低氧,山莨菪碱对肺内小动脉平滑肌细胞产生血栓素A2和前列环素的影响

本工作观察了急性重度低氧及山莨菪碱（anisodamine，Am）对分离培养家兔肺内小动脉平滑肌细胞（PASMCS）培养液中TXB2和6-酮-PGF1a含量及它们的比值的影响。结果是：重度低氧明显增加PASMCS培养液中TXB2和6-酮-PGF1a含量及它们的比值。常氧和低氧条件下，终浓度为2.5×10－5×mol／L的山莨菪碱显著降低TXB2的含量，但6-酮-PGF1a的含量无变化。这提示：急性重度低氧可能通过增加PASMCS产生和释放TXA2和PGI2及它们的比值而致肺血管收缩，山莨菪碱可能通过抑制PASMCs产生ThA2和降低ThB2与PGI2的比值逆转低氧所致的肺血管收缩效应。

EFFECTS OF HYPOXIA AND ANISODAMINE ON PRODUCTS OF TXA_2 and PGI_2 IN CULTURED INTRA-PULMONARY ARTERIOLAR SMOOTH MUSCLE CELLS

The changes of contents of TXB2 and 6-Keto-PGF1a were studied in severely acute hypoxic cultured intra-pulmonary aIteriolar 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 pulmonare vascular constriction through increased production of PASMCs and liheration of TXA2, or PGI2, and increased TXA2/PGI2 ratio. The latter effect of hypoxia could be prevented by anisodamine, which antagonized theeffect of hypoxia induced pulmonary vasoconstriction.