Oxygen delivery and utilization in dogs with a sublethal dose of cobalt chloride.

Four groups of eight dogs each were anesthetized with pentobarbital, paralyzed with succinylcholine, and ventilated at constant rate. Control measurements were made for 30 min, then 15 mg/kg of cobaltous chloride was given slowly intravenously to one group. A second group was also given 1 mg/kg per h propranolol (beta-block); a third group was given NaHCO3 to correct pH changes after CoCl2; and a fourth group had both beta-block and NaHCO3. Vo2 was measured every 10 min for 4 h and blood was taken frequently for lactate, pyruvate, and blood gas measurements. Cobalt transiently decreased Vo2 in all groups but significantly more in those with beta-block (groups 2 and 4). Cardiac output and mean arterial pressure were also decreased in all groups but to similar extent. Recovery of Vo2 was complete, usually within 60 min with little evidence of deficit repayment. Total O2 transport (Q X Cao2) appeared to limit Vo2 below 12 ml/kg times min. Above that value, histotoxic effects of CoCl2 reduced Vo2 approximately 20%. Excess lactate (XL) in arterial blood was linearly correlated with measured O2 deficit during the acute reaction of CoCl2, in all but group 3, similar to results previously obtained in hypoxic hypoxia.