# Pelvic ganglia inflammation as a factor leading to organ crosstalk and coordinated development of bladder and erectile dysfunction following pelvic surgery.

> **NIH NIH R01** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2024 · $675,090

## Abstract

Pelvic ganglia inflammation as a factor leading to organ crosstalk and coordinated development of
bladder and erectile dysfunction following pelvic surgery.
Abstract:
Patients undergoing radical prostatectomy are at high risk of developing both bladder and erectile dysfunction,
even when minimally nerve-sparing approaches are used to avoid direct damage to the urogenital organs and
their neurovasculature. The goal of this proposal is to identify mechanisms that result in this coordinated
development of bladder and erectile dysfunction (ED) following pelvic surgery.
We recently reported that in rats, simple laparotomy results in ED 3 days after surgery, and is accompanied by
systemic and also local inflammatory responses in penile cavernosal tissue, cavernous nerve (CN) and major
pelvic ganglia (MPG). Interestingly, even though this surgical procedure avoids direct nerve injury, the profile of
molecular changes in cavernosal tissue was strongly indicative of CN injury, suggesting that development of ED
following nerve-sparing pelvic surgery may involve a systemic inflammatory response, resulting in indirect nerve
injury. In preliminary data presented here, we demonstrate that in both rat models of minimally invasive pelvic
surgery and direct CN injury, the development of ED is accompanied by significant changes in bladder function.
Moreover, we also observed an inflammatory response at the level of the MPG, which innervates both cavernosal
and bladder tissues. A pathological inflammatory response in the MPG may therefore mediate pelvic organ
crosstalk leading to the coordinated development of bladder and erectile dysfunction.
These observations have led us to the hypothesis that even following minimally invasive, nerve-sparing
pelvic surgery that avoids direct damage to the urogenital organs, there is a pathological inflammatory
response in the MPG that mediates pelvic organ crosstalk and coordinated development of bladder and
erectile dysfunction. Furthermore, we hypothesize that modulating the inflammatory response will improve
post-operative urogenital function outcomes.
We will test these hypotheses with three Specific Aims. In Aim 1 we will utilize animal models to compare the
impact of different levels of pelvic surgical trauma (naïve rats compared with those undergoing laparotomy,
sham-CN injury, CN crush or CN transection) to correlate the time-course and severity of post-operative bladder
and erectile dysfunction with the levels of the inflammatory response (systemically, in urogenital tissue, and in
the CN and MPG). In Aim 2, we will investigate the impact of post-surgical inflammation on the MPG and
determine the extent to which MPG molecular and structural remodeling provide a substrate for pelvic organ
crosstalk leading to coordinated post-surgical development of bladder and erectile dysfunction. In Aim 3 we will
use anti-inflammatory drugs to determine the role of the inflammatory response on the coordinated development
of urogenital...

## Key facts

- **NIH application ID:** 10857817
- **Project number:** 1R01DK139328-01
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** KELVIN P DAVIES
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $675,090
- **Award type:** 1
- **Project period:** 2024-04-15 → 2029-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10857817

## Citation

> US National Institutes of Health, RePORTER application 10857817, Pelvic ganglia inflammation as a factor leading to organ crosstalk and coordinated development of bladder and erectile dysfunction following pelvic surgery. (1R01DK139328-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10857817. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*