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机构地区:[1]深圳市红十字会医院检验科和内科
出 处:《标记免疫分析与临床》1994年第3期137-140,共4页Labeled Immunoassays and Clinical Medicine
摘 要:为了探讨慢性阻塞性肺病(COPD)患者血栓素A_2(TXA_2)和前列环素(PGI_2)与肺动脉高压的关系,我们对伴有和不伴有肺动脉高压的30例缓解期COPD患者血浆中血栓素B_2(TXB_2)及6-酮-前列腺素F_(1α)(6-keto-PGF_(1α))的含量变化进行了观察,还对7例伴肺动脉高压的COPD患者不同病期的肺动脉平均压(PaP)、血浆TXB_2及6-keto-PGF_(1α).水平作了对比分析。结果发现,缓解期COPD患者中,伴肺动脉高压者血浆TXB_2明显增高,6-keto-PGF_(1α)显著下降,TXB_2/6-keto-PGF_(1α)明显增大,与不伴肺动脉高压者比较,差异非常显著(P均<0.01),而不伴肺动脉高压者的这些指标与正常人的比较,则无统计学意义(P均>0.05);与急性期比较,COPD患者缓解期PaP明显下降,TXB_2亦显著降低,6-keto-PGF_(1α)明显升高,TXB_2/6-keto-PGF_(1α)缩小(P均<0.01);相关分析发现,伴肺动脉高压者PaP与TXB_2呈明显正相关,与6-keto-PGF_(1α)呈负相关(n=28,r=+0.46、-0.39,P均<0.05)To investigate the changes of Thromboxane A2 (TXA2) and Prostacyclin (PGI2) and their relation with pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD),the mean pulmonary arterial pressure (PaP) and plasma level of Thromboxane B2 and 6-keto-PGF1α were simultaneously measured in 30 remission COPD patients with or without pulmonary hypertension and 19 normal subjects.Meanwhile, PaP, plasma level of TXB2 and 6-keto-PGF1α in different stages of COPD were compared in 7 COPD patients with pulmonary hypertension. Results showed that plasma level of TXB2 was significantly increased, that of 6-keto-PGF1α was markedly decreased,and TXB2/6-keto-PGF1α ratio was greatly elevated in remission COPD patients with pulmonary hypertension as compared with those without pulmonary hypertension (P<0.01). There was no difference in plasma level of TXB2 and 6-keto-PGF1α and TXB2/6-keto-PGF1αratio between normal subjects and remission COPD patients without pulmonary hypertension (P>0.05).In remission stage of 7 COPD patients with pulmonary hypertension, PaP was markedly decreased,plasma level of TXB was also considerably reduced, that of 6-keto-PGF1α was increased and TXB2/6-keto-PGF1αratio was apparently decreased in comparison with those of exacerbation stage (P<0.01). PaP was positively correlated with plasma level of TXB2 and inversely with that of 6-keto-PGF1αin COPD patients with pulmonary hypertension (n=28,r=+0.46 and-0.39,P<0.05). These findings suggest that the imbalance between TXA2 and PGI2 plays an important role in the development of pulmonary hypertension in COPD patients.
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