Effects of hypogastric neurectomy on escape responses to uterine distention in the rat

Jennifer L. Temple, Heather B. Bradshaw, Elizabeth C. Wood, Karen J. Berkley
In: Pain · 1999 · vol. 82(Supplement 1) , pp. S13–S20 · doi:10.1016/s0304-3959(99)00133-5 · PMID:10491968 · W1989954943
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Abstract

Anatomical data indicate that the rat uterine horn is innervated primarily by afferent fibers in the hypogastric nerves, suggesting that hypogastric neurectomy, but not pelvic or pudendal neurectomy, should eliminate behavioral responses to uterine horn stimulation. To test this hypothesis, detection and escape responses of rats to different volumes of uterine horn distention (via an indwelling intrauterine balloon) were compared before and after bilateral hypogastric (n = 9), sham-hypogastric (n = 3), pelvic (n = 3), or pudendal (n = 2) neurectomies. As predicted, sham-hypogastric, pelvic, and pudendal neurectomies had no effect on the rats' responses. However, although hypogastric neurectomy completely eliminated responses in five rats whose postmortem evaluation revealed no signs that the uterine balloons had evoked any pelvic pathophysiology, the neurectomy had no effect on the responses of an additional four rats. Postmortem evaluation of these rats revealed gross signs of severe pathology in the vicinity of the balloon in two rats, and evidence that the balloon had shifted caudally so that it was stimulating the cervix rather than the uterine horn in a third. In the fourth rat, pathophysiology had been deliberately induced by the prior implantation of a small pellet that released approximately 1 microg/day of prostaglandin PF2alpha over the uterine horn. Similar findings have been reported in clinical studies on the efficacy of hypogastric ('presacral') neurectomy for dysmenorrhea. Together, the findings support the hypothesis that the major source of afferent innervation of the uterine horn in healthy rats and women is the hypogastric nerve but that the situation changes under conditions of pelvic pathology. Such changes could include additional activation of afferent fibers in nerves that supply other pelvic organs, activation by the uterine pathophysiology of latent uterine innervation from afferent fibers in the pelvic, vagus or ovarian plexus nerves, or some form of central sensitization.

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dysmenorrhea

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