Effect of repeated ACTH-stimulation on early embryonic development and hormonal profiles in sows

Razdan, P; Mwanza, A.M.; Kindahl, H.; Rodriguez‐Martinez, Heriberto; Hultén, Fredrik; Einarsson, S.

doi:10.1016/s0378-4320(01)00182-8

Cited by 38 publications

(29 citation statements)

References 20 publications

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“…reproductive hormones, embryo development), and often effects were found (e.g. Razdan et al, 2002;Razdan et al, 2004a,b), although they did not seem to result in negative effects on embryo survival. Relatively little information is available on the influence of specific management stressors on reproductive processes, let alone on farrowing rate and/or litter size.…”

Section: Stressmentioning

confidence: 99%

Group housing of sows in early pregnancy: A review of success and risk factors

Geudeke²,

et al. 2009

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Section: Stressmentioning

confidence: 99%

Group housing of sows in early pregnancy: A review of success and risk factors

Geudeke²,

et al. 2009

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“…restrain of snout, electric foot shock, transportation or jugular puncture) induces elevated cortisol levels, it may not result in deleterious effects [14][15][16]. Studies with different models of stress i m i t a t i o n h a v e d e m o n s t r a t e d t h a t b o t h administration of ACTH or cortisol impaired reproductive function in female pigs when given in a way which resulted in a sustained elevation of cortisol in plasma [17][18][19]. Furthermore, cortisol was shown to affect the LH secretion preferentially by reducing the frequency and amplitude of GnRH pulses [20,21], and by effects at pituitary level [22].…”

mentioning

confidence: 99%

Alteration of Reproductive Hormone Levels in Pregnant Sows Induced by Repeated ACTH Application and Its Possible Influence on Pre- and Post-natal Hormone Secretion of Piglets

Brüssow¹,

Schneider²,

Kanitz

et al. 2005

Journal of Reproduction and Development

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Abstract. Prenatal stress has been seen as a reason for reproductive failures in pig offspring mostly originated or mediated by changed maternal functions. Experiments were conducted in pregnant gilts (n=32) to characterize effects of elevated maternal glucocorticoids on the secretion of reproductive hormones (LH, progesterone) during the 1 st (EXP 1), 2 nd (EXP 2) and 3 rd (EXP 3) trimester of pregnancy (TP). Transiently elevated cortisol release was repeatedly achieved by application of 100 IU adenocorticotropic hormone (ACTH) (Synacthen Depot®) six times every second day beginning either on day 28 (EXP 1), day 49 (EXP 2) or day 75 of pregnancy (EXP 3). Glucocorticoid concentrations were examined in umbilical blood vessels of fetuses which mothers were subjected to ACTH at 2 nd and 3 rd TP (EXP 4). Furthermore, the pituitary function of newborn piglets of EXP 2 was checked by a LH-RH challenge test. In sows, LH concentrations were at low basal level (0.1-0.2 ng/ ml) but with pulsatory release pattern during each TP. The number of LH pulses/6 h (LSM ± SE) of saline treated Controls increased with ongoing pregnancy and decreased to the 3 rd TP (1.3 ± 0.2 in EXP 1 vs. 2.0 ± 0.1 in EXP 2 vs. 1.4 ± 0.1 in EXP 3, p<0.05). After ACTH treatment the number of LH pulses left unchanged in Experiments 1 and 2 (1.3 ± 0.2 and 1.5 ± 0.1) and decreased in EXP 3 (0.8 ± 0.2, p<0.05). Differences (p<0.05) were obtained comparing the LH pulse number of ACTH and saline treated sows at the 2 nd and 3 rd TP. Moreover, areas under the curve (AUC) of each LH pulse and of LH over baseline were significantly reduced by treatment. Levels of progesterone increased (p<0.05) for 150 to 170 min after each ACTH application both in EXP 1 and EXP 2, but not in EXP 3. The mean progesterone concentration was different between trimesters, and ACTH and Controls (1 st TP: 30.0 ± 0.9 and 24.4 ± 0.7 ng/ml; 2 nd TP: 35.5 ± 0.9 and 29.1 ± 1.0 ng/ml; 3 rd TP: 13.6 ± 0.2 and 13.1 ± 0.1 ng/ml; p<0.05). In fetuses (n=87) recovered 3 h after ACTH or saline (EXP 4), the plasma cortisol concentrations were significantly increased in umbilical vein (93.7 ± 5.5 vs. 47.0 ± 5.3 nmol/l) and artery (95.7 ± 5.4 vs. 66.4 ± 5.4 nmol/l), and in periphery (46.8 ± 5.3 vs. 27.1 ± 5.3 nmol/l) compared to controls. Plasma ACTH concentrations, however, did not differ in fetuses of both treatment groups. Postnatal LH-RH challenge tests (1 st and 28 th day post partum) induced LH surges in female piglets (n=67) both of ACTH and saline treated sows, but did not differ between groups (1 st day: 7.2 ± 0.8 vs. 8.1 ± 0.7 ng/ml; 28 th day: 10.5 ± 1.7 vs. 13.6 ± 2.2 ng/ml). However, basal LH of piglets whose mothers were submitted to ACTH during 2 nd TP was lower on 1 st day (1.7 ± 0.2 vs. 2.3 ± 0.2 ng/ml, p<0.05) but not on 28 th day (1.0 ± 0.2 vs. 1.1 ± 0.2 ng/ml). However in both groups, the basal LH was always higher on 1 st as on 28 th day (p<0.05). Thus, chronic intermittent ACTH administration is able to influence the release pattern of maternal reproductive hormones. However, ...

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“…In this way, the injections of ACTH in sows during standing estrus may have altered the intraluminal environment of the sperm reservoir in the oviduct because most of the treated females presented increased amounts of mucus in the oviduct lumen, attributed to the higher levels of progesterone in peripheral blood [40]. Furthermore, in a different study, the repeated administration of ACTH for 48 hours after ovulation also caused changes in the endocrine profile that might have changed the oviductal milieu, which was revealed by a low number of spermatozoa attached to the ZP and a decrease in the embryo yield [41]. These in vivo observations are in agreement with the present findings where the observed reduced binding ability of the plasma-exposed spermatozoa might be because of a higher proportion of AR spermatozoa.…”

Section: Discussionmentioning

confidence: 97%