Gazzola C, Magner T, Lisle A T, Hunter R A
Queensland Department of Primary Industries, Rockhampton, Australia.
Comp Biochem Physiol A Physiol. 1995 May;111(1):73-7. doi: 10.1016/0300-9629(95)98522-i.
Brahman steers (Bos indicus) were treated with the alpha 2-adrenergic agonists, guanfacin.HCl (4-440 micrograms/kg), UK14304.HCl (20-125 micrograms/kg) and clonidine.HCl (0.2-5 micrograms/kg). All three agonists produced dose-dependent reductions in metabolic rate, heart rate and rectal temperature (P < 0.001). Brahman heifers were infused with idazoxan.HCl (10 micrograms/kg/hr), an alpha 2-adrenergic antagonist, alone and in combination with an intramuscular injection of guanfacin.HCl (80 micrograms/kg). Idazoxan alone did not alter rectal temperature but it blocked the guanfacin-induced lowering of rectal temperature (P = 0.05 for the interaction between the two drugs). Idazoxan alone raised metabolic rate (P = 0.01). Guanfacin lowered metabolic rate (P = 0.007) and heart rate (P = 0.03), but the blocking of the guanfacin effect by idazoxan could not be demonstrated (P > 0.05) for either. The same heifers treated with 0.5, 1.0 and 5 micrograms/kg prazosin.HCl, an alpha 1-adrenergic antagonist, had significant changes in metabolic rate (P = 0.003) and heart rate (P = 0.008) at 0.5 and 5 micrograms/kg. Metabolic rate and heart rate decreased at the lower dose and increased at the higher dose. These results with cattle parallel previous results in rats (Gazzola, 1993) where a minimal, conceptual model for the partial control of resting metabolic rate by the sympathetic nervous system was postulated. The model indicates points of control in the sympathetic nervous system which could be manipulated so as to alter the metabolic rate of farm animals.
