可乐定对严重烫伤大鼠心肌Giα表达的影响

Effects of clonidine on the expression of myocardial Giα after severe scald in rats

目的 探讨可乐定对严重体表烫伤大鼠心肌抑制性G蛋白α亚基 (Giα)表达的作用及机制。方法 通过建立大鼠背部 3 0 %体表面积Ⅲ度烫伤模型 ,分别采用间接酶法、Westernblot测定了烫伤大鼠早期心肌AC活性、Giα水平。结果 可乐定 0 3、1、3mg kg ,可剂量依赖性地抑制烫伤后心肌Giα的增加。可乐定 0 .3～ 3mg kg还可显著升高烫伤后心肌AC基础活性 ,而 1～ 3mg kg可明显升高心肌Gpp (NH)p刺激活性 ,0 .3mg kg对心肌Gpp (NH)p刺激活性无明显影响 ;I1咪唑啉受体阻断剂efaroxan( 5、10mg kg)可部分逆转可乐定抑制烫伤大鼠心肌Giα升高的作用。结论 可乐定可抑制烫伤后心肌Giα的升高 ,其机制可能与可乐定激动I1

Objective To investigate the effects of clonidine on the expression of myocardial α subunit of inhibitory G protein (Giα) in severely scalded rats and the mechanisms. Methods A scald model of 30% total body surface area Ⅲdegree burn on the back of rats was established. The basal and Gpp (NH) p, forsklin stimulated activity of adenylate cyclase (AC), and Giα in cardiac myocytes were determined by indirect enzyme radiochemical assay and Western blotting, respectively. Results Clonidine at the dosage of 1-3 mg·kg -1 inhibited significantly the increase in the myocardial Giα levels. Clonidine at the dosage of 0.3-3 mg·kg -1 partially reversed the decrease in the basal activity, and clonidine at the dosage of 1-3 mg·kg -1 showed the similar effect on the decrease in the Gpp (NH) p stimulated activity. Efaroxan, an I 1 imidazoline receptor antagonist, could partially reverse the inhibitory effect of clonidine on myocardial Giα levels. Conclusion Clonidine can inhibit the elevation of myocardial Giα levels, and the mechanisms of the inhibition may possibly be associated with the stimulatory effect of clonidine on I 1 imidazoline receptors.