Expression of uterine oxytocin receptors and blood progesterone, 13,14-dihydro-15-Keto-Prostaglandin F2α, and ionized calcium levels in dystocic bitches.

This study aimed to examine the etiology of canine dystocia by measuring the relative expression of oxytocin receptor (OXTR) mRNA and the concentration of serum progesterone, plasma PGF_2α metabolite (PGFM), and blood ionized calcium (iCa) near term and in dystocia. Altogether 58 bitches were included in this study, 41 of which underwent cesarean section (CS). The four CS groups were based on history: complete uterine inertia (CUI; n = 7), partial uterine inertia (PUI; n = 13), obstructive dystocia (OD; n = 10), and elective cesarean section (ECS; n = 11). An additional group of medically treated dystocia without CS (MD; n = 8) and a control group (C; n = 9) with normal parturition (without CS and medical treatment) were also formed. Blood samples were taken prior to CS or medical treatment. Progesterone concentrations were highest in the ECS and a significant difference (p < 0.05) was observed between the ECS and the OD and between the ECS and the combined dystocia (CUI, PUI, OD, MD) groups (COMB). Highest concentrations of PGFM was observed in the C, the difference being significant (p < 0.05) between the C and the ECS and between the C and the COMB group. The progesterone:PGFM ratio was significantly (p < 0.05) higher in the ECS than in the C and the COMB group. No significant difference (p > 0.05) was observed in iCa concentrations between the groups. Relative OXTR mRNA expression was evaluated with real-time PCR from full-thickness uterine samples taken from the incision site during CS. The expression was highest in the ECS and the difference in expression was significant (p < 0.05) between the ECS and the OD and between ECS and the combined dystocia (CUI, PUI, OD) groups (COMB2). The study supports previous reports of decreasing progesterone and increasing PGFM during prepartum luteolysis. Upregulation of OXTR occurs near term. In obstructive dystocia, a prolonged influence of oxytocin and uterine exhaustion may lead to downregulation of OXTR. Complete primary uterine inertia may have a different etiology as no clear decrease in OXTR was observed in CUI as in OD. It remains unclear if parturition ceases because of uterine inertia or if uterine inertia occurs because of ceased parturition and desensitization of receptors.