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.

The aetiology of primary uterine inertia (PUI), which is the most common cause of canine dystocia, is still not elucidated. Prostaglandins (PGs) play a crucial role in parturition. We hypothesized that the expression of prostaglandin endoperoxidase synthase 2 (PTGS2), PGF2α synthase (PGFS), and corresponding receptor (PTGFR) is altered in PUI. We investigated PTGS2, PGFS, and PTGFR mRNA expression, and PTGS2 and PGFS protein expression in interplacental (IP) and uteroplacental sites (UP) in bitches with PUI, obstructive dystocia (OD), and prepartum (PC). PTGS2, PGFS, and PTGFR mRNA expression did not differ significantly between PUI and OD (IP/UP). PTGFR ratio in UP was higher in PC than in OD (p = 0.014). PTGS2 immunopositivity was noted in foetal trophoblasts, luminal and superficial glandular epithelial cells, smooth muscle cells of both myometrial layers, and weakly and sporadically in deep uterine glands. PGFS was localized in luminal epithelial cells and in the epithelium of superficial uterine glands. PTGS2 and PGFS staining was similar between PUI and OD, while PGFS protein expression differed between OD and PC (p = 0.0215). For PTGS2, the longitudinal myometrial layer of IP stained significantly stronger than the circular layer, independent of groups. These results do not support a role for PTGS2, PGFS, and PTGFR in PUI. Reduced PGFS expression in IP during parturition compared with PC and the overall lack of placental PGFS expression confirm that PGFS is not the main source of prepartal PGF2alpha increase. The difference in PTGS2 expression between IP myometrial layers warrants further investigation into its physiological relevance.

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.

An altered oxytocin and progesterone receptor (OXTR and PGR, respectively) expression was postulated in canine uterine inertia (UI), which is the lack of functional myometrial contractions. OXTR and PGR expressions were compared in uterine tissue obtained during C-section due to primary UI (PUI; n = 12) and obstructive dystocia (OD, n = 8). In PUI, the influence of litter size was studied (small/normal/large litter: PUI-S/N/L: n = 5/4/3). Staining intensity in immunohistochemistry was scored for the longitudinal and circular myometrial layer and summarized per dog (IP-Myoscore). Mean P4 did not differ significantly between PUI (n = 9) and OD (n = 7). OXTR and PGR expressions (ratios) were significantly higher in PUI (OXTR: p = 0.0019; PGR: p = 0.0339), also for OXTR in PUI-N versus OD (p = 0.0034). A trend for a higher PGR IP-Myoscore was identified (PUI-N vs. OD, p = 0.0626) as well as an influence of litter size (lowest PGR-Myoscore in PUI-L, p = 0.0391). In conclusion, PUI was not related to higher P4, but potentially increased PGR availability compared to OD. It remains to be clarified whether OXTR is upregulated in PUI due to a counterregulatory mechanism to overcome myometrial quiescence or downregulated in OD due to physiological slow OXTR desensitization associated with an advanced duration of labor. Identified OXTR differences between myometrial layers indicate the need for further research.

Chronic asymptomatic orchitis (CAO) is a common cause of acquired non-obstructive azoospermia in dogs. To understand the impact and mode of action of apoptosis, we investigated TUNEL, Bax, Bcl-2, Fas/Fas ligand, and caspase 3/8/9 in testicular biopsies of CAO-affected dogs and compared the results to undisturbed spermatogenesis in healthy males (CG). TUNEL⁺ cells were significantly increased in CAO, correlating with the disturbance of spermatogenesis. Bcl-2, Bax (p < 0.01 each), caspase 9 (p < 0.05), Fas, caspase 8 (p < 0.01 each), and caspase 3 (p < 0.05) were significantly increased at the mRNA level, whereas FasL expression was downregulated. Cleaved caspase 3 staining was sporadic in CAO but not in CG. Sertoli cells, some peritubular (CAO/CG) and interstitial immune cells (CAO) stained Bcl-2⁺, with significantly more immunopositive cells in both compartments in CAO compared to CG. Bcl-2 and CD20 co-expressing B lymphocytes were encountered interstitially and in CAO occasionally also found intratubally, underlining their contribution to the maintenance of CAO. Our results support the crucial role of the intrinsic and extrinsic apoptotic pathways in the pathophysiology of canine CAO. Autoprotective Bcl-2 expression in Sertoli cells and B lymphocytes seems to be functional, however, thereby also maintaining and promoting the disease by immune cell activation.