Stress-associated concentrations of plasma cortisol cannot account for reduced lymphocyte function and changes in serum enzymes in lambs exposed to restraint and isolation stress.

Lambs were used to evaluate the effect of stress-associated plasma concentrations of cortisol on measures of immune function. Lambs given restraint and isolation stress (RIS) were isolated from visual and tactile contact with other lambs for 6 h on three consecutive days. Additional lambs were infused with cortisol (CORT) to increase plasma concentrations similar to those in lambs subjected to RIS. Control lambs (CON) were undisturbed. On the 1st and 3rd d of the experiment, plasma was obtained hourly during treatment for quantification of cortisol and ACTH. Blood mononuclear cells were obtained 24 h before the 1st d of treatment and daily at the conclusion of treatment for responses to phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM); for production of interleukin 2 (IL2); and for identification of cells expressing major histocompatibility complex class II antigens (MHCII). Combined fitted profiles of cortisol in RIS and CORT lambs differed (P < .005) from those in CON on both days evaluated. Fitted profiles of cortisol were similar between RIS and CORT lambs on the 1st d of treatment but differed (P < .005) on the 3rd d. Combined fitted profiles of ACTH from CON and CORT lambs differed from those of RIS lambs on both days of treatment (P < .005). Lymphocyte responses to PHA (P < .01), Con A (P < .01), and PWM (P < .07) were less in RIS than in CON but did not differ between CON and CORT. Treatment did not affect IL2 or MHCII. Increased plasma cortisol measured during RIS cannot alone account for reduced lymphocyte proliferative responses.

Influence of treadmill exercise on pituitary-adrenal secretions, other blood constituents, and meat quality of sheep.

Whether lambs were used to evaluate the influence of treadmill exercise (TME) on physiological responses and meat quality. Lambs were exercised at either 5.6, 7.2, or 8.8 km/h on a 9 degrees incline for 10 min, followed by a 10-min walk at 4.0 km/h and 0 degrees incline, or were unexercised controls (C; n = 3/treatment). Heart rates were determined at -15, 1, 3, 6, 10, and 15 min relative to the onset of exercise. Blood was collected at 2.5-min intervals during and after exercise for determination of plasma concentrations of ACTH, cortisol, and lactate. In addition, blood collected during exercise was evaluated for hematocrit and for concentrations of glucose, hemoglobin, and total protein. Exercised lambs had greater (P < .01) heart rates than C lambs during and after exercise. Blood from TME lambs also had greater (P < .001) hematocrit percentages, total protein, and hemoglobin concentrations. Areas under the ACTH and cortisol response curves were greater (P < .001) for TME than for C lambs. Areas under glucose response curves were greater for all TME treatments (P < .001) than for C and greater (P < .001) for lambs exercised at 8.8 km/h than for lambs exercised at 5.6 km/h. Areas beneath lactate response curves were greater (P < .001) for lambs exercised at 8.8 km/h than for lambs exercised at 7.2 km/h and C lambs. Carcasses from lambs exercised at 5.6 km/h had lesser (P < .05) longissimus muscle (LM) glycogen concentrations at slaughter than carcasses from lambs exercised at either 7.2 or 8.8 km/h and C lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic hormone and cortisol response to corticotropin-releasing factor and lysine vasopressin in pigs.

Two experiments were conducted to evaluate the ability of corticotropin-releasing factor (CRF) and lysine vasopressin (LVP) to stimulate the secretion of ACTH and cortisol in pigs. In Exp. 1, barrows were blocked by weight (average BW 97 +/- 1 kg) and received an i.v. bolus of 10 (n = 4), 50 (n = 4), or 100 (n = 3) micrograms of LVP. Samples of plasma were obtained at 10-min intervals for 2 h before and for 2 h after peptide treatment. The percentage of change in plasma concentration of ACTH (average of the concentration 1 h after LVP compared with the average of the 1 h before LVP) was greater (P < .001) for 100 micrograms (452.3 +/- 4.7%) than for 10 (81.5 +/- 5.7%) or 50 micrograms (233.6 +/- 11.3%). Furthermore, the ACTH response was greater (P < .001) to 50 micrograms than to 10 micrograms. The cortisol responses to treatment (average of the concentration 2 h after LVP compared to the average of the 2 h before LVP) were similar in pigs given 50 (132.8 +/- 5.3%) and 100 (123.2 +/- 2.4%) micrograms, but both were greater (P < .001) than the response to 10 micrograms (38.2 +/- 1.4%). In Exp. 2, a dose of LVP was chosen that provided a total mass of peptide similar to the lowest dose in Exp. 1, but this time the peptide was administered at .11 nmol/kg BW. This dose of LVP was chosen because it resulted in neither maximum ACTH nor cortisol secretion in Exp. 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of repeated restraint and isolation stress and electrolyte administration on pituitary-adrenal secretions, electrolytes, and other blood constituents of sheep.

Crossbred lambs (n = 24) were blocked by weight and assigned within blocks to four treatments applied in two replications of a 2 x 2 factorial arrangement. Main effects included no stress (NS) or three consecutive days of restraint and isolation stress (RIS) and treatment with either water (W) or an electrolyte (E) solution. Each lamb in the RIS treatment group was moved from its home stanchion to another room, isolated from visual and tactile contact with other lambs, and restrained for 6 h on three consecutive days. Lambs received either distilled W or E (320 mL) on each of the 3 d of stressor treatment. On the morning of the 3rd d of stressor treatment, blood samples were collected at 1-h intervals for 6 h for determination of concentrations of ACTH, cortisol, and lactate. Also, blood was collected at the conclusion of, and 18 h after, the termination of stressor treatment (at slaughter) to measure serum electrolyte concentrations and other blood constituents. Polynomial curves fit to plasma concentrations of ACTH, cortisol, and lactate data differed (P < .005) between RIS and NS lambs during the last 6-h stressor bout. Stressed lambs had lower (P < .05) serum calcium and alkaline phosphatase concentrations than did NS lambs. Serum glutamic oxaloacetic transaminase was increased (P < .05) 20- to 30-fold in RIS lambs. Restraint and isolation stress caused clear increases in plasma concentrations of ACTH, cortisol, lactate, and glutamic oxaloacetic transaminase but had minimal effects on serum electrolytes. Electrolyte treatment had no appreciable effect on pituitary-adrenal secretions or any other measured component of blood.

Vasoconstrictor-mediated release of lactate from the perfused rat hindlimb.

The effects of different vasomodulators on lactate release by the constant-flow-perfused rat hindlimb were examined and compared with that by perfused mesenteric artery, incubated preparations of aortas, soleus and epitrochlearis muscles, and perifused soleus muscles. Infusion of vasopressin (0.5 nM), angiotensin II (5 nM), norepinephrine (50 nM), and methoxamine (10 microM) into the hindlimbs of 180- to 200-g rats increased the perfusion pressure by 112-167% from 30.4 +/- 0.8 mmHg, O2 consumption by 26-68% from 6.4 +/- 0.2 mumol.g-1 x h-1, and lactate efflux by 148-380% from 5.41 +/- 0.25 mumol.g-1 x h-1. Hindlimbs of 100- to 120-g rats responded similarly to angiotensin II. Isoproterenol (1 microM) had no effect on O2 uptake or perfusion pressure but increased lactate release by 118%. Nitroprusside (0.5 mM) markedly inhibited the vasoconstrictor-mediated increases in lactate release, perfusion pressure, and O2 consumption by the hindlimb but had no effect on isoproterenol-mediated lactate efflux. Serotonin (6.7 microM) increased lactate release from the perfused mesenteric artery by 120% from 5.48 mol.g-1 x h-1. Lactate release by incubated aorta was increased by angiotensin II (50 nM), isoproterenol (1 microM), and mechanical stretch. The increase mediated by angiotensin II was blocked by glycerol trinitrate (2.2 microM), which had no effect on lactate release by isoproterenol. Neither angiotensin II (5 nM) nor vasopressin (0.5 nM) increased lactate release from incubated soleus and epitrochlearis muscles; however, lactate release was increased by isoproterenol, and this increase was unaffected by glycerol trinitrate (2.2 microM).(ABSTRACT TRUNCATED AT 250 WORDS)