfused lungs, L-NMMA added 30 or 90 min after isolation did not alter baseline pressure in N rats but caused its increase in CH rats. Whereas iNOS messenger ribonucleic acid (mRNA) was detectable by reverse-transcriptase polymerase chain reaction in the PA wall of N or CH rats after 4 h of incubation, it was absent in both at the time of isolation. In contrast, there was evidence of iNOS mRNA in lungs from CH rats at the time of isolation but no signal in those from N rats. In conclusion, there is induction of nitric oxide synthase activity in pulmonary arteries from normoxic and chronically hypoxic rats after prolonged incubation, but this effect is more pronounced in pulmonary arteries from chronically hypoxic rats.