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本研究采用家兔失血性休克模型，测定失血性休克条件下血浆和组织ＰＬＡ＿２活性的变化和红细胞膜流动性的改变。结果表明失血性休克前和休克后１、２、５小时血浆ＰＬＡ＿２分别为４６．９±１２．２ｍＭ／Ｌ、９４．０±５０．０、１１９．２±６２．４、１７４．５±８５．３ｍＭ／Ｌ，休克后血浆ＰＬＡ＿２比伤前显著升高（Ｐ＜０．０１），为伤前的２．０、２．５、３．７倍。失血性休克５ｈ后肝、心、肺、肠粘膜中ＰＬＡ＿２含量为假手术组的２．４７５、３．４７５、３．３３９、４．６５７倍，显著高于假手术组。同时失血性休克时红细胞膜流动性降低，膜脂分子排列有序性升高，细胞膜荧光偏振度升高，红细胞膜脂区微粘度升高。血浆ＰＬＡ＿２的升高和细胞膜流动性改变呈显著正相关（ｒ＞０．９３）。结果说明：失血性休克时ＰＬＡ＿２水平升高可能是血液动力学衰竭和膜损伤的重要原因，ＰＬＡ＿２是失血性休克的一个关键酶和重要的体液因子。
In this study, rabbit hemorrhagic shock model was used to determine the change of plasma PLA_2 activity and erythrocyte membrane fluidity in hemorrhagic shock. The results showed that plasma PLA 2 before hemorrhagic shock and at 1, 2 and 5 hours after shock were 46.9 ± 12.2 mM / L, 94.0 ± 50.0, 119.2 ± 62.4 and 174.5 ± 85 .3mM / L, PLA2 after shock was significantly higher than that before injury (P <0.01), 2.0, 2.5, 3.7 times before injury. The content of PLA_2 in liver, heart, lung and intestinal mucosa after hemorrhagic shock for 5h was 2.475, 3.475, 3.339 and 4.657 times higher than that in sham operation group, which was significantly higher than that in sham operation group. At the same time hemorrhagic shock, erythrocyte membrane fluidity decreased, membrane lipid molecules arranged in an orderly manner, cell membrane fluorescence polarization increased, erythrocyte membrane lipid micro-viscosity increased. There was a significant positive correlation between plasma PLA_2 and cell membrane fluidity (r> 0.93). The results showed that elevated PLA 2 level in hemorrhagic shock may be an important reason for hemodynamic failure and membrane damage. PLA 2 is a key enzyme and an important humoral factor in hemorrhagic shock.