Molecular and Histologic Evidence of Novel Erectile Dysfunction Rat Model as an Aging Atherosclerosis Model: A Preliminary Study

Abstract

Purpose

To validate a novel arteriogenic erectile dysfunction (ED) model with atherosclerosis (AS) based on molecular and histologic evidence induced by chronic pelvic ischemia (CPI) and determine effect of phosphodiesterase-5 inhibitor treatment.

Materials and Methods

Twenty 16-week-old male Sprague–Dawley rats were divided into three experimental groups (Group I, untreated sham-operated rats with regular diet; Group II, CPI with cholesterol diet; Group III, CPI model with cholesterol diet and mirodenafil). Erectile function was accessed using maximum intracavernous pressure (ICP) and ICP/mean arterial pressure (MAP). Molecular changes were examined by western blot analysis using hypoxia inducible factor 1-alpha (HIF-1α), endothelial nitric oxide synthase (eNOS), and transforming growth factor beta-1 (TGF-β1) antibodies. Collagen change was evaluated by Masson's trichrome staining.

Results

In vivo measurements of ICP and ICP/MAP in Group II were significantly lower than those in Group I (p<0.01). Smooth muscle/collagen ratio in Group II was significantly lower than that in Group I (p<0.05). After treatment with mirodenafil for four weeks, Group III showed significantly higher levels of ICP and ICP/MAP than Group II (p<0.05). Western blot analysis showed that HIF-1α and TGF-β1 levels were significantly higher in Group II whereas eNOS levels were significantly lower in Group II than those in Group I or III.

Conclusions

A novel arteriogenic ED with AS model is successfully induced by CPI and validated based on molecular and histologic evidences.