Plasma progesterone and prolactin concentrations in overtly pseudopregnant bitches: A clinical study

Contents Concentrations of progesterone, prolactin and relaxin in serum at predetermined intervals after ovulation (day 0) in non‐pregnant and pregnant normocyclic Beagles were assayed and results compared with those observed in German Shepherd dogs (GSD) in a previous study. The goal was to determine possible reproductive hormone specificities related to the GSD breed. Furthermore, the effects of medroxyprogesterone acetate (MPA)‐treatment in non‐pregnant Beagles and of progesterone supplementation in pregnant Beagles on the hormone concentrations were examined. Mean concentrations of progesterone and prolactin were not different in the non‐pregnant Beagles compared with those seen in non‐pregnant GSD, except at days 50–60, when progesterone concentrations were found to be higher in Beagles (p < 0.05). Mean progesterone concentrations in pregnant Beagles at days 50–60 after ovulation (day 0) were higher (p < 0.05) than in GSD at that time, but not at earlier time periods. Prolactin concentrations were higher (p < 0.05) in Beagles throughout pregnancy compared with those in the GSD. Mean relaxin concentrations were numerically but not significantly lower in GSD than in Beagles throughout pregnancy. A 10‐day oral MPA treatment did not affect progesterone or prolactin secretion in normocyclic non‐pregnant Beagles. Medroxyprogesterone acetate serum concentrations were approximately 3.9 ng/ml during treatment and decreased to 0.42 and 0.021 ng/ml within 5 and 15 days after end of treatment, respectively. Intramuscular progesterone supplementation from days 30 to 40 in pregnant Beagles resulted in higher concentrations of progesterone in the 36‐ to 45‐day time periods; prolactin and relaxin concentrations were not significantly affected during or after treatment compared with administration of placebo. The results suggest a tendency towards deficient luteal function in the short‐cycle GSD bitches previously studied, which in pregnancy may reflect the observed decreased prolactin concentrations; the possibility that GSD relaxin secretion is deficiency required needs further study. As oral treatment with MPA did not affect progesterone and prolactin release, it may be useful for studying luteal function in pregnant bitches with suspected hypoluteoidism.

Section: Discussionmentioning

confidence: 61%

Comparison of Selected Endocrine Parameters During Luteal Phase and Pregnancy in German Shepherd Dogs and Beagles

Günzel‐Apel¹,

Beste²,

Nottorf³

et al. 2009

“…The prepartum rise in prolactin suggests a possible prior ongoing inhibitory role of progesterone. Such is, in part, supported by reports that ovariectomy during the luteal phase may precipitate a rise in prolactin (Lee et al 2006), and even a clinical pseudopregnancy, a prolactindependent phenomenon usually attributable to a rise in prolactin (Tsutsui et al 2007). Additionally, administration of a progestin antagonist at mid-luteal phase or in late pregnancy can cause a transient rise in prolactin (Fieni et al 2001;Baan et al 2008).…”

Section: Pre-partum Luteolysismentioning

confidence: 85%

Endocrinologic Control of Normal Canine Ovarian Function

Concannon

2009

134

In dogs, the termination of the 3-10-month obligate anoestrus involves selection of a cohort of LH-sensitive follicles, presumably from a wave of dominant small antral follicles that would otherwise undergo atresia. The number and size of such follicles appears to increase, especially during the last 50 days of anoestrus when the already elevated concentrations of FSH become further elevated. The final selection and eventual terminal development of these follicles is caused by an increased frequency of high-amplitude LH pulses at the end of anoestrus. Concomitant increases in FSH are typically small or negligible. High concentrations of FSH in anoestrus are likely to be important in maintaining, if not stimulating, overlapping waves of dominant follicles throughout anoestrus, their expression of aromatase activity and basal oestradiol secretion sufficient to suppress LH by negative feedback. An attractive hypothesis is that late anoestrus increases in LH-stimulate synthesis of precursor androgen for already available FSH-dependent aromatase. After 7 or more days of elevated LH, and perhaps 2-5 days of semi-autonomous growth, with maximal oestradiol production reached, follicle capacity to further increase oestradiol becomes limited and excess progesterone becomes increasingly secreted. The pre-ovulatory LH surge and oestrus onset are then triggered - often synchronously and in concert with the terminal maturation of the follicles - by central effects of the large decrease in the oestrogen to progestin ratio. Follicular endocrine and paracrine events during and following the LH surge are likely similar to those reported for other species. The prolonged luteal phase lengths of 55-75 days in non-pregnant bitches bracket the 64 +/- 1 day in pregnancy and represent a genetically programmed luteal cell lifespan approximating gestation length as occurs in the luteal phase of hysterectomized animals of most polyoestrous artiodactyls and rodents. The 30-40-day slow regression after day 20 to 30 involves periodic cell death, diminution in cell size, low levels of apoptosis and minimal or modest involvement of endogenous prostaglandin F (PGF) production. The canine corpus luteum (CL) is dependent on both LH and prolactin as stimulating luteotrophins by day 15, and as required luteotrophins by days 20-25, if not earlier. Thereafter, both luteotrophins likely have cellular mechanisms of action similar to those reported for other species. Progesterone secretion during pregnancy is greatly enhanced by characteristic, and probably relaxin-stimulated, increases in prolactin concentration starting at or after day 25, and persisting to term. Near term, foetoplacental maturation results in the placental release of large, luteolytic amounts of PGF for 1-2 days pre-partum. Pre-partum luteolysis, like that induced by exogenous prostaglandin, likely involves a cascade enhanced by the removal of progesterone inhibition of PGF release and some degree of intra-luteal PGF synthesis. That a likely twofold or greater increase in progesterone ...

“…A lack of relationship between serum PRL and clinical PSP signs was previously reported and can be explained by different peripheral sensitivity or molecular forms of this hormone (Gobello et al. 2001d; Tsutsui et al. 2007).…”

Section: Discussionmentioning

confidence: 83%

Effect of Short‐Term Restricted Food Intake on Canine Pseudopregnancy

Hermo

Gerez

et al. 2009

A non-pharmaceutical, dietary option may be useful to manage clinical pseudopregnancy (PSP). To describe the effect of short-term food restriction on canine PSP, 16 privately owned, overtly pseudopregnant bitches were randomly assigned to one of the following groups: Limit-fed (increasing amounts of a restricted maintenance: 50%, 40%, 30% restriction for 2, 3 and 2 days respectively) during 7 days (n = 8) or Maintenance-fed of the same food and period (n = 8). The bitches were physically examined and blood samples were taken for prolactin and progesterone determinations on days 2, 5 and 8. By day 8, none of the bitches had completely regressed the condition although all (8/8) the animals of the Limit-fed and two (25%) of the Maintenance-fed group improved in condition decreasing mammary size and secretion (p < 0.05). No day or group effects were observed for serum prolactin and progesterone concentrations (>0.05). It is concluded that although an 8-day food restriction did not cure PSP, it seemed to hasten PSP signs involution in these bitches. No endocrine change was related to these clinical findings.