Urethral function after chronic cauda equina lesions in cats. I. The contribution of mechanical factors and sympathetic innervation to proximal sphincter dysfunction.
We investigated the contribution of mechanical and sympathetic neural factors to proximal urethral sphincter dysfunction in the cat after chronic sacral rhizotomy. Concomitant vesicostomy prevented a decrease in the urethral pressure profile measured three months post-rhizotomy. Sympathetic influences on basal urethral perfusion pressure were the same in neurally-intact and chronic rhizotomised cats. A significant prazosin-sensitive component of basal urethral perfusion pressure remained after section of all extrinsic urethral innervation in both neurally-intact and chronic cats. Local intra-arterial 6-hydroxydopamine also abolished this component. After rhizotomy, noradrenaline content in the proximal urethra was significantly increased but there was no change in sensitivity to sympathetic stimulation. A small (5% of control) atropine-sensitive and prazosin-resistant constriction was seen only after chronic sacral rhizotomy. We conclude that a mechanical factor associated with bladder expression and not an alteration in sympathetic control is the major factor leading to diminished proximal urethral closure after vesicourethral lower motor neuron lesion. Furthermore, short adrenergic neurons have an important role in the maintenance of urethral pressure in the normal state and after lower motor neuron lesion.[1]References
- Urethral function after chronic cauda equina lesions in cats. I. The contribution of mechanical factors and sympathetic innervation to proximal sphincter dysfunction. Flood, H.D., Downie, J.W., Awad, S.A. J. Urol. (1990) [Pubmed]
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