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机构地区:[1]中国医学科学院基础医学研究所病理生理研究室,昆明医学院生理教研室
出 处:《基础医学与临床》1995年第1期40-44,共5页Basic and Clinical Medicine
摘 要:本文观察常压缺氧24h及1,2,4w(6h/d,6d/w)后大鼠血小板数及聚集率和血浆及肺TXB_2和6-keto-PGF_(1α)的动态变化。结果表明(1)缺氧大鼠血小板数呈先增加、后恢复、再下降,血小板聚集率呈先减少、后增加再减少的动态变化。(2)血浆TXB_2和6-keto-PGF_(1α)均明显升高,(3)肺组织6-keto-PGF_(1α)升高早于TXB_2,提示PGI_2参干旱期缺氧肺血管张力调节。(4)缺氧大鼠2周时肺动脉高压达到高峰,右心室明显肥厚,而肺组织TXB_2至缺氧4周后才见增加,表明TXB_2不是缺氧早期肺血管收缩的主要因素。e Stuied the changes of the platelet number and aggregation rate,the TXB_2and 6-keto-PGF_(1α) in plasma and lung in hyooxic pulmonary hypertension inrats.The results showed that platelet number increased after 24 h hypoxia:re-turned to the control level at 1 and 2 w,then decreased by 4 w of hypoxia.Theaggregation rate of the platelets decreased by 24 h of hypoxia, then increesedat 1 and 2 w but declined again after 4 w of hypoxia. The Plasma TXB_2 and 6-keto-PGF_(1α)both slgnificantly increased at all time obaerved.The ratio ofTXB_2/6-keto一PGF_(1α)higher all along than that of the control.However,thechanhges of TXB_2 and 6-keto PGF_(1α)in the lung were not the same as that ofthe plasma.6-keto-PGF_(1α)increased as early as in 1 w of hypoxia and kepthigher at 2 and 4w of hypoxia,while TXB_2 in the lung did not increase untilafter 4w of hypoxia.This result suggests that prostacyclin other than TXA_2 maypart icipate in the modulation of Pulmonary vascular tone during the early stageof the hypoxic hypertension,Since the animals developed the pulmonary hyperten-sion and the right ventricular hypertrophy as early as in 1 w of hypoxia whilethe TXA_2 in the lung tissue remained unchanged,it suggested that TXA_2 is notan unavoidable factor for the develpment of the hypoxic pulmonary hyperten-sion in rats.
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