血小板激活因子在SMAO休克发病过程中的变化及山莨菪碱的影响

Platelet activating factor in the pathogenesis of SMAO shock and therapeutic effect of anisodamine

本工作在家兔肠系膜上动脉闭塞性休克(SMAO休克)模型上观察血浆PAF活性变化及山莨菪碱的影响。结果发现SMAO休克动物血浆PAF水平随休克过程发展进行性增加(基础值为3.88±0.82AU/ml,开夹后2小时为9.71±1.26AU/ml,P<0.01)。血浆PAF水平与动物血压呈显著负相关关系(r=-0.97,P<0.01)。夹闭SMA前直用山茛菪碱(5mg/kg),能防止血压明显下降,降低动物死亡率,并显著抑制血浆PAF活性的增加(基础值为4.66±0.74AU/ml,开夹后2小时为7.06±0.90AU/ml,与对照组比较P<0.05)。实验结果提示山莨菪碱抑制缺血小肠产生或释放PAF可能是其抗休克效应的机制之一。

The changes of PAF activity and the effects of anisodamine (654-2) were studied in the superior mesenteric artery occlusion (SMAO)shock in rabbits. The results showed that plasma PAF activity increased from 3.88±0.82 AU/ml before SM-AO to 9.71±1.26 AU/ml (P<0.01) 2hr after release of SMAO. There was a significant negative correlation between the level of plasma PAF and MABP in the rabbits (r=-0.97, P<0.01). Pretreatmeht with 654-2 alleviated hypotension and plasma PAF increase (from 4.66±0.74 AU/ml to 7.06±0.90 AU/ml, compared to control shock animals P<0.05). It also improved survival. The above results suggest that 654-2 depressed the synthesis or release of PAF from intestinal ischemia-reperfusion, which is probably one of the chief mechanisms of its anitshock action.