AB308. SPR-35 Sympathetic reinnervation of the urinary bladder using somatic donor nerves in a canine model of lower motoneuron lesioned bladder

Objective: Preganglionic sympathetic axons to pelvic viscera originate from lumbar preganglionic neurons and contribute to sympathetic chain ganglia and lumbar splanchnic nerves to the inferior mesenteric ganglia (many via the hypogastric nerve). Postganglionic sympathetic axons to the urinary bladder originate mostly from L7–S2 sympathetic chain ganglia and inferior mesenteric ganglion. We tested if after bladder decentralization and transfer of a lumbar originating nerve, postganglionic sympathetic axons will sprout from the lumbar nerves to reinnervate the urinary bladder.

Methods: A canine lower motoneuron lesioned bladder model was created by transecting sacral nerve roots that increased detrusor pressure using intraoperative electrical stimulation, and all roots caudal to S1. Female hounds underwent bladder decentralization and then femoral or genitofemoral nerve transfer (FNT, n=10, and GFNT, n=17, respectively) to the anterior vesicle branch of the pelvic nerve, or remained decentralized (n=3). Six sham/unoperated controls were included. Bladder emptying in animals without vesicostomies was accomplished by the Credé maneuver during the 8-month recovery period (242±6.2 days). Three weeks prior to euthanasia, a retrograde dye, Fluorogold, was injected into the bladder wall lateral to ureteral orifices. At euthanasia, T10 through coccygeal sympathetic ganglia and the inferior mesenteric ganglia were collected and examined for retrogradely labeled neuronal cell bodies. Multifactoral ANOVAs were performed (with the factors segment and group). The Bonferroni method of post hoc analysis for multiple comparisons with adjusted P values (adjusted down from P<0.05) was used to compare group differences.

Results: Increased numbers of fluorogold labeled cell bodies were observed in sympathetic ganglia of appropriate segments (mainly L4 and L5 in FNT animals; mainly L2 and L4 in GFNT animals), compared to sham/unoperated controls which showed fluorogold labeled cell bodies in S1–S3 sympathetic ganglia (P<0.01 each segment). Numbers of fluorogold labeled cells were also higher in sympathetic ganglia at vertebral levels L5 and L3 in FNT and GFNT animals, respectively, compared to decentralized controls (P<0.05 each). Low numbers of fluorogold labeled cells were visible in S1–S3 sympathetic ganglia of decentralized and FNT animals. The inferior mesenteric ganglia contained increased fluorogold labeled cells from the urinary bladder in both FNT and GFNT animals, compared to sham/unoperated controls (P<0.01 each).

Conclusions: Transfer of the femoral nerve to the anterior vesicle branch of the pelvic nerve lead to increased innervation of the bladder from lumbar postganglionic sympathetic ganglia, segments that did not contribute innervation in sham/unoperated controls. Functional consequences of this new innervation pattern should be explored in future studies.

Funding Source(s): NIH-NINDS NS070267

Keywords: Innervation; spinal cord injury; bladder; neural plasticity; dog