Rui L, Cai Y
Institute of Basic Medical Sciences, CAMS, Beijing.
Chin Med Sci J. 1991 Sep;6(3):145-7.
This experiment was designed to determine whether chronic hypoxia affects endothelium-dependent relaxation and cGMP content of rat pulmonary artery (PA). Both Ach and ATP were found to induce endothelium-dependent relaxation of PA; and this relaxation was not prevented by indomethacin, but was completely abolished by methylene blue. Chronic hypoxia significantly depressed the endothelium-dependent relaxation: the relaxation responses of intra-PA (IPA) and extra-PA (EPA) to 10(-6) mol/L Ach in the hypoxic group were 61.3% and 59.2% of those in control, and the relaxation responses of IPA and EPA to 1.8 x 10(-5) mol/L ATP in the hypoxic group were 64.9% and 55.2% of those in the control, respectively. Chronic hypoxia significantly decreased the basic level and Ach-induced accumulation of cGMP in the PA. Our data suggest that chronic hypoxia might depress rat pulmonary artery endothelium-dependent relaxation through the inhibition of cytosolic soluble guanylate cyclase in vascular smooth muscle cells.
本实验旨在确定慢性缺氧是否会影响大鼠肺动脉(PA)的内皮依赖性舒张以及环磷酸鸟苷(cGMP)含量。发现乙酰胆碱(Ach)和三磷酸腺苷(ATP)均可诱导PA的内皮依赖性舒张;且这种舒张不受吲哚美辛的抑制,但可被亚甲蓝完全消除。慢性缺氧显著抑制内皮依赖性舒张:缺氧组肺动脉内(IPA)和肺动脉外(EPA)对10⁻⁶mol/L Ach的舒张反应分别为对照组的61.3%和59.2%,缺氧组IPA和EPA对1.8×10⁻⁵mol/L ATP的舒张反应分别为对照组的64.9%和55.2%。慢性缺氧显著降低PA中cGMP的基础水平以及Ach诱导的cGMP积累。我们的数据表明,慢性缺氧可能通过抑制血管平滑肌细胞中的胞质可溶性鸟苷酸环化酶来抑制大鼠肺动脉内皮依赖性舒张。