Effects of peripheral blood polymorphonuclear leukocyte function and blood components in Japanese black steers administered ACTH in a cold environment.

Abstract

An examination of the effects of artificial stress induced by adrenocorticotropin (ACTH) on total and differential leukocyte counts, plasma cortisol levels, metabolic profiles and peripheral blood polymorphonuclear leukocyte (PMN) function was performed on Japanese Black steers kept in a cold environment, with the following regimes; 1) -5 degrees C x ACTH (100 IU/day for 3 days), 2) 0 degrees C x ACTH, 3) 15 degrees C x ACTH and 4) 15 degrees C x PBS. Blood samples were collected before and at 1, 2, 24, 48, 72 and 96 hr prior to the application of the stressor. The plasma cortisol level was found to greatly increase at one hr after the first treatment of ACTH, particularly so in animals exposed to -5 degrees C. Total leukocytes (-5 degrees C and 0 degrees C experiments, respectively), the monocytes (-5 degrees C), neutrophils and eosinophils (-5 degrees C, 0 degrees C and 15 degrees C, respectively) obviously increased just after the first administration, although lymphocyte counts at -5 degrees C were inversely related to those described above. All of these tendencies were augmented by the cold environment except for eosinophils. The chemiluminescent (CL) response of PMN decreased in the ACTH-administered steers at an early stage of post-administration, however, it tended to recover from the lower-than-base value in the cold-affected steers. ACTH administration resulted in higher plasma glucose (Glu) compared to a control, although only steers housed at -5 degrees C evidently showed lower plasma inorganic phosphorus (IP). No abnormal serum acute phase protein, or immunosuppressor, was noted. ACTH thus appears not only to promote physiological reactions but also to temporarily suppress PMN cellular immune function in Japanese Black steers. Although, a cold environment rapidly restored the CL activity to over the pre-administrational value, suggesting that a vital response was activated by crymo-stimuli.