Nava F, Calapai G, De Sarro A, Caputi A P
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
Eur J Pharmacol. 1996 Aug 15;309(3):223-7. doi: 10.1016/0014-2999(96)00352-4.
The involvement of interleukin-1 in antidipsogenic effects induced by intraperitoneal (i.p.) administration of lipopolysaccharide (0.32, 0.64 and 0.96 mg/kg) in 24-h water-deprived rats, was evaluated by injection of human interleukin-1 receptor antagonist (10, 25 and 50 micrograms/rat) into the lateral cerebral ventricle (i.c.v.). The effects of either lipopolysacharide or human interleukin-1 receptor antagonist treatment on rectal temperature of 24-h water-deprived rats, were examined. Our date show that human interleukin-1 receptor antagonist administration is able to reverse, dose dependently, fever, but not lipopolysaccharide inhibition of thirst. The reduction of pyrogenic, but not of antidipsogenic, effects of lipopolysaccharide following human interleukin-1 receptor antagonist administration suggests that lipopolysaccharide inhibition of thirst is not dependent on interleukin-1 induced fever and that interleukin-1 is not a direct mediator implicated in inhibition of water intake provoked by peripheral injection of lipopolysaccharide.
通过向24小时禁水大鼠的侧脑室注射人白细胞介素-1受体拮抗剂（10、25和50微克/只大鼠），评估白细胞介素-1在腹腔注射脂多糖（0.32、0.64和0.96毫克/千克）诱导的抗渴作用中的参与情况。研究了脂多糖或人白细胞介素-1受体拮抗剂处理对24小时禁水大鼠直肠温度的影响。我们的数据表明，注射人白细胞介素-1受体拮抗剂能够剂量依赖性地逆转发热，但不能逆转脂多糖对口渴的抑制作用。注射人白细胞介素-1受体拮抗剂后，脂多糖的致热作用减弱，但抗渴作用未减弱，这表明脂多糖对口渴的抑制作用不依赖于白细胞介素-1诱导的发热，且白细胞介素-1不是外周注射脂多糖引起的饮水抑制的直接介质。
