THE EFFECTS OF BRONCHODILATORS ON SPONTANEOUS VENTILATION AND OXYGEN-CONSUMPTION IN RHESUS-MONKEYS

The effects of breathing normal saline, salmeterol, fenoterol, ipratro pium bromide, or formoterol, and of i.v. infusion of theophylline on o xygen consumption (VO2), carbon dioxide production (VCO2), minute vent ilation (VE), heart and respiratory rates, and end-tidal carbon dioxid e tension (PETCO2) have been defined in 10 anesthetized, intubated rhe sus monkeys (mean age 7.0 y, weight 10.2 kg), VO2 increased over contr ol by +17.1% after salmeterol (p < 0.001), +33.3% after fenoterol (p < 0.001), +23.7% after formoterol (p < 0.001), +3.9% after theophylline (p < 0.01), but did not change after ipratropium bromide and normal s aline. VE increased by 63.0% after fenoterol (p < 0.001), 49.8% after formoterol (p < 0.001), 31.7% after salmeterol (p < 0.01), and 29.7% a fter theophylline (p < 0.001), but not after ipratropium bromide or no rmal saline. Heart rate response was greatest after fenoterol, formote rol, and salmeterol, respectively. PETCO2 dropped dramatically after t heophylline (-15.7%, p < 0.001), but not at all with any of the inhale d beta(2)-adrenoceptor agonists. In seven animals, salbutamol (albuter ol) caused an increase in VE and VO2 of 50.1% and 45.9%, respectively, whereas in the presence of a beta(2)-adrenoceptor antagonist {racemic or (+/-)-propranolol (0.1 mg/kg i.v.)}, inhaled salbutamol (2.5 mg/mL for 10 min) could not increase VE (+6.2%, p > 0.05) and VO2 (+1.6%, p > 0.05). The increase in VO2 and VE after administration of beta(2)-a gonists may be partly the result of direct stimulation of the respirat ory center and partly a response to increased metabolic rate. The dram atic increase in VO2 and VE after salbutamol was suppressed in the pre sence of propranolol, which is consistent with a beta-receptor-mediate d mechanism.