Objective: To describe detection of severe acute respiratory syndrome (SARS)-coronavirus 2 (CoV-2) in seminal fluid of patients recovering from coronavirus disease 2019 (COVID-19) and to describe the expression profile of angiotensin-converting enzyme 2 (ACE2) and Transmembrane Serine Protease 2 (TMPRSS2) within the testicle. Design: Observational, cross-sectional study. Setting: Tertiary referral center. Patient(s): Thirty-four adult Chinese males diagnosed with COVID-19 through confirmatory quantitative reverse transcriptasepolymerase chain reaction (qRT-PCR) from pharyngeal swab samples. Intervention(s): None. Main Outcome Measure(s): Identification of SARS-CoV-2 on qRT-PCR of single ejaculated semen samples. Semen quality was not assessed. Expression patterns of ACE2 and TMPRSS2 in the human testis are explored through previously published single-cell transcriptome datasets. Result(s): Six patients (19%) demonstrated scrotal discomfort suggestive of viral orchitis around the time of COVID-19 confirmation. Severe acute respiratory syndrome-CoV-2 was not detected in semen after a median of 31 days (interquartile range, 29-36 days) from COVID-19 diagnosis. Single-cell transcriptome analysis demonstrates sparse expression of ACE2 and TMPRSS2, with almost no overlapping gene expression. Conclusion(s): Severe acute respiratory syndrome-CoV-2 was not detected in the semen of patients recovering from COVID-19 1 month after COVID-19 diagnosis. Angiotensin-converting enzyme 2-mediated viral entry of SARS-CoV-2 into target host cells is unlikely to occur within the human testicle based on ACE2 and TMPRSS2 expression. The long-term effects of SARS-CoV-2 on male reproductive function remain unknown. (Fertil Steril Ò 2020;113:1135-9. Ó2020 by American Society for Reproductive Medicine.) El resumen está disponible en Español al final del artículo.

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Introduction Radical prostatectomy (RP) is associated with erectile dysfunction (ED). A single, placebo-controlled, human study has assessed the effects of regular sildenafil use after RP and demonstrated an increased chance of preservation of preoperative erectile function. Aim This study was undertaken to define the effects of such a regimen in an animal model. Methods Using the cavernous nerve (CN) crush injury model, animals were divided into a number of groups: no CN injury (sham), bilateral CN injury exposed to either no sildenafil (control) or sildenafil at two doses (10 and 20 mg/kg) subcutaneously daily for three different durations (3, 10, 28 days). Main Outcome Measures At these time points, CN electrical stimulation was used to assess erectile function by mean intracavernosal pressure (ICP)/mean arterial pressure (MAP) ratio. For the structural analyses, whole rat penes were harvested. Staining for Masson's trichrome was utilized to calculate the smooth muscle-collagen ratio. Immunohistochemical antibody staining was performed for endothelial (CD31 and eNOS) and neural (GAP43, NGF, and nNOS) factors and immunoblotting was performed to analyze the AKT/eNOS pathway. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) assay was used for the assessment of apoptotic indices and the CN architecture was evaluated by transmission electron microscopy (TEM). Results Erectile function was improved with sildenafil in a time- and dose-dependent fashion with maximization of erectile function recovery occurring with daily 20 mg/kg at the 28-day time point. Sildenafil use resulted in smooth muscle-collagen ratio protection and CD31 and eNOS expression preservation. Sildenafil reduced apoptotic indices significantly compared with control. Animals exposed to sildenafil had increased phosphorylation of akt and eNOS. Tem demonstrated distinct differences in architecture between control and sildenafil groups toward an increased amount of myelinized nerve fibers. Conclusions Sildenafil use in the CN crush injury model preserves erectile function that appears to be mediated predominantly through preservation of smooth muscle content and endothelial function as well as through reduction in apoptosis.

Introduction The rat model of cavernous nerve (CN) injury has been developed in an effort to define the functional and structural consequences of neural trauma in the corpus cavernosum. However, there is no universally accepted method of inducing nerve injury in this model, with neurotomy and crush models being used currently. To address this issue, we induced CN injury using various techniques in an effort to compare the hemodynamic sequelae of these injuries. Methods Twenty-five adult male Sprague–Dawley rats were divided into five groups: (1) control: laparotomy only; (2) exposure: laparotomy and exposure of cavernous nerves bilaterally without nerve manipulation; (3) neurotomy; bilateral neurotomy; (4) bulldog crush: bilateral nerve crush with bulldog vascular clamp; and (5) hemostat nerve crush: bilateral nerve crush with a hemostat. Ten days later, a second operation was performed during which systemic mean arterial pressure (MAP) and intracavernosal pressure (ICP) were measured in response to CN stimulation proximal to the site of injury. Hemodynamic endpoints assessed included ICP/MAP ratio, rate of tumescence, and rate of detumescence. Results The ICP/MAP ratio (mean ± 95% confidence interval) in the control group was 70 ± 4%. ICP/MAP ratios were significantly reduced in all CN injury groups compared with control group: exposure: 41 ± 10% (P < 0.001); neurotomy: 35 ± 15% (P < 0.001); bulldog crush: 39 ± 13% (P < 0.001); hemostat crush: 31 ± 9% (P < 0.0001). No significant difference existed in ICP/MAP ratios between the injury groups. Of note, the exposure group also demonstrated significant functional alterations. The rates of tumescence and detumescence were significantly reduced in all groups compared with the control group. Conclusion No significant difference in the magnitude and consistency of hemodynamic alterations has been demonstrated in all CN injury models assessed in this study.