Abstract

The contribution of changes in ureter motility produced by a stone to the pain of ureteric calculosis is unclear. In this study we measured ureter motility as changes in intraureter pressure in anesthetized rats 1, 4, and 8 d ys after implantation of an artificial calculus (n = 33) and compared it with motility in normal (n = 8) and ligated (n = 4) ureters. Partial obstruction of the ureter by the stone produced a 478% increase in the amplitude of contractions, a 70% decrease in the rate of contractions, and a 66% decrease in the baseline pressure. The pressures reached during contractions were equivalent to those evoking nociceptive reactions in animals and humans. These changes persisted in rats that had spontaneously eliminated the stone. Complete obstruction of the ureter by the stone or by ligation abolished contractions. We conclude that the increased motility caused by a stone likely contributes to the development and maintenance of visceral pain and referred hyperalgesia in ureteric colic and to the persistence of referred hyperalgesia after elimination of the stone.

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