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本文观察了大鼠感染性休克和内毒素性休克时血浆6-酮-PGF_1α和TXB_2的动态变化。通过结扎盲肠加穿孔造成大鼠细菌性腹膜炎,随之产生感染性休克。静脉注射大肠杆菌内毒素使大鼠产生内毒素休克。在这两种休克模型中,血浆6-酮-PGF_(1α)均明显升高,似与病情程度同步;血浆FXB_2的变化规律不一致。内毒素休克时血浆TXB_2持续升高,而结扎盲肠加穿孔组大鼠仅在术后5.5小时时血浆TXB_2显著升高,随后持续下降,术后约16小时时明显低于术前水平。感染性休克过程中血浆6-酮-PGF_(1α)和TXB_2的比值与动脉血压呈显著负相关,提示血浆PGI_2的增高和/或FXA_2的下降可能是介导感染性休克低血压的原因之一。
In this paper, the dynamic changes of 6-keto-PGF 1α and TXB 2 in septic shock and endotoxic shock in rats were observed. Bacterial peritonitis was induced in rats by puncturing the cecal and perforation followed by septic shock. Intravenous injection of E. coli endotoxin causes endotoxic shock in rats. In both shock models, plasma 6-keto-PGF_ (1α) were significantly increased, with the degree of illness seems to be synchronized; changes in plasma FXB_2 inconsistent. TXB_2 increased continuously in endotoxic shock, while TXB_2 increased significantly at 5.5 hours after operation in ligation of cecal and perforation rats, and then decreased continuously. The level of TXB_2 was significantly lower than preoperative level at about 16 hours postoperatively. The ratio of plasma 6-keto-PGF_ (1α) and TXB_2 during septic shock was significantly negatively correlated with arterial blood pressure, suggesting that increased plasma PGI_2 and / or decreased FXA_2 may be one of the causes of septic shock and hypotension .