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通过家兔内毒素休克模型重点观察了磷脂酶Ａ２（ＰＬＡ２）抑制剂磷酸氯喹和地塞米松对血中ＰＬＡ２及其相关脂介质的影响。实验分成４组：（１）假手术组（ＳＯ）；（２）内毒素休克组（ＥＳ）；（３）磷酸氯喹预处理组（ＣＱ）；（４）地塞米松预处理组（ＤＸＭ）．分别于给药前、内毒素或生理盐水注射后５、３０ｍｉｎ，１、３、５、８ｈ取血测ＰＬＡ２血小板活化因子（ＰＡＦ）、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ，同时连续监测平均动脉压（ＭＡＰ）、心率和呼吸，观察动物８ｈ存活率、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ浓度均明显升高，ＰＬＡ２抑制剂能显著抑制ＰＬＡ２及ＰＡＦ活性，其中磷酸氯喹对ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ的抑制最为显著。此外，ＰＬＡ２抑制剂可使家兔８ｈ存活率由４８％提高到７５％（ＣＱ组）和７０％（ＤＸＭ组）。提示，用ＰＬＡ２的抑制剂磷酸氯喹和地塞米松均能显著抑制内毒素休克时ＰＬＡ_２的活性及相关脂介质如ＰＡＦ、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ的升高，提高动物存活率，有效地改善休克动物的预后。
The effects of phospholipase A2 (PLA2) inhibitor chloroquine phosphate and dexamethasone on PLA2 and its related lipid mediators in blood were mainly observed through the rabbit endotoxin shock model. The experiment was divided into 4 groups: (1) Sham operation group (SO); (2) endotoxin shock group (ES); (3) chloroquine phosphate preconditioning group . The levels of PLA2 and TXB2 / 6-keto-PGF1a were measured at 5, 30, 1, 3, 5 and 8h after administration of endotoxin or saline respectively. Mean arterial pressure MAP), heart rate and respiration. The animals were observed for 8h survival rate, TXB2 / 6-keto-PGF1a concentration were significantly increased, PLA2 inhibitor can significantly inhibit PLA2 and PAF activity, of which chloroquine phosphate TXB2 / 6-keto-PGF1a inhibition The most significant. In addition, the PLA2 inhibitor increased the 8 h survival rate of rabbits from 48% to 75% (CQ group) and 70% (DXM group). These results suggest that both PLA2 and dexamethasone, inhibitors of PLA2, can significantly inhibit the activity of PLA2 and the increase of related lipid mediators such as PAF and TXB2 / 6-keto-PGF1a during endotoxic shock and improve the animal survival rate effectively The prognosis of shock animals.