Visceral pain is a sort of pain, which is caused by activation of sore sensor in visceral organs when they get nociceptive stimulation. When visceral hyperalgesia occur, the variety of the sensitivity of nerve fibre, which controls the organ, is same as that of soma hyperalgesia, which takes place when skin hurt or inflammation. They both represent the trait of excess sensitivity. Come to light, visceral hyperalgesia is participated by peripheral mechanism and central mechanism. We have summarized the knowledge about central sensitization of visceral hyperalgesia in this article which consists of four sections. The first section sums up the conception and four traits of visceral pain. The second one summarizes the conception of visceral hyperalgesia, which is a phenomenon of threshold of pain decline or sensitivity of pain enhance in damnification, inflammation or persistent nociceptive stimulation, and three phenomena in the inflammatory visceral hyperalgesic experiments. The third part narrates the central sensitization of visceral hyperalgesia, which is comprised of seven segments. It also narrates the relations of the excitability amino acid, NMDA receptors, P substance, NK1 receptors, NO, Calcitonin Gene Related P eptide (CGRP), and extracellular signal-regulated kinases 1/2 (ERK1/2) to the central sensitization of visceral hyperalgesia. Last one, we sum up five others mechanisms of central hyperalgesia.
Objective To investigate the role of activated ERK1/2 in spinal cord in the development of gallbladder pain in rabbit. Methods Rabbits were divided into consisted of eight groups: nave group, surgery group, saline group, formalin group, U0126 100 μg/kg group,200 μg/kg group,400 μg/kg group and DMSO( menstruum )group, with six animals in each. The relationship between the activation of pERK1/2 in spinal cord and nociceptive behaviors, as well as the effect of U0126, which was the inhibitor of MEK1/2(upstream protein of ERK1/2 ) on gallbladder pain in rabbits were observed by Western blot and behavior test. Results There was a significant increase of pERK1/2 expression in spinal cord, as well as the increase of behaviors of gasping cheek and licking abdomen in 30 minutes after injection of 0.5ml formalin into gallbladder. The duration of behaviors were respective 23.17±1.47 and 23.00±1.41(P<0.01)in the rabbits with gallbladder pain. Administration of U0126(100 μg/kg^400 μg/kg, intravenous injection, 10 min before administration of formalin) dose-dependently attenuated nociceptive behaviors in rabbits with gallbladder pain caused by formalin. The most effective dose was 400 μg/kg . It decreased the nociceptive behaviors of grasping cheek and licking abdomen to 7.17±1.17 and 9.00±1.4(P<0.01).But it could not restrain these nociceptive behaviors completely. Conclusion It has suggested that activated ERK1/2 in spinal cord partly participates in the development of acute inflammative gallbladder pain caused by formalin in rabbits.
