Abstract

The pharmacology of bradykinin has enticed investigators to prove the involvement of the kinin system in various pathological states, including protozoan diseases. In Plasmodium knowlesi malaria of rhesus monkeys, the significance of the kinin system was reported by British investigators, who showed that plasma kininogen of the infected primates was almost depleted near death, in spite of failure of the detection of free kinin in the plasma (1, 2). In addition, the increase of kallikrein contents and kininase activity in plasma were also reported in the infected monkeys (2, 3). On the other hand, Urbanitz, et al. claimed that the reduced concentration of plasma kininogen did not mean directly the involvement of the kinin system in various types of shock, because the reduction of plasma kininogen levels was simultaneously accompanied with the reduction of plasma protein concentration in shocks (4, 5). As it is known that plasma protein concentration decreases gradually with the increased degree of parasitaemia in the monkey n malaria (6), the apparent reduction of plasma kininogen in the infection mentioned above may be one of the features of the general prostration without true consumption of kininogen and release of kinin. Therefore, the reduction of kininogen in malaria must be re-examined in these respects. The present paper reports, in the severe cases of mice infected with Plasmodium berghei (NK 65), the success of the detection of free kinin in venous blood and the real consumption of plasma kininogen. The latter finding was supported by the reduction of the concentration expressed in μg/mg protein or globulin. Its pathophysiological significance is also discussed.

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