Antinociceptive Effects Of Clonidine On Somatic Pain And Visceral Pain Evoked By Myocardial Ischemia

Objective The purpose of the study was to investigate the potential antinociceptive effects of clonidine on the changes in the discharge rate of neurons in parafascicular (PF) nucleus of thalamus evoked by mechanical stimulation and coronary artery occlusion.Methods①Divide the 12 rats detected noxious stimulation responding neuron(NSRN) by microelectrode into 2 groups, 6 animals each. All the neuroes were recorded continually:the basic discharge frequency; the discharge frequency after mechanical stimulation; the discharge frequency after mechanical stimulation after injection of clonidine (one group 10μg and the other 30μg) 5min later; the discharge frequency after mechanical stimulation after injection of yohimbine 5min later.Compare the 4 class discharge frequency,and analyse the efficacy of clonidine and yohimbine.②M ade the myocardial model of rat by occlusion of coronary artery(CAO), Divide the 24 rats detected NSRN showed response to CAO into 4 groups,Each group take action as: GroupI CAO+NS0.1ml, iv; GroupII CAO+clonidine30μg, iv; GroupIII CAO+clonidine100μg, iv; GroupIV CAO+clonidine100μg+yohimbine200μg, iv; The clonidine was administered intravenously 15 minutes and the yohimbine was 25 minutes after the onset of CAO. The experiment recordings lasted for 60 minutes.Results①clonidine 30μg significantly suppressed the increase in the discharges of NSRN induced by mechanical stimulation ,and this efficacy can be blocked by theα2-recepter antagonist yohimbine②clonidine 100μg significantly suppressed the increase in the discharges of NSRN induced by CAO ,and this efficacy can be blocked by theα2-recepter antagonist yohimbineConclusions①Clonidine can effectively suppress the nociceptive stimulus evoked by somatic pain and visceral pain.②The transmition and modulation mechanism about somatic pain and visceral pain is different.