Hioki A, Yoshino M, Kano S, Ohtomo H
Parasitol Res. 1987;73(4):298-302. doi: 10.1007/BF00531081.
Pathophysiological significance of hypoxia in malarial infection was investigated in mice infected with Plasmodium berghei NK65. Intraperitoneal inoculation of mice with 1 X 10(7) parasitized red blood cells resulted in death of the hosts 6-7 days later. Anaemia of infected animals developed on day 4 after inoculation and oxygen affinity of whole blood, measured as P50 act pH, increased simultaneously. This change may be a physiological adaptive response to a reduction in oxygen delivery to the tissues to day 5. However, the blood oxygen supply on day 6 appeared to be deteriorating and this is thought to be an important factor contributing to the death of the host. The value of adenylate energy charge in red cells during malarial infection, however, was comparatively well-maintained. Allopurinol stimulated the multiplication of malaria parasites and seems to have induced collapse in host-parasite balance more rapidly. Decrease in blood pH and in blood oxygen transport may be important factors for the pathogenesis of the allopurinol-treated hosts.
在感染伯氏疟原虫NK65的小鼠中研究了疟疾感染中缺氧的病理生理意义。给小鼠腹腔接种1×10⁷个寄生红细胞后，宿主在6 - 7天后死亡。接种后第4天，感染动物出现贫血，同时以P50 act pH衡量的全血氧亲和力增加。这种变化可能是对组织氧输送减少至第5天的一种生理适应性反应。然而，第6天的血液氧供应似乎在恶化，这被认为是导致宿主死亡的一个重要因素。然而，疟疾感染期间红细胞中的腺苷酸能荷值相对保持良好。别嘌呤醇刺激疟原虫增殖，似乎更快地导致宿主 - 寄生虫平衡崩溃。血液pH值和血液氧运输的降低可能是别嘌呤醇处理的宿主发病机制的重要因素。
