Chicks were conditioned by exposure to heat stress (36 +/- 1 C; to 80% RH) for 24 h at the age of 5, or 5 and 7 d. During conditioning, weight gain was depressed. Due to accelerated growth during the postconditioning period, a complete compensation for lost weight gain was achieved by the group conditioned at 5 d, but only a partial compensation was obtained in the group conditioned at both 5 and 7 d. At the age of 42 d, challenge with acute heat stress (35 +/- 1 C; 20 to 30% RH) resulted in a large increase in cloacal temperature of the controls and a more moderate increase in the conditioned chickens. Mortality during the thermal challenge was significantly higher in the control than that of the previously exposed (conditioned) groups. Conditioning at an early age resulted in hemodynamic changes (significant decrease in heart weight and hematocrit) and reduced plasma triiodothyronine (T3) concentration. The results suggest that reduced T3 and hemodynamic changes may be part of the mechanism associated with improved thermotolerance by early age temperature conditioning.
The energy requirements for growth and maintenance were studied in male and female chicks and turkeys, kept in environmental chambers for 4 to 5 weeks following the brooding period. In both species and sexes, the maintenance requirement decreased with constant temperatures from 12 to 24 C, reaching a low between 24 and 28 C, followed by an increase as the temperature was raised further. At 12 C, the maintenance ranged between 2.45 and 2.70 kcal/g 2 / 3 , for chicks and turkeys, respectively. Requirements for weight gain averaged 1.87 kcal/g and .7 kcal/g in chicks and turkeys, respectively. This species difference was explained on the basis of carcass composition. Turkeys fed a high-protein diet had an apparently greater maintenance requirement than those fed a diet appropriate for their age. Weight gain decreased between 19 and 34 C in chicks and between 18 C and 32 C in turkeys. Feeding of a high protein diet tended to reduce but did not overcome the growth depression by temperature. In turkeys, weight gain at 12 C was inferior to that at 18 C for both sexes. The calculated amino acid per kilocalorie dietary requirements for 6-week-old chicks increased with temperature to a peak at 27 C, followed by a decrease as the temperature was raised further. (
Hemodynamic changes were studied in broiler chickens during exposure to constant temperatures (10 to 35 C) or diurnal temperature cycles (10:30 C and 15:35 C), and during acute heat or cold. Packed cell volume (PCV) was significantly high at low constant temperatures (10 and 15 C), whereas at high temperatures (30 and 35 C) plasma volume (PV) was significantly high. A linear relationship between hematocrit and heart weight was observed and indicates an adaptation of heart mass to changes in cardiac output and hematocrit to meet the demands of increased basal metabolic rate. Only during the diurnal temperature cycle of 15:35 C did a significant increase in PV occur when ambient temperature (Ta) was raised form 15 to 35 C. Acute exposure of chickens to high temperature did not affect PV or PCV, but resulted in hyperthermia (44.7 +/- 0.4 C). Changes in PCV are probably related to modulation of the supply of oxygen to accommodate changes in heat production. The significant hypervolemia observed at high temperatures could occur to provide the fluid needed for heat dissipation by panting. The lack of response of the blood system to acute temperature changes may be at least partially responsible for the chickens' failure to control body temperature.
Due to the importance of Ca2+ in the regulation of vital cellular and tissue functions, the concentration of Ca2+ in body fluids is closely guarded by an efficient feedback control system. This system includes Ca(2+)-transporting subsystems (bone, and kidney), Ca2+ sensing, possibly by a calcium-sensing receptor, and calcium-regulating hormones (parathyroid hormone [PTH], calcitonin [CT], and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]). In humans and birds, acute Ca2+ perturbations are handled mainly by modulation of kidney Ca2+ reabsorption and by bone Ca2+ flow under PTH and possibly CT regulation, respectively. Chronic perturbations are also handled by the more sluggish but economic regulatory action of 1,25(OH2)D3 on intestinal calcium absorption. Peptide hormone secretion is modulated by Ca2+ and several secretagogues. The hormones' signal is produced by interaction with their respective receptors, which evokes the cAMP and phospholipase C-IP3-Ca2+ signal transduction pathways. 1,25 (OH)2D3 operates through a cytoplasmic receptor in controlling transcription and through a membrane receptor that activates the Ca2+ and phospholipase C messenger system. The calciotropic hormones also influence processes not directly associated with Ca2+ regulation, such as cell differentiation, and may thus affect the calcium-regulating subsystems also indirectly.
A method is described for the preparation of isolated bovine parathyroid cells. Fresh, minced bovine parathyroid tissue is incubated with 2 mg/ml collagenase and 50 mug/ml DNAse for 1 h at 37 C with periodic pipetting. Parthyroid cells are separated from contaminating fat cells and red cells by low speed centrifugation. The resulting cell preparation is indistinguishable from parathyroid cells in intact bovine glands by light and electron microscopy. Hormone release is linear for at least 3 h at both high (2.0 mM) and low (0.5 mM) calcium concentrations and is inversely proportional to divalent cation concentration between 0.3 mM and 1.0 mM calcium as been observed previously both in vivo and in vitro. As in previous studies, hormone release is also stimulated up to 2-fold by 10(6) M (-)isoproterenol, an effect blocked by 10(-6)M (-)propranolol, suggesting a beta-adrenergic effect. Such a cell preparation should be useful for studying hormone binding and effects on cyclic nudleotides and cellular transport phenomena in both normal amd abnormal tissue.
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