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本文报道30只急性心梗大鼠心梗24小时血 TXB_2、6-K-PGF_(1α)、PRA 和 AT Ⅱ水平,以20只大鼠作对照。同时测定心梗大鼠梗塞前后24小时尿 TXB_2、6-K-PGF_(1α)浓度改变。其结果:心梗大鼠血 TXB_2、6-K-PGF_(1α)浓度较对照组明显升高(P<0.01)。心梗后24小时尿 TXB_2、6-K-PGF_(1α)及其肌肝矫正值较心梗前24小时显著升高(P<0.01),提示 TXA_2、PGI_2参与急性心梗的病理过程。相关分析未见血、尿 TXB_2、6-K-PGF_(1α)及其比值与大鼠尸检梗塞范围有相关性(P>0.05)。但发现心梗组血 PRA、AT Ⅱ较对照组显著升高(P<0.01)。
This article reports the levels of TXB_2, 6-K-PGF_ (1α), PRA and AT Ⅱ in 24 hours of myocardial infarction in 30 acute myocardial infarction rats. Twenty rats were used as control. The concentration of TXB_2, 6-K-PGF_ (1α) in 24 hours before and after infarction in MI rats was also measured. Results: The concentration of TXB_2, 6-K-PGF_ (1α) in myocardial infarction rats was significantly higher than that in control group (P <0.01). TXB_2, 6-K-PGF_ (1α) and their myo-liver corrections 24 hours after myocardial infarction were significantly higher than those of 24 hours before myocardial infarction (P <0.01), suggesting that TXA_2 and PGI_2 are involved in the pathogenesis of acute myocardial infarction. There was no correlation between blood TXB_2, 6-K-PGF_ (1α) and the ratio of urine and autopsy infarct extent (P> 0.05). However, it was found that the levels of PRA and AT Ⅱ in myocardial infarction group were significantly higher than those in control group (P <0.01).