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肺泡低氧引起肺血管收缩的机制至今尚未完全阐明。前列环素(PGI_2)及血栓素A_2(TXA_2)对肺血管有强烈舒缩作用,两者的平衡对维持肺血管张力起重要作用。TXA_2主要来源于激活的血小板,而体外诱导血小板聚集性在一定程度上代表血小板活性。本文在常压10％低氧条件下,测定雄性Wistar大鼠缺氧后不同时间血浆和肺组织中TXB_2(TXA_2稳定代谢产物)及6-Keto-PGF_(1α)(PGI_2稳定代谢产物)的变化,以及血小板计数(PC)、体外诱导血小板聚集率(MAR)的变化,探讨上述指标与缺氧肺动脉高压的关系。
The mechanism by which alveolar hypoxia causes pulmonary vasoconstriction has not yet been fully elucidated. Prostacyclin (PGI_2) and thromboxane A_2 (TXA_2) have a strong systolic and diastolic effect on pulmonary arteries, and their balance plays an important role in the maintenance of pulmonary vascular tone. TXA 2 is mainly derived from activated platelets, while platelet aggregation induced in vitro, to a certain extent, represents platelet activity. In this paper, the changes of TXB_2 (TXA 2 stable metabolites) and 6-Keto-PGF_ (1α) (PGI_2 stable metabolites) in plasma and lung tissue of male Wistar rats at different time after hypoxia were measured under 10% , Platelet count (PC) and in vitro induced platelet aggregation rate (MAR), and to explore the relationship between these indexes and hypoxic pulmonary hypertension.