Onabanjo A O, Maegraith B G
Br J Exp Pathol. 1970 Oct;51(5):523-33.
Methods for the fractionation and estimation of serum kallikrein in the blood of healthy and rhesus monkeys infected with are discussed. A total mean increase of 4·5 ng. bradykinin equivalents/μg. protein content of kallikrein was shown to be present in the systemic circulation in the -infected animal. A remarkable fall in the bradykininogen (BKG) content in infected animal is also observed. The kallikrein from an infected animal is observed to be more active than that from control in enhancing capillary permeability, and in the development of small vessels damage including diapedesis and haemorrhage. This action of kininogenase is unaffected by prior treatment of guinea-pig with anti-histamine drugs, but is almost blocked if kallikrein is incubated with protease inhibitors before i.d. injection. The action of kallikrein would suggest a 2-fold effect; that is, acting directly on the vessel walls and is also mediated by the release of kallidin (or kinin) from the precursor. Kallikrein fraction 4a, present only in the infected monkey, was found to be very active in initiating inflammatory reactions. The gross reduction in BKG level or its disappearance in the circulation in infected animals would invariably suggest a large turnover of kinins, but this latter substance is yet to be determined. The kininogenase from both healthy and infected animals produced hypotension in rabbits when injected i.v. at a relatively low dose. It is concluded that the increase in kallikrein concentration contemporaneous with the fall of kininogen in malarial infection (and possibly with increase in kinin or kallidin content) are concerned in the inflammatory phenomena involved in the pathogenesis of malaria.
本文讨论了健康恒河猴和感染[具体感染物未明确]的恒河猴血液中血清激肽释放酶的分离和测定方法。结果表明，感染动物的体循环中激肽释放酶的总平均增加量为4.5纳克缓激肽当量/微克蛋白质含量。还观察到感染动物中缓激肽原（BKG）含量显著下降。观察发现，感染动物的激肽释放酶在增强毛细血管通透性以及在包括血细胞渗出和出血在内的小血管损伤发展方面比对照动物的激肽释放酶更具活性。激肽原酶的这种作用不受用抗组胺药物预先处理豚鼠的影响，但如果在皮内注射前将激肽释放酶与蛋白酶抑制剂一起孵育，则其作用几乎被阻断。激肽释放酶的作用表明有双重效应；也就是说，它直接作用于血管壁，也通过从前体释放胰激肽（或激肽）来介导。仅在感染的猴子中存在的激肽释放酶组分4a在引发炎症反应方面非常活跃。感染动物循环中BKG水平的大幅降低或其消失必然表明激肽有大量周转，但后一种物质尚未确定。当以相对低剂量静脉注射时，来自健康和感染动物的激肽原酶均在兔子中产生低血压。得出的结论是，疟疾感染中激肽释放酶浓度的增加与激肽原的下降（可能与激肽或胰激肽含量的增加）同时发生，与疟疾发病机制中涉及的炎症现象有关。
