What Happens in Male Dogs after Treatment with a 4.7 mg Deslorelin Implant? II. Recovery of Testicular Function after Implant Removal

Although deslorelin slow-release implants are widely used in the clinic, detailed published information about the recovery of testosterone concentrations (T), semen quality, and testicular and prostatic volume (TV, PV) after treatment is still missing. This article aims to characterize changes during restart after a five-months treatment and subsequent implant removal. Seven male Beagle dogs were treated with deslorelin (treatment group, TG), and three saline-treated dogs served as controls (CG). Deslorelin implants were removed after five months (D ex), followed by detailed andrological examinations for TV, PV, semen collection, and blood sampling for T-analysis with/without GnRH/hCG stimulation tests. TV, PV, and T increased rapidly after D ex in TG, not differing from CG from D91 (TV), D49 (PV), and D14 (T). The first sperm-containing ejaculates were collected between D49 and 70, whereas the samples were normospermic between D84 and 133. A T increase (>0.1 ng/mL) subsequent to the GnRH/hCG stimulation test was observed from D28/29 onwards, respectively. Histological assessment of testicular tissue at the end of the observational period (D149 after implant removal) revealed normal spermatogenesis. Our data confirm that the restart of endocrine and germinative testicular function is highly variable, but nevertheless, all of the effects induced were reversible

What Happens in Male Dogs after Treatment with a 4.7 mg Deslorelin Implant? I. Flare up and Downregulation

Although registered since 2007, knowledge about changes in testosterone concentrations (T), testicular and prostatic volumes (TV, PV) and semen quality, as well as the time point of infertility following treatment with a 4.7 mg deslorelin (DES) slow-release implant, is limited. Therefore, seven sexually mature male dogs were treated with DES (TG); three male dogs treated with saline served as controls (CG). The study assessed local tolerance, TV, PV, semen parameters and T subsequent to GnRH/hCG stimulation in regular intervals. Local tolerance was good. In TG, T was increased right after treatment, but decreased four hours afterwards. Subsequently, TV, PV, semen quality and T decreased over time in TG, but not CG. T was basal (≤0.1 ng/mL) from D28 onwards. Response to GnRH/hCG stimulation was variable, with two TG dogs having increased T post-stimulation on all study days independent of pre-treatment concentrations. A(zoo)spermia in TG was observed from D35–D77 in all seven dogs. Whereas treatment was still effective in six TG dogs five months after implant insertion, it was fully reversed in one dog in terms of T and spermatozoa on the last examination. These results indicate high variation in individual dogs, necessary to consider when advising dog owners

Investigations on the potential role of prostaglandin E2 in canine uterine inertia

Prostaglandin (PG) E2 plays a crucial role in the endocrine network of canine parturition and we hypothesized that PGE2, 15-hydroxyprostaglandin dehydrogenase (HPGD) and PG-transporter (PGT) might be involved in the development of primary uterine inertia (PUI). We investigated PTGE synthase (PTGES), PTGE receptors 2/4 (PTGER2/4), HPGD and PGT expression on the mRNA- and protein-level in interplacental (IP) and uteroplacental (UP) tissues of bitches presented with dystocia undergoing emergency caesarean section. Groups were formed retrospectively based on strict criteria: PUI (n = 12; small/normal/large litter - PUI-S/N/L: n = 5/4/3), and obstructive dystocia (OD, n = 8). Respective mRNA expressions (ratio) between PUI and OD in IP and UP, between PUI dogs with different litter sizes, between PUI-N and OD in IP, and overall between IP and UP were compared. PTGES, PTGER2, PTGER4, HPGD and PGT mRNA expressions did not differ significantly between PUI and OD in IP or UP. PUI-N PTGES mRNA expression was higher than PUI-S/L (P = 0.0203/P = 0.0186) and OD (P = 0.0314). Higher PTGES (P = 0.0112) and a tendency for higher PTGER2 (P = 0.059) mRNA-expressions were detected in UP versus IP. Other than hypothesized, we did not find a difference in PGE2 production and signaling between PUI and OD, indicating that altered uterine PTGES, PTGER2, PTGER4, HPGD and PGT expression was likely not causative for PUI. However, higher PTGES expression in PUI-N compared to OD might point to a possible role of PGE2 during the course of parturition. Higher PTGES expression in PUI-N compared to PUI-S/L indicates an influence of litter size, the underlying cause and biological relevance of which remain to be clarified