Electrocautery‐induced cavernous nerve injury in rats that mimics radical prostatectomy in humans

Abstract

Objective• To investigate the early and delayed effects of cavernous nerve electrocautery injury (CNEI) in a rat model, with the expectation that this model could be used to test rehabilitation therapies for erectile dysfunction (ED) after radical prostatectomy (RP). Materials and Methods• In all, 30 male Sprague-Dawley rats were randomly divided equally into two groups (15 per group). The control group received CNs exposure surgery only and the experimental group received bilateral CNEI.• At 1, 4 and 16 weeks after surgery (five rats at each time point), the ratio of maximal intracavernosal pressure (ICP) to mean arterial pressure (MAP) was measured in the two groups. Neurofilament expression in the dorsal penile nerves was assessed by immunofluorescent staining and Masson's trichrome staining was used to assess the smooth muscle to collagen ratio in both groups. Results• At the 1-week follow-up, the mean ICP/MAP was significantly lower in the CNEI group compared with the control group, at 9.94% vs 70.06% (P < 0.05).• The mean ICP/MAP in the CNEI group was substantially increased at the 4-(35.97%) and 16-week (37.11%)follow-ups compared with the 1-week follow-up (P < 0.05).• At all three follow-up time points, the CNEI group had significantly decreased neurofilament staining compared with the control group (P < 0.05). Also, neurofilament expressions in the CNEI group at both 4 and 16 weeks were significantly higher than that at 1 week (P < 0.05), but there was no difference between 4 and 16 weeks (P > 0.05).• The smooth muscle to collagen ratio in the CNEI group was significantly lower than in the control group at the 4-and 16-week follow-ups (P < 0.05), and the ratio at 16 weeks was further reduced compared with that at 4 weeks (P < 0.05). Conclusions• In the CNEI rat model, we found the damaging effects of CNEI were accompanied by a decline in ICP, reduced numbers of nerve fibres in the dorsal penile nerve, and exacerbated fibrosis in the corpus cavernosum.• This may provide a basis for studying potential preventative measures or treatment strategies to ameliorate ED caused by CNEI during RP.

Comparison of two cannulation methods for assessment of intracavernosal pressure in a rat model

“…Both our study and Cellek’s study [ 35 ] found that stimulation of the MPG would cause contraction of the bladder, pelvic floor and rectum. This would result in an inaccurate measurement of CN-mediated neurotransmissions, as the CN is the main innervation responsible for the erection [ 36 ]. (4) In the method of cannulation into the shaft of the penis, the cannulating needle should enter the penile shaft at about a 10-degree angle.…”

Intravenous Infusion of Bone Marrow–Derived Mesenchymal Stem Cells Reduces Erectile Dysfunction Following Cavernous Nerve Injury in Rats

“…Although most experimental animal models of CN injury are mechanically created trauma models such as “crush,” “freezing,” and ligation, 18 thermal damage also could be a potential cause of ED. 19 We applied electrical coagulation to the bilateral CNs for 0.5 second at 50 kHz and 16 W using a bipolar forceps. This condition provided a stable platform to study the therapeutic effects of infused bone marrow–derived MSCs after CN injury.…”

Axotomy of tributaries of the pelvic and pudendal nerves induces changes in the neurochemistry of mouse dorsal root ganglion neurons and the spinal cord

“…Using this model, the consequences of the deafferentation of autonomic pelvic ganglia on their neurochemistry and nerve regeneration (Calenda et al 2012; Girard et al 2013; Keast 2006; Song et al 2014), on erectile dysfunction (Calenda et al 2012; Karakiewicz et al 1996; Song et al 2014; Yamashita et al 2009) or bladder and urethral functions (Lee et al 2013) have been examined. Axotomy of the pelvic nerve or its tributaries [lumbar 6 (L6) and sacral 1 (S1) spinal nerves axotomy] was introduced for the study of the neural and behavioral effects of vaginocervical stimulation (Pfaus et al 2006), neurochemical changes in the lumbar sympathetic chain (LSC) (see Brumovsky et al 2011b), changes in colonic transit (Ridolfi et al 2011), or the physiology of parturition (Martinez-Gomez et al 1998; Tovar et al 2013).…”