Pituitary-Adrenocortical and Lymphocyte Responses to Bromocriptine-induced Hypoprolactinemia, Adrenocorticotropic Hormone, and Restraint in Swine

Abstract

A study was conducted with castrated male pigs (barrows) to evaluate effects of bromocriptine-induced hypoprolactinemia (6 days) on basal and adrenocorticotropic hormone (ACTH)-altered (single injection) pituitary-adrenocortical function, on lymphocyte proliferative responses, and on interleukin 2 production. In addition, the study was designed to measure the short time course of pituitary-adrenocortical and lymphocyte responses to ACTH and to a 30-min restraint stressor. Blood samples were taken via indwelling jugular catheters at -0.5, +0.5, +2, and +5 hr (with reference to time of acute treatment exposure) on Day 6 of the study. Lymphocyte responses were measured only at the 2-hr interval. Exposure (6 days) to bromocriptine (CB154) was associated with 53% reductions (P less than 0.05) in plasma prolactin (1.37 +/- 0.13 vs 0.60 +/- 0.04 vs 0.68 +/- 0.08 ng/ml) when averaged across all time intervals in control, CB154-treated, and CB154 + ACTH-treated pigs, respectively. The reductions in plasma prolactin were associated with a reduction (P less than 0.05) in basal plasma cortisol at only one time interval (+0.5 hr) when CB154-treated pigs were compared with controls (17.7 +/- 4.2 vs 26.9 +/- 3.2 ng/ml). CB154 had no effect on plasma ACTH or growth hormone concentrations for the time periods at which they were measured. CB154 treatment produced numerical, but not statistically significant, 38% reductions in interleukin 2 production (6.31 +/- 1.8 vs 3.91 +/- 1.47 units/ml). Lymphocyte proliferative responses to the mitogen concanavalin A and interleukin 2 production decreased 65 and 75% (P less than 0.05), respectively, 2 hr subsequent to ACTH administration when compared with control animals. Hence, under the conditions of this study, only a modest association between lowered plasma prolactin concentrations and basal cortisol concentrations was evident. The data suggest the absence of dopamine regulation of basal plasma ACTH in pigs and provide evidence for a rapidly occurring inhibitory effect of ACTH administration on specific lymphocyte activities.

Cell-mediated immune function in lambs chronically treated with dexamethasone.

“…In agreement with this observation, restraint stress also decreased production of IL-2 by lymphocytes from lambs (Cop pinger et al, 1991). Also, treatment with ACTH decreased IL-2 production in cattle (Blecha and Baker, 1986) and pigs (Klemcke et al, 1990). In contrast, identical doses of DEX did not reduce production of IL-2 by lambs in our previous study (Minton et al, 1991).…”

“…Stressors can reduce the ability of lymphocytes from lambs to proliferate in response to mitogens (Coppinger et al, 1991), an effect also seen in cattle (Blecha et al, 1984) and pigs (Klemcke et al, 1990). In general, reduced proliferative responses of lymphocytes from stressed animals is thought to be the result of the suppressive action of glucocorti- coids.…”

“…Dexamethasone @EX) is a potent, synthetic glucocorticoid that has been used as a model treatment to study the effects of elevated adrenal glucocorticoids on the function of the immune system of cattie (Roth, 1985; Roth and Flaming, 1990). The immunological responses to DEX have been generalized to represent responses to stressor-induced elevations in endogenous glucocorticoids be- concentrations of cortisol and can reduce some measures of immunological function (Blecha et al, 1984;Klemcke et al, 1990;Coppinger et al, 1991). Indeed, cell-mediated immune functions of cattle are reduced by treatment with DEX (Roth and Kaeberle, 1985).…”

Function of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system in models of acute stress in domestic farm animals2

“…For example, exposure of lambs to a single 6-h bout of RIS or to heat stress for 24 h activated the PA axis but did not alter lymphocyte blastogenic response to mitogens (Minton and Blecha, 1990). Similarly, restraint of pigs for 30 min also increased plasma ACTH and cortisol but did not alter lymphocyte proliferation in response to mitogens or affect production of IL-2 in vitro (Klemcke et al, 1990). Furthermore, our 3-d RIS model stressor MINTON system in lambs, which consistently reduced lymphocyte proliferation in response to mitogens, did not alter IL-2 production in our latest two studies (Minton et al, 1992.…”

Recovering from an Epidemic of Teen Pregnancy: The Role of Rural Faith Leaders in Building Community Resilience

“…Corticosteroids and catecholamines are mediators of the inflammatory response, and this response is an example of a function that can be harmful to the animal if left unchecked (Black, 2002). The suppression of the immune system via GC is mainly seen in chronic stress situations (Minton, 1994;Klemcke et al, 1990;Minton and Blecha, 1990). Conversely, for people with Addison's disease in which the body does not produce ACTH, there is chronic stimulation and excess white blood cell (WBC) concentrations (Sapolsky et al, 2000).…”