Hu D H, Liu H J, Ma C T
Laboratory of Cardiovascular Physiology, Hunan Medical University, Changsha.
Sheng Li Xue Bao. 1997 Dec;49(6):671-4.
The changes of contents of TXB2 and 6-Keto-PGF1a were studied in severely acute hypoxic cultured intra-pulmonary arteriolar smooth muscle cells (PASMCs) under the action of anisodamine. The results demonstrated that the contents of TXB2 and 6-Keto-PGF1a and their ratio were significantly increased in severe acute hypoxic PASMCs' medium. The content of TXB2 decreased significantly, but the content of 6-Keto-PGF1a was hardly affected by anisodamine under normoxia and hypoxia. These findings suggest that acute and severe hypoxia results in pulmonary vascular constriction through increased production of PASMCs and liberation of TXA2, or PGI2, and increased TXA2/PGI2 ratio. The latter effect of hypoxia could be prevented by anisodamine, which antagonized the effect of hypoxia induced pulmonary vasoconstriction.
研究了山莨菪碱作用下严重急性缺氧培养的肺小动脉平滑肌细胞(PASMCs)中血栓素B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1a)含量的变化。结果表明,严重急性缺氧PASMCs培养基中TXB2和6-Keto-PGF1a的含量及其比值显著升高。在常氧和缺氧条件下,山莨菪碱可使TXB2含量显著降低,但对6-Keto-PGF1a含量几乎无影响。这些结果提示,急性严重缺氧通过增加PASMCs生成及释放血栓素A2(TXA2)或前列环素(PGI2),以及升高TXA2/PGI2比值导致肺血管收缩。缺氧的后一种效应可被山莨菪碱阻断,山莨菪碱可拮抗缺氧诱导的肺血管收缩作用。