Investigation of a Saphenous-Hypogastric Bladder Reflex Pathway

Franz, Karly 1 ; Yoo, Paul 1, 2

1. Institute of Biomaterials and Biomedical Engineering, University of Toronto; 2. Department of Electrical and Computer Engineering, University of Toronto  

Background: Overactive bladder (OAB) is a symptomatic disorder characterized by frequent urination, incontinence, and nocturia. There are several treatment options available, including drugs and surgical intervention; however, they come at high costs with undesirable side effects. Recent studies have shown that electrically stimulating the saphenous nerve in rats causes a decreased urination rate. Thus, saphenous stimulation could be a minimally invasive and cost effective OAB treatment option for patients. However, the neural pathways that form a saphenous-bladder mechanism are not fully understood. Electrically activating the hypogastric nerve is also known to inhibit bladder function, and interestingly the spinal projections of both the hypogastric and saphenous nerves overlap within the same lumbar region. Therefore, the goal of this study was to investigate whether the bladder-inhibitory reflex evoked by saphenous nerve stimulation is mediated through the hypogastric nerve.

Methods: Acute experiments were conducted in urethane anesthetized rats. The bladder was continuously infused with 0.1% acetic acid to approximate OAB pathophysiology. Following a baseline period (no stimulation), changes in bladder function were measured in response to 40 minute trials of saphenous nerve stimulation applied at 10 Hz and at amplitudes of 50 µA and 100 µA. The hypogastric nerve was then bilaterally transected below the inferior mesenteric ganglion, and the stimulation protocol was repeated.

Results: Preliminary results showed that saphenous nerve stimulation at 50 µA caused a decrease in the bladder contraction rate, during the intra-stimulation (up to a 17.7 % decrease) and post-stimulation (up to a 15.9 % decrease) periods. In contrast, saphenous nerve stimulation applied after hypogastric nerve transection resulted in smaller changes in the bladder contraction rate both during the intra-stimulation (4.3% decrease) and post stimulation (9.7% decrease) periods at 50 µA.  Similar behavior was observed when stimulating at 100 µA. The pre-transection phase showed up to a 9.7 % decrease in the bladder contraction rate during stimulation and a 27.4% decrease during the post-stimulation phase. After hypogastric nerve transection, there was up to a 10.3% decrease in the bladder contraction rate during stimulation and 0.86% decrease during post-stimulation.

Conclusion: Our results show the bladder-inhibitory responses evoked by saphenous nerve stimulation persist following transection of the hypogastric nerve. This suggests that the hypogastric nerve contributes to the bladder-inhibitory effects of saphenous nerve stimulation in anesthetized rats.