Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Journal Article (Academic article)

Urinary retention is the inability to empty the bladder completely, and may result from bladder hypocontractility, increases in outlet resistance or both. Chronic urinary retention can lead to several urological complications and is often refractory to pharmacologic, behavioral and surgical treatments. We sought to determine whether electrical stimulation of sensory fibers in the pudendal nerve could engage an augmenting reflex and thereby improve bladder emptying in an animal model of urinary retention. We measured the efficiency of bladder emptying with and without concomitant electrical stimulation of pudendal nerve afferents in urethane-anesthetized rats. Voiding efficiency (VE = voided volume/initial volume) was reduced from 72 +/- 7\% to 29 +/- 7\% following unilateral transection of the sensory branch of the pudendal nerve (UST) and from 70 +/- 5\% to 18 +/- 4\% following bilateral transection (BST). Unilateral electrical stimulation of the proximal transected sensory pudendal nerve during distention-evoked voiding contractions significantly improved VE. Low-intensity stimulation at frequencies of 1-50 Hz increased VE to 40-51\% following UST and to 39-49\% following,BST, while high-intensity stimulation was ineffective at increasing VE. The increase in VE was mediated by increases in the duration of distention-evoked voiding bladder contractions, rather than increases in contraction amplitude. These results are consistent with an essential role for pudendal sensory feedback in efficient bladder emptying, and raise the possibility that electrical activation of pudendal nerve afferents may provide a new approach to restore efficient bladder emptying in persons with urinary retention.

Full Text

Duke Authors

Cited Authors

  • Peng, CW; Chen, JJJ; Cheng, CL; Grill, WM

Published Date

  • June 2008

Published In

Volume / Issue

  • 5 / 2

Start / End Page

  • 144 - 154

PubMed ID

  • 18430976

Pubmed Central ID

  • PMC3656418

International Standard Serial Number (ISSN)

  • 1741-2560