Su Y C, Wang D X
Department of Pathophysiology, Tongji Medical University, Wuhan.
J Tongji Med Univ. 1993;13(2):88-92. doi: 10.1007/BF02887922.
The effect of hypoxia on the production and release of vasoactive substances from endothelial cells of pulmonary artery (PAECs) and aorta (AECs) was studied. The results indicated that the overall effect of the long half-life vasoactive substances released from PAECs and AECs was vasoconstrictive. The long half-life lipid-soluble substances produced by PAECs and AECs were vasodilative, and did not change in hypoxia. However, the long half-life water-soluble heat-unstable and heat-stable ones were vasoconstrictive. Hypoxia could reduce the release of the former and promote that of the latter which might be peptides. The PAECs could release specific long half-life mediator which was pulmonary artery-constrictive, water-soluble, heat-unstable, and not related to hypoxia. Hypoxia inhibited the production of PGI2, a short half-life vasodilator, in PAECs, but not in AECs.
研究了缺氧对肺动脉内皮细胞(PAECs)和主动脉内皮细胞(AECs)血管活性物质产生和释放的影响。结果表明,PAECs和AECs释放的长半衰期血管活性物质的总体作用是血管收缩。PAECs和AECs产生的长半衰期脂溶性物质具有血管舒张作用,且在缺氧状态下无变化。然而,长半衰期水溶性热不稳定和热稳定物质具有血管收缩作用。缺氧可减少前者的释放并促进后者(可能是肽类)的释放。PAECs可释放特定的长半衰期介质,该介质具有肺动脉收缩作用、水溶性、热不稳定且与缺氧无关。缺氧抑制PAECs中半衰期较短的血管舒张剂前列环素(PGI2)的产生,但不抑制AECs中PGI2的产生。