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以糖原腹腔注入由其中渗出液提取PMNs进行体外白细胞功能-释放功能研究是较理想的。实验观察到,内毒素即使浓度高达8mg/ml也不能直接作用于PMNs,使之释放β-g;但经内毒素或Zymosan激活补体可明显增加β-g释放;乙酰胆碱本身对PMNs释放β-g无明显作用,但乙酰胆碱可加强Zymosan所致β-g释放;654-2对补体引起的β-g释放无明显影响,但可明显抑制乙酰胆碱加强Zymosan引起的β-g释放;组胺可明显抑制Zymosan所引起的β-g释放;这种抑制作用是由组胺Ⅱ型受体介导的。可以认为,休克和炎症时调节PMNs释放溶酶体酶的机制是多方面的。
To glycogen intraperitoneal injection of exudate PMNs extraction of leukocyte function - release function in vitro is more ideal. It has been observed experimentally that endotoxin can not directly act on PMNs even at a concentration of 8 mg / ml, and release β-g; however, activation of complement by endotoxin or Zymosan can significantly increase the release of β-g; acetylcholine itself releases β-g However, acetylcholine increased the release of β-g from Zymosan; 654-2 had no significant effect on complement-induced release of β-g, but significantly inhibited the release of β-g from Zymosan induced by acetylcholine; histamine significantly inhibited Zymosan induced beta-g release; this inhibition is mediated by histamine type II receptors. It is believed that the mechanisms by which PMNs release lysosomal enzymes during shock and inflammation are multifaceted.