Effects of a ‘CO<sub>2</sub> buffer’ on hypercapnia of apneic oxygenation

Gabriel G. Nahas, E. C. Jordan, J. C. Ligou

American Journal of Physiology-Legacy Content · 1959 · 39 citations · 0 references

Concepts

Abstract

Eight dogs maintained in ‘apneic oxygenation’ for 60 minutes were given a .3 M intravenous infusion of 2-amino-2-(hydroxymethyl)-1, 3-propanediol (THAM) in a .3% NaCl solution at the rate of 1.1 ml/ kg/min. After 1 hour of apnea, arterial O 2 saturation was 100%, plasma CO 2 53.2 mm/l., plasma HCO – 3 50.6 mm/l., arterial blood pH 7.37 and PaCO 2 98 mm Hg. Blood pressure remained close to the preapneic control period and intracranial pressure did not change significantly. Plasma catecholamines levels did not change. There was a fall in hematocrit, in Na + and Cl – plasma concentration while K + did not change. After a 20-minute lag, urine output equaled fluid input. Urinary pH was 7.54, HCO – 3 concentration 89 mm/l., THAM 85 mm/l. and 18–28% of the total CO 2 produced by the animal during apnea was recovered in the urine excreted during that time. All the animals survived, indicating that the dog will tolerate well a plasma concentration of CO 2 over twice its normal level when its two fractions HCO – 3 and H 2 CO 3 are in suitable proportion to maintain the biological neutrality of the internal environment (e.g. 7.40). In the presence of a normal pH and an elevated pCO 2 there is no measurable stimulation of the sympathoadrenal system and the circulation is not altered.