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麻醉狗注内毒素前左心血TXB_2/6-keto-PGF_(1α)及PAR均明显低于右心血;内毒素休克时,左、右心血TXB_2/6-keto—PGF_(1α)及PAR明显上升,且左、右心血之间的浓度梯度差消失;消炎痛明显减轻内毒素休克时的前述改变。注内毒素前及内毒素休克早期TXB_2/6-keto-PGF_(1α)与PAR之间呈显著正相关。结果提示:肺解聚功能与肺代谢TXA_2、PGI_2有关;内毒素休克早期,肺代谢TXA_2,PGI_2的失调是肺解聚功能受损原因之一。
The blood TXB_2/6-keto-PGF_(1α) and PAR in the anesthetized dogs were significantly lower than those in the right heart blood before endotoxin injection; TXB_2/6-keto-PGF_(1α) and PAR increased significantly in endotoxin shock. , and the concentration gradient difference between left and right heart blood disappears; indomethacin significantly reduces the aforementioned changes in endotoxin shock. There was a significant positive correlation between TXB_2/6-keto-PGF_(1α) and PAR before and after endotoxin injection. The results suggest that the function of pulmonary depolymerization is related to the metabolism of TXA_2 and PGI_2 in the lung; in the early stage of endotoxin shock, the imbalance of TXA_2 and PGI_2 metabolism in the lung is one of the causes of impaired lung depolymerization.