| Background:Labor pain, a kind of physically visceral pain, is one of the most serious pain that women expierenced in their lives. In2700cases of maternal observational studies have shown that85%of women think the pain experiences moderate to severe during labor. The drastic pain in labor can produce a series of adverse effects on maternal and fetal. So more and more patients focus on how to allievate and cure the labor pain., Although there are lots of researches about the labor pain,its mechanism is still unkown. The pain of the first stage of labor originate in the lower uterine segment and uterine cervix, a kind typically acute visceral pain. The uterine cervix, which am involved in the whole parturition, is the vicseral sensitive areas and the innervation from uterine cervix is most abundant in the female genital tract. From the above, uterine cervical distention is the main site where pain in labor arises. Researches have shown that the spinal cord is the central part of pain transmission, also the neurotransmitter and the protein channels is vital for us to understand labor pain in the spinal cord level. Recently, the related studies Detected that TRPV1channel has an expression in uterine cervix.TRPV1is an important membrane receptor and can mediate or integrate all kinds of harmful stimulus.TRPV1can be activated by inflammatory mediators, then produces the nociceptive signals. Some researches referred that the application of TRPV1channel blockers can cause pain sensitization by estrogen, which suggests that TRPV1may participate in the formation of the labor pain, but that has not further confirmed.Objection:To observe different levels of distension on the influence of TRPV1expression in the spinal cord, and analyses its role and mechanism in acute uterine cervical distension.Materials and Method:A total of54adult female virgin Sprague-Dawley rats weighing220-250g, purchased from Shanghai Slac Laboratory Animal Co. Ltd., Shanghai, China, were used. Food, but not water, was withheld for8h before the study. Animals were anesthetized with inhalation of isoflurane. The right common carotid artery were cathetered, in order to the continuous monitoring of blood pressure and heart rate. A lower abdominal laparotomy was performed to expose the uterus after1%lidocaine local infiltration anesthesia, and two fine metal rods were placed through the cervical osses, with one side attached to a metal stand and the other side connected to a force transducer. As the experimental group, we induced the expansion of uterine cervix by hanging different weights (50g、100g) through the pulley. In contrast, the control group only exposed the uterine cervix without expansion. To examine reflex responses induced by UCD, uninsulated needle electrodes were inserted in the rectus abdominis in its right inguinal part, never changed in its position, and EMG activity monitored using a window discriminator (Med-U/4C6.5.5v)Then, the halothane concentration was adjusted to0.5-1%, at which theanimal showed no gross movement during UCD stimulation. A constant UCD stimulation of75g or100g was applied for60min and the recovery was held for1hour. Then rats were put to death by dividing atlanto-occipital articulation, and rapidly removed to the ice for taking out the lumbosacal spinal cord, in order to make arrangements for molecular experiment.Results:Compared with the control group, uterine cervical distension can increase the expression of cFos in deep dorsal horn and central canal regions of the spinal cord in a distension force-dependent manner (the numbers of cFos-positive neurons in DDH and CR:UCDOg:14±1.6;UCD50g:62±5.2; UCD100g:80±1.5; P<0.05). At the same time the expression of TRPV1in the spinal cord lever of experimental group was higher than control group (P<0.05).Conclusion:1. To demonstrate that uterine cervical distension caused a similar pattern of c-fos protein expression in the spinal cord which seen in other visceral noxious stimulus and to observe that the expression of c-Fos increased in line with distension force. Thus, this model can be feasible for studying labor pain by uterine cervical distension.2. TRPV1expression changed in the spinal cord level with a distension force-dependent uterine cervical distension, which shows that TRPVlmay participate in pain transmission and regulation induced by uterine cervical distension in the level of spinal cord. |
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