European Society for Sexual Medicine Consensus Statement on the Use of the Cavernous Nerve Injury Rodent Model to Study Postradical Prostatectomy Erectile Dysfunction

Introduction: Rodent animal models are currently the most used in vivo model in translational studies looking into the pathophysiology of erectile dysfunction after nerve-sparing radical prostatectomy. Aim: This European Society for Sexual Medicine (ESSM) statement aims to guide scientists toward utilization of the rodent model in an appropriate, timely, and proficient fashion. Methods: MEDLINE and EMBASE databases were searched for basic science studies, using a rodent animal model, looking into the consequence of pelvic nerve injury on erectile function. Main outcome measures: The authors present a consensus on how to best perform experiments with this rodent model, the details of the technique, and highlight possible pitfalls. Results: Owing to the specific issue—basic science—Oxford 2011 Levels of Evidence criteria cannot be applied. However, ESSM statements on this topic will be provided in which we summarize the ESSM position on various aspects of the model such as the use of the Animal Research Reporting In Vivo Experiments guideline and the of common range parameter for nerve stimulation. We also highlighted the translational limits of the model. Conclusion: The following statements were formulated as a suggestive guidance for scientists using the cavernous nerve injury model. With this, we hope to standardize and further improve the quality of research in this field. It must be noted that this model has its limitations

Acute intermittent hypoxia in rat in vivo elicits a robust increase in tonic sympathetic nerve activity that is independent of respiratory drive

Acute intermittent hypoxia (AIH) elicits long-term increases in respiratory and sympathetic outflow (long-term facilitation, LTF). It is still unclear whether sympathetic LTF is totally dependent on changes in respiration, even though respiratory drive modulates sympathetic nerve activity (SNA). In urethane-anaesthetized, vagotomized mechanically ventilated Sprague–Dawley rats, we investigated the effect of ten 45 s episodes of 10% O2–90% N2 on splanchnic sympathetic nerve activity (sSNA) and phrenic nerve activity (PNA). We then tested whether or not hypoxic sympathetic chemoreceptor and baroreceptor reflexes were changed 60 min after AIH. We found that 17 animals manifested a sustained increase of sSNA (+51.2 ± 4.7%) 60 min after AIH, but only 10 of these rats also expressed phrenic LTF compared with the time controls (rats not exposed to hypoxia, n = 5). Inspiratory triggered averages of integrated sSNA showed respiratory modulation of SNA regardless of whether or not phrenic LTF had developed. The hypoxic chemoreceptor reflex was enhanced by 60 min after the development of AIH (peak change from 76.9 ± 13.9 to 159.5 ± 24.9%). Finally, sympathetic baroreceptor reflex sensitivity increased after sympathetic LTF was established (Gainmax from 1.79 ± 0.18 to 2.60 ± 0.28% mmHg−1). Our findings indicate that respiratory–sympathetic coupling does contribute to sympathetic LTF, but that an additional tonic increase of sympathetic tone is also present that is independent of the level of PNA. Sympathetic LTF is not linked to the change in baroreflex function, since the baroreflex appears to be enhanced rather than impaired, but does play an important role in the enhancement of the hypoxic chemoreflex