Ulugöl A, Karadag H, Dökmeci D, Dökmeci I
Department of Pharmacology, Faculty of Medicine, Trakya University, Edirne, Turkey.
Yonsei Med J. 1996 Apr;37(2):97-103. doi: 10.3349/ymj.1996.37.2.97.
Contribution of histamine H1- and H2-receptors to the effect of compound 48/80, a potent histamine releaser, upon asphyxiation and body temperature in mice was investigated in the present experiments. Compound 48/80 showed an apparent protective potency against hypoxia and significantly prolonged the latencies for convulsions and death in a dose-dependent manner. Compound 48/80 also decreased the body temperature, which was in relation with the antihypoxic effect. Both the H1-receptor antagonist, dimethindene, and the H2-receptor antagonist, ranitidine, attenuated the hypothermic effect of compound 48/80, indicating the involvement of central histamine through both the H1- and H2-receptors. Ranitidine had no effect on the protective effect of compound 48/80 against hypoxia-induced lethality, whereas dimethindene completely antagonized it. These results suggest that the protective effect of compound 48/80 against hypoxia is mediated through histamine H1-receptors and is not related to its ability to induce hypothermia.
本实验研究了组胺H1和H2受体在强效组胺释放剂化合物48/80对小鼠窒息和体温影响中的作用。化合物48/80对缺氧表现出明显的保护作用，并以剂量依赖方式显著延长惊厥和死亡的潜伏期。化合物48/80还降低了体温，这与抗缺氧作用有关。H1受体拮抗剂二甲茚定和H2受体拮抗剂雷尼替丁均减弱了化合物48/80的降温作用，表明中枢组胺通过H1和H2受体发挥作用。雷尼替丁对化合物48/80抗缺氧致死的保护作用无影响，而二甲茚定则完全拮抗该作用。这些结果表明，化合物48/80对缺氧的保护作用是通过组胺H1受体介导的，与其诱导体温降低的能力无关。
