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Vertebrate reproductive science and technology
RESEARCH ARTICLE

121 RELATIONSHIP BETWEEN PROSTAGLANDIN E2 METABOLITE, UTERINE ARTERIAL VASODILATORY CHANGES, AND PROGESTERONE DURING THE OESTROUS CYCLE AND EARLY PREGNANCY IN BEEF COWS

H. L. Sánchez-RodrÍguez A , J. M. Feugang A , R. C. Youngblood A , R. C. Vann B , S. T. Willard C and P. L. Ryan A D
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- Author Affiliations

A Department of Animal and Dairy Sciences, Mississippi State University, Mississippi State, MS, USA;

B MAFES-Brown Loam Branch Experiment Station, Mississippi State University, Raymond, MS, USA;

C Department of Biochemistry, Molecular Biology, Entomology and Pathology, Mississippi State, MS, USA;

D Department of Pathobiology and Population Medicine, Mississippi State, MS, USA

Reproduction, Fertility and Development 25(1) 207-208 https://doi.org/10.1071/RDv25n1Ab121
Published: 4 December 2012

Abstract

Vasodilation of the female reproductive vasculature is essential to supply the increasing demands associated with reproductive processes; including maintenance of a healthy functional luteal structure, and the establishment and continuance of pregnancy. Due to its vasodilatory effects, prostaglandin E2 has been identified as a potential candidate sustaining such vascular effects. Here, the relationship between systemic concentrations of prostaglandin E2 metabolite (PGEM) and progesterone (P4), and uterine arterial vasodilatory changes were evaluated during the oestrous cycle and early pregnancy. Synchronised Angus cows (n = 19) were artificially inseminated (AI) and examined for pregnancy 45 d post-AI. Jugular blood samples were collected on Days 0, 3, 6, 10, 16, 20, 25, and 32 (Day 0 = AI) for serum PGEM and P4 evaluation. Vasodilatory changes of the uterine arteries were also characterised using the B-mode ultrasound luminal circumference (UAC). Retrospective comparisons were carried out between pregnant (n = 10) and nonpregnant (n = 9) animals. The GLM Procedure of SAS (SAS Institute Inc., Cary, NC, USA) was used to evaluate the effects of pregnancy status and sampling day over PGEM, UAC, and P4. Pearson correlations between PGEM, UAC, and P4 were obtained by the CORR Procedure of SAS. All variables were measured in triplicate and thresholds for significance and tendency were fixed at P ≤ 0.05 and 0.06 to 0.10, respectively. From Day 0 to Day 20, the overall PGEM concentration tended to be higher in nonpregnant cows compared to pregnant ones (P = 0.08; 90.97 ± 4.38 v. 78.28 ± 3.01 pg mL–1, respectively), while a shift in favor of pregnant cows was observed at Day 32 (P = 0.29; 89.88 ± 14.23 v. 106.3 ± 7.17 pg mL–1, respectively). Both uterine arteries showed similar UAC (P ≥ 0.05); therefore, they were combined in one average value per animal each sampling day. There was an overall increase of the UAC over time, from 10.49 ± 0.01 mm at Day 0 to 12.17 ± 0.02 mm at Day 20 (P ≤ 0.0001), but no significant differences were found between pregnant and nonpregnant cows during this period (P ≥ 0.05). An overall sharp increase in P4 concentrations was observed from Day 3 to Day 16 (0.60 ± 0.12 to 9.66 ± 0.45 ng mL–1, P ≤ 0.0001); while from Day 16 to Day 32, pregnant cows maintained steady and higher P4 concentrations than nonpregnant ones (9.87 ± 0.31 v. 4.40 ± 1.09 ng mL–1, respectively; P = 0.002). As expected, nonpregnant cows showed a sharp decrease in P4 concentrations from Day 16 to Day 25, followed by a second increase at Day 32 (9.27 ± 0.20, 0.85 ± 0.33, and 6.04 ± 1.67 ng mL–1, respectively; P = 0.0007). The UAC and PGEM concentrations were positively correlated in pregnant (r = 0.48; P = 0.002), but not in nonpregnant animals (r = 0.29; P = 0.21). Similarly, UAC and P4 concentrations were also positively associated in pregnant (r = 0.47; P = 0.002), but not in nonpregnant cows (r = 0.01; P = 0.96). Our findings support the role of PGE2 as a potential mediator of the vascular function in the female reproductive tract and, subsequently, as an essential factor to ensure adequate P4 production able to sustain early pregnancy in the bovine.

USDA-ARS Grant#58-6402-3-0120.