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It is established that reflex inhibition of bladder function can be achieved by electrically stimulating the sacral spinal nerve, pudendal nerve, and the tibial nerve in anesthetized animals. Recent work in our lab has shown that electrical stimulation of the saphenous nerve (SAFN) can also elicit bladder-inhibitory responses; however, the mechanism of this reflex is unknown. Given that the hypogastric nerve (HGN) modulates bladder function and projects to similar lumbar spinal regions as the SAFN in rats, we hypothesized that the bladder-inhibitory effects of SAFN stimulation involves a spinal-mediated mechanism. In this study, we investigated the effects of bilateral HGN transection on the bladder-inhibitory effects of SAFN stimulation.
Acute experiments were conducted in 11 urethane-anesthetized rats (250-300g, female), where the effects of bilateral HGN transection on SAFN stimulation were tested in the same (n=4) or in separate (n=7, 3 post-transection rats) animals. Using a surgically implanted suprapubic catheter, the bladder was infused continuously with 0.1% acetic acid (AA). Following 60-minute baseline period, changes in bladder function were measured in response to 40-minute stimulation trials applied at 10 Hz and at amplitudes of 50 µA and 100 µA. Electrical pulses were delivered via a bipolar nerve cuff electrode placed around the SAFN. Bilateral HGN transection was performed caudal to the inferior mesenteric ganglion.
Bladder atonicity, characterized by loss of bladder activity and urethral sphincter muscle bursting, was observed in response to SAFN stimulation trials applied at 50 µA and 100 µA. In rats where SAFN stimulation was tested in the same animal (n=4), atonic bladder episodes occurred in 1 of 4 rats before HGN transection, but in 3 of 4 rats after HGN transection. These episodes lasted 10.6 minutes and 11.6 ± 4.0 minutes, respectively. In rats where SAFN stimulation was tested in separate animals (n=7), bladder inhibition periods occurred in 1 of 4 rats with HGN intact, but in 2 of 3 rats with HGN transected. The duration of these episodes was 7.0 minutes and 45.2 ± 24.4 minutes, respectively.
The increased incidence of SAFN-mediated bladder activity loss following HGN transection, as shown in both experimental groups, supports the hypothesis that a neuromechanistic relationship may exist between the SAFN and bladder sympathetic tract. Further studies using sympatholytics must be done to provide more selective sympathetic inhibition to determine specific neural pathways activated by SAFN stimulation.