Hoffman W E, Albrecht R F, Miletich D J
Brain Res. 1986 Mar 5;367(1-2):73-6. doi: 10.1016/0006-8993(86)91580-5.
The mechanisms by which intracerebroventricular (i.v.t.) prostaglandin E2 (PGE2) produce hyperthermia in the rat were investigated. I.v.t. PGE2 produced dose-related increases in blood pressure, heart rate and rectal temperature which were significant with a dose of 0.5 ng. Oxygen consumption also increased and remained above baseline over an hour with 50 and 500 ng PGE2 doses. Ganglionic blockade with hexamethonium (20 mg/kg) attenuated the blood pressure and heart rate response to PGE2 but metabolic rate and rectal temperature increases were unchanged. Propranolol (2 mg/kg i.v.) decreased the heart rate response to PGE2 but had no significant effect on blood pressure, metabolic rate and rectal temperature responses. These results suggest a similar sensitivity of central receptors for mediating cardiovascular and metabolic rate/temperature increases but suggest that the mechanisms mediating these effects are separate.
研究了脑室内注射前列腺素E2(PGE2)在大鼠中产生高热的机制。脑室内注射PGE2会使血压、心率和直肠温度呈剂量相关增加,0.5纳克剂量时这些变化具有统计学意义。氧耗也增加,50纳克和500纳克PGE2剂量时,在一小时内氧耗一直高于基线水平。用六甲铵(20毫克/千克)进行神经节阻断可减弱对PGE2的血压和心率反应,但代谢率和直肠温度升高未改变。静脉注射普萘洛尔(2毫克/千克)可降低对PGE2的心率反应,但对血压、代谢率和直肠温度反应无显著影响。这些结果表明,介导心血管和代谢率/温度升高的中枢受体具有相似的敏感性,但提示介导这些效应的机制是分开的。