Factor XII activation and inhibition in inflammation.
Factor XII activation and inhibition in inflammation.
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炎症中因子 XII 的激活和抑制。
DOI：
10.1007/978-3-0348-7397-0_11
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Colman,RW
中科院分区：
文献类型：
--
作者：
Colman,RW
临床败血症期间的生化观察通过对钾likrein-kinin系统的酶、辅助因子和抑制剂的功能和免疫学测量表明，这些蛋白酶的激活发生在低血压革兰氏阴性败血症和成人呼吸窘迫综合征期间。利用动物败血症模型，我们证明了蛋白酶抑制剂或对接触系统蛋白的中和性单克隆抗体抑制或阻止了钾激肽的形成和激肽原的减少。此外，还可以预防不可逆的低血压期，延长生存期。因此，缓激肽是低血压的重要介质之一。相比之下，接触系统在相关的DIC中作用很小。在体外循环中，钾激肽的形成导致中性粒细胞脱颗粒和弹性蛋白酶的释放。kallikrein的选择性抑制剂不仅阻断其激活，而且在抑制弹性蛋白酶释放方面起主导作用。
Biochemical observations during clinical sepsis using functional and immunological measurements of enzymes, cofactors and inhibitors of the kallikrein-kinin system indicate that activation of these proteases occur during hypotensive gram-negative septicemia and adult respiratory distress syndrome. Using animal models of septicemia, we demonstrated that protease inhibitors or neutralizing monoclonal antibodies to proteins of the contact system inhibit or prevent the formation of kallikrein and the decrease in kininogen. In addition, the irreversible phase of hypotension can be prevented and survival prolonged. Thus, bradykinin is one of the important mediators of hypotension. In contrast, the contact system plays little role in the associated DIC. In cardiopulmonary bypass, the formation of kallikrein leads to neutrophil degranulation and release of elastase. Selective inhibitors of kallikrein not only block its activation but play a predominant role in inhibiting elastase release.