No abstract

Healthy multiparous Holstein-Friesian cows (n = 22, parity: 2-4) from a large-scale dairy herd in Hungary were subjected to an intravenous glucose tolerance test 10-15 days after calving. AluI genotype of growth hormone, several plasma metabolites and metabolic hormones were determined, and current and previous lactation yields were recorded. We also used the Revised Quantitative Insulin Sensitivity Check Index (RQUICKI) and its modified version (RQUICKI BHB ) for the estimation of peripheral insulin sensitivity. The majority of cows (n = 18) was leucine homozygous (LL), four were heterozygous (LV) and there were no valine homozygous (VV) animals in the population. Current average milk production was not different between AluI genotypes, but LV cows tended to have higher 305-day previous lactation yields (P = 0.13). AluI polymorphism was not associated with any of the calculated glucose and leptin parameters of the intravenous glucose tolerance test (P > 0.58). Heterozygous cows were prone to higher basal insulin levels (P = 0.064), longer time to reach half of the maximal and basal insulin concentrations (P = 0.035 and P = 0.054, respectively) and larger insulin area under the curve (P = 0.032). Both RQUICKI and RQUICKI BHB estimated decreased insulin sensitivity in LV compared to LL cows (P = 0.055 and P = 0.044, respectively). Higher plasma NEFA and BHB levels accounted for slower glucose disappearance and lower insulin release and insulin clearance rate (P < 0.05). Average yield was inversely related to glucose area under the curve (P = 0.040) and time to reach baseline concentration (P = 0.005). Plasma cortisol lowered glucose clearance rate (P = 0.040) and prolonged time to reach basal levels (P = 0.006). More weight loss was associated with higher glucose peak and prolonged glucose disappearance time (P = 0.055 and P = 0.024, respectively). All cows became cyclic and showed signs of estrus during the study period. There were no differences between leucine homozygous and heterozygous animals in the onset of ovarian activity and in the time of first observed estrus (P > 0.540). We conclude that Holstein-Friesian cows heterozygous for AluI polymorphism of the growth hormone gene may be more likely to develop insulin resistance during early lactation than leucine homozygous cows. Decreased insulin sensitivity could be part of a homeorhetic adaptation process that supports nutrient partioning for the use of the mammary gland and may allow LV cows to reach higher yields throughout lactation.

Bitches with dystocia most often present with clinical signs of uterine inertia (UI). The aetiology of myometrial dysfunction in most of these cases is still not elucidated. We compared blood ionized calcium (iCa) and glucose concentrations in bitches diagnosed with primary UI (PUI, n = 14), secondary UI (SUI, n = 6) or obstructive dystocia (OD, n = 6), and we described their haematology profiles. Bitches diagnosed with UI had a patent birth canal and delivered no puppies yet (PUI) or only part of the whole litter (SUI). The OD group had no UI and showed strong abdominal contractions. Blood iCa did not differ between the PUI, SUI and OD groups and was not influenced by litter size. There was a significant positive relationship (R = .241, p = .013) between iCa concentrations and the dam's body weight. Glucose concentrations were also not significantly different between dystocia groups or influenced by body weight and litter size. Hypocalcaemia was detected in 11 bitches, and hypoglycaemia in two bitches. Pregnancy-associated anaemia was seen in about one-third of the bitches. Eight of 12 dogs had increased platelet counts, and ten had leukocytosis with mature neutrophilia. Although iCa did not differ between dystocia groups, low concentrations may have contributed to the development of UI in some of the small size bitches. Hypoglycaemia was uncommon, and therefore, we consider low glucose concentrations not to have played an important role in the pathogenesis of UI in our study population. Pregnancy-associated anaemia, thrombocytosis, leukocytosis and mature neutrophilia were common findings in otherwise healthy bitches diagnosed with different forms of dystocia.

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.