Abstract
The neuropharmacology of increased bladder stiffness, which may contribute to upper tract damage and incontinence, was investigated in 76 cats, β-blockade increased but combined α1-adrenergic with muscarinic blockade decreased filling phase stiffness in normal cats. Bladder wall stiffness during the early filling phase was unaffected by chronic S2 ventrodorsal rhizotomy or L7-S3 ventral rhizotomy, but was decreased when L7-S3 dorsal rhizotomy or total sympathectomy was combined with the ventral root lesion, implying that sacral dorsal roots and sympathetic efferents maintain normal detrusor stiffness. Acute sympathectomy increased stiffness in all the former 3 chronic groups, implying that a tonic or reflex sympathetic inhibition operates independently of the L7-S3 dorsal roots. Stiffness during early filling phase decreased with acute ventral rhizotomy. This change persisted with chronic sympathectomy but returned to normal if sympathetic nerves were left intact. These results suggest that bladder stiffness is modulated by tonic or reflexic sympathetic activity, which is influenced by L7-S3 afferents. Detrusor stiffness during the later stages of filling, which was decreased by acute sympathectomy in chronic groups but increased by chronic sympathectomy, was reduced by interference with adrenergic or muscarinic mechanisms after either lesion. Therefore, a peripheral pathway with facilitatory α1-adrenergic and muscarinic receptors is involved in the production of increased late stage stiffness after chronic sympathetic damage. We propose that the increased bladder stiffness seen in congenital sacral lesions may be analogous to the stiffness during late stages of filling reported here. Our results also imply that the presence of this increased stiffness is closely associated with chronic sympathetic damage. Whether the increased stiffness in congenital and traumatic neural lesions in humans arises from sympathetic damage remains to be determined.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
