Metabolic responses of the whole body, portal-drained viscera and hindquarter to adrenaline infusion: Effects of nonselective and selective β-adrenoceptor blockade

Abstract

Miaron, J. O. O. and Christopherson, R. J. 1997. Metabolic responses of the whole body, portal-drained viscera and hindquarter to adrenalin infusion: Effects of nonselective and selective β-adrenoceptor blockade. Can. J. Anim. Sci. 77: 307-316. Propranolol, a nonselective β-blocker and selective β-blockers (metoprolol a β 1 -blocker and ICI 118551 a β 2 -blocker) were used to investigate the β-adrenoceptor-mediated adrenaline-induced increase in whole-body and organ VO 2 in five whether sheep. Transit time blood flow probes were chronically implanted on the portal vein and the external iliac artery and sampling catheters were placed in the mesenteric artery, iliac vein and portal vein. Oxygen consumption by the whole body was measured by open circuit calorimetry, and oxygen consumption by the portal-drained viscera and the hindquarter was determined from A-VO 2 differences and organ blood flow. Absolute pre-infusion VO 2 values for the whole body, portal-drained viscera and hindquarters were 236 ± 7.4, 61 ± 6.0 and 13 ± 3.1 mL min -1 respectively. The mean changes in VO 2 in response to infusion were 74 vs. 11, 26, 10 and 12 mL min -1 (SE = 9.1) for whole body; 31 vs. -2, -15, 13 and -4 mL min -1 (SE = 7.3) for portal-drained viscera and 8 vs.-0.4, 2.1, 1.0 and -2.7 mL min -1 ; SE = 4.3) for hindquarters during adrenaline, control, propranolol, metoprolol and ICI 118551 treatments, respectively. Adrenaline increased VO 2 (P < 0.05) in the whole body and portal-drained viscera, but not hindquarters relative to controls. All β-blockers suppressed (P < 0.05) the adrenaline-induced increase in VO 2 except for the portal-drained viscera where metoprolol was less effective and the hindquarters where β-blockers had no effect. The blood flow pattern was similar to VO 2 responses for the portal-drained viscera. The nonselective β 1 and β 2 blockers were effective in reducing the adrenaline-induced increases in blood flow from the portal-drained viscera and to the hindquarters, with more pronounced β 2 -adrenoceptor-mediated haemodynamic effects. The results indicate that the β-adrenoceptor system modulates whole body VO 2 , clearly establishes that adrenaline induces an increased VO 2 in portal-drained viscera which can be reversed by a β 2 or nonselective β blocker and implicates β adrenoceptors as an influencing factor in the maintenance energy requirements of ruminants. Sci. 77: 307-316. Le propanolol, un β-agoniste non sélectif et des β-agonistes sélectifs : métopropol, β 1 -agoniste et ICI 118551, β 2 -agoniste ont été utilisés pour examiner sur cinq agneaux mâles castrés l'accroissement adréno-induit, à médiation par les β-adrénorécepteurs, du VO 2 du corps entier et des organes. Des sondes de débit sanguin à temps de passage étaient implantées à demeure autour de la veine porte et de l'artère iliaque externe et des cathéters de prélèvement étaient installés dans l'artère mésen-térique, dans la veine iliaque et dans la veine porte. La consommation d'oxygène par le corps entier était mesurée par calorimétrie en circ...

Metabolic responses of the whole body, portal-drained viscera and hind quarter to acute cold exposure and feeding in sheep: Effects of nonselective and selective β-adrenoceptor blockade

“…These data also confirm previous conclusion by other workers that cold exposure had little or no effect on the oxygen consumption of the portal-drained viscera of the sheep (Thompson et al 1975). Evidently, the endogenous release of adrenaline, unlike the exogenous adrenaline (Miaron and Christopherson 1997) was not sufficient to induce an increase in portal-drained viscera metabolism in sheep during an acute cold exposure. One cannot, however, rule out a potential role for the adrenoceptor processes in the modulation of portal-drained viscera metabolism in sheep exposed to a more prolonged thermal exposure which is usually associated with increased gut mass, since data on the possible modulatory role of the adrenoceptor system in the gut of ruminants exposed to a prolonged cold exposure are lacking.…”

“…Thus, there is not complete agreement in the literature with respect to the role of β-adrenoceptors in regulating the heat production response to feeding. An elevation in thermogenesis occurs in response to adrenaline and noradrenaline (Graham and Christopherson 1981;Miaron and Christopherson 1997) and may be blocked by β-adrenoceptor antagonists (Webster et al 1969;Miaron and Christopherson 1997) and, hence, constitutes a basis for β-adrenoceptor modulation of the energy requirement in sheep. A decrease in whole blood amino acid concentration has been reported during fasting (Ericksson et al 1988) and lower plasma levels are associated with trauma-and cold-related stressors (Souba and Dauglas 1983);Kelly 1987).…”

“…Water and salt were available ad libitum. Blood flow probes were implanted surgically on the portal vein and external iliac artery for use in measurement of blood flow in these vessels and blood sampling catheters were also implanted as previously described by Miaron and Christopherson (1997). Experimental procedures and care of animals of this study were conducted in accordance with the guidelines of the Canadian Council on Animal Care.…”

“…Whole body oxygen consumption, portal-drained viscera and hindquarter blood flow and oxygen consumption rates (products of blood flow and the A-V oxygen differences) were determined by methods described by Miaron and Christopherson (1997). Prior to infusion a pre-infusion zero time measurement was made and, thereafter, sampling was at scheduled intervals of 1 h. AMINO ACID ANALYSIS.…”

Effect of aminophylline on metabolic and thermoregulatory responses during hypothermia associated with cold exposure in lambs

“…Catecholamines are involved in the physiological response of ruminants to cold stress (Christopherson et al 1978) and appear to increase metabolic heat production in both adult and young ruminants (Alexander 1979;Graham and Christopherson 1981;Miaron and Christopherson 1997). One of the means by which catecholamines enhance metabolism is through stimulation of adenylate cyclase resulting in formation of 3′, 5′ adenosine monophosphate in target tissues (Lundholm et al 1968;Robison et al 1971).…”