Effects of a ‘CO2 buffer’ on hypercapnia of apneic oxygenation
- 1 December 1959
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 197 (6), 1308-1316
- https://doi.org/10.1152/ajplegacy.1959.197.6.1308
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 O2 saturation was 100%, plasma CO2 53.2 mm/l., plasma HCO–3 50.6 mm/l., arterial blood pH 7.37 and PaCO2 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 CO2 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 CO2 over twice its normal level when its two fractions HCO–3 and H2CO3 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 pCO2 there is no measurable stimulation of the sympathoadrenal system and the circulation is not altered.Keywords
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