EFFECT OF PCO2 ON THE RELATION OF LACTATE AND EXCESS LACTATE TO O2 DEFICIT
Abstract
When anesthetized dogs were made hypoxic at constant ventilation, increases in arterial lactate (delta L) compared as well to net O2 deficit (NOD) as did excess lactate (XL). It was asked whether this would hold true if PCO2 was varied during hypoxia. Twelve dogs were made hypoxic for 30 minutes while eucapnic (PCO2 = 40 torr) and again while hypercapnic (PCO2 = 77 torr), with appropriate control and recovery periods. Another group of 12 dogs were treated similarly except one hypoxic period was hypocapnic (PCO2 = 18 torr) and the other eucapnic. NOD was estimated from the total decrease in VO2 during hypoxia by assuming that baseline VO2 would have been unchanged if PO2 was not limited, and by estimating the change in O2 stores during hypoxia. Net O2 repayment (NOR) was estimated similarly. In a graph of delta L against NOD, three different lines were obtained according to the PCO2 level. The same was true for XL against NOD. In 36 or 48 comparisons, NOR was less than NOD. Of the 12 comparisons in which NOR was larger, 7 were hypocapnic, 4 were eucapnic, and only 1 was hypercapnic. In addition to direct effects of altered intracellular pH on lactate metabolism, PCO2 may also alter baseline energy demand during hypoxia by its effect on calorigenesis of liberated catecholamines.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 1967
- Accession Number
- AD0666647
Entities
People
- Stephen M Cain
Organizations
- United States Air Force School of Aerospace Medicine