Nerves in the Areas Posterior to the Prostate Base Contribute to Erectile Function: An Intraoperative Electrical Stimulation Assessment.

OBJECTIVE: To confirm the distribution of functional nerves involved in erectile function at the posterior of the prostate base, intraoperative nerve stimulation was performed during robot-assisted radical prostatectomy (RARP) METHODS: Several points at the posterior of the prostate and the posterolateral typical neurovascular bundle (NVB) were electrically stimulated at the level of the prostate base during RARP in patients with clinically localized prostate cancer. The prostate pedicle (PP), medial side of the PP (MPP), Denonvilliers' fascia (DF), and typical NVB were stimulated using bipolar electrodes. The changes in pressure at the middle of the urethra were measured using an inserted balloon-catheter to detect the increase in cavernosal pressure. RESULTS: Although the study included only 12 patients, each stimulation of the PP, MPP, and NVB induced evident urethral pressure responses in all patients. The median amplitude of the pressure responses was 5.49 (IQR 3.11-8.42), 6.00 (IQR 3.70-8.30), and 3.22 (IQR 2.48-7.19) cm H2O at the PP, MPP, and NVB, respectively. The amplitude of responses at the PP and MPP was not small compared with the responses at the typical NVB. Stimulations at the DF induced unstable weak urethral response alone or no response in all patients. CONCLUSION: We showed that electrostimulation of the PP and MPP increases the cavernosal pressure similar to the typical NVB stimulation. These findings indicate that maximal preservation of the tissues at the posterior area of the prostate base can contribute to optimal recovery of postoperative erectile function after nerve-sparing RARP.

Dehydroepiandrosterone sulfate and cytochrome P450 inducers alleviate fatty liver in male rats fed an orotic acid-supplemented diet.

The effects of the peroxisome proliferator, dehydroepiandrosterone sulfate (DHEAS), and the typical cytochrome P450 (CYP) inducers phenobarbital (PB) and 3-methylcholanthrene (3-MC) on fatty liver were examined in rats. Treating rats with orotic acid caused marked accumulation of lipid droplets in the liver. This effect of orotic acid was almost eradicated by co-treatment with DHEAS and PB. While DHEAS or PB alone also alleviated fatty liver, treatment with 3-MC caused little effect on a reduction in lipid droplets. Histopathological examinations revealed numerous peroxisomes in the liver of rats treated with DHEAS. In addition, a significant increase in the expression on hepatic CYPs was observed in rats the fatty liver of which was attenuated. Regarding other enzymes associated with hepatic fatty acid oxidation, the expression levels of sirtuin 1, sirtuin 6, and carnitine palmitoyltransferase 1 were also upregulated most markedly by treatment with DHEAS alone. Thus, the attenuation in fatty liver observed in the present study is likely due to peroxisome proliferation and the induction of fatty acid-metabolizing enzymes by DHEAS and typical CYP inducers.

Increase of galanin-like immunoreactivity in rat hypothalamic arcuate neurons after peripheral nerve injury.

Galanin and galanin receptors are widely distributed within the central nervous system, and may play important roles in pain signaling and modulation. In the present study, we examined the galanin immunoreactivity (IR) in the hypothalamus and the amygdala following peripheral nerve injury. Four weeks after the operation, the ipsilateral mechanical threshold in the spared nerve injury (SNI) group (0.87 +/- 0.33 g) was significantly lower than that in the sham group (12.53 +/- 3.41 g; P < 0.05). In the SNI group, the number of galanin-IR neurons per section in the arcuate nucleus (Arc) of the hypothalamus was 10.2 +/- 1.7, significantly higher than that in the sham group (5.6 +/- 1.0; P < 0.05). These data suggest that the galanin-ergic neurons in the Arc may be involved in the functional modulation of descending pain modulation system following peripheral nerve injury.