Kamei J, Ohsawa M, Misawa M, Nagase H, Kasuya Y
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hoshi University, Tokyo, Japan.
Nihon Shinkei Seishin Yakurigaku Zasshi. 1995 Apr;15(2):165-9.
The effect of diabetes on the morphine-induced inhibition of gastrointestinal transit was examined in mice. Morphine dose-dependently inhibited gastrointestinal transit after s.c. administration in both non-diabetic mice and diabetic mice. There was no significant difference between the ED50 values for this antitransit effect of morphine in non-diabetic and diabetic mice. The gastrointestinal antitransit effect of morphine was significantly antagonized by pretreatment with beta-funaltrexamine (40 mg/kg, s.c.), a selective mu-opioid receptor antagonist, in both non-diabetic and diabetic mice. However, pretreatment with naloxonazine (35 mg/kg, s.c.), a selective mu 1-opioid receptor antagonist, had no effect on the antitransit properties of morphine. These results suggest that diabetes failed to alter the mu 2-opioid receptor-mediated antitransit effect of morphine.
在小鼠中研究了糖尿病对吗啡诱导的胃肠蠕动抑制作用的影响。皮下注射吗啡后,非糖尿病小鼠和糖尿病小鼠的胃肠蠕动均呈剂量依赖性受到抑制。吗啡对非糖尿病小鼠和糖尿病小鼠这种抗蠕动作用的半数有效剂量(ED50)值之间没有显著差异。在非糖尿病小鼠和糖尿病小鼠中,用选择性μ阿片受体拮抗剂β-芬太尼环唑(40毫克/千克,皮下注射)预处理可显著拮抗吗啡的胃肠抗蠕动作用。然而,用选择性μ1阿片受体拮抗剂纳洛酮嗪(35毫克/千克,皮下注射)预处理对吗啡的抗蠕动特性没有影响。这些结果表明,糖尿病未能改变吗啡由μ2阿片受体介导的抗蠕动作用。