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1.本文报告了青霉素过敏休克机制的实验研究,主要观察了动物过敏休克模型的建立及肥大细胞脱颗粒反应。2.实验证明,青霉噻唑蛋白为引起过敏反应的过敏原,使豚鼠致敏后用青霉噻唑蛋白1～2mg或含杂质的青霉素G10万单位作为抗原心内注射进行攻击,动物立即出现比较典型的休克症状;死后剖验,心脏停止于舒张状态,两肺呈严重肺气肿,组织镜检心、肝及肾等组织也呈休克的病理改变。3.体外大鼠腹腔肥大细胞脱粒反应的被动免疫实验证明,致敏豚鼠血清加不同抗原在体外对肥大细胞脱粒反应有明显影响,如青霉噻唑蛋白使肥大细胞脱颗粒为82.3%,青霉素G为76.7%,青霉素聚合物为83.9%,正常对照者仅为19.4%,此种反应是青霉素过敏休克时介质释放的前提条件。4.本文并对青霉素过敏休克机制、肥大细胞脱颗粒反应的意义和影响因素以及过敏休克模型建立进一步改进,进行了讨论。
1. This paper reports the experimental study on the mechanism of allergic shock induced by penicillin. The establishment of an animal model of allergic shock and the degranulation of mast cells were mainly observed. 2. Experiments show that the penicillin thiazole protein is an allergen that causes allergic reactions, the guinea pig sensitized with penicillin thiazole 1 ~ 2mg or impurity penicillin G million units as an antigen intracardiac injection attack, the animals immediately appear to compare Typical shock symptoms; post mortem test, the heart stopped in the diastolic state, both lungs were severe emphysema, histological microscopy heart, liver and kidney and other organizations also showed pathological changes in shock. In vitro rat peritoneal mast cells thylakoid reaction passive immunization experiments showed that sensitized guinea pig serum plus different antigens in vitro mast cell degranulation had a significant effect, such as penicillin thiazole protein mast cells degranulation of 82.3%, penicillin G Was 76.7%, penicillin polymer was 83.9%, normal control was only 19.4%, this response is a prerequisite for penicillin anaphylactic shock when the media release. The paper also discusses the significance and influencing factors of allergic shock mechanism of penicillin, the degranulation reaction of mast cells and the further improvement of allergic shock model.