Abstract
Rapid recovery from severe carbon monoxide poisoning under X-ray treatment 1 , 2 and spectrographic evidence of the reduction of blood CO after X-ray treatment 3 have previously been reported. A recent publication has described progressive discontinuous stages of decreased resistance to CO among young rats and rabbits during the first few days after birth. 4
Some attempts have lately been made to determine the factors responsible for these phenomena. Each of several kinds of effects has been considered and there may be others not yet investigated.
The release of reserve red cells from the spleen in response to X-ray injury to circulating cells has often been described, 5 but a latent period, or lag, of 6 hours or more is associated with this process. In CO recovery the effect must be maximal within so short a time after the onset of asphyxia that the release of this reserve seems to be ruled out.
Possible recombination of CO and O2 in the blood and tissues to form CO2 ereduce the amount of CO present was checked in 12 experiments carried on in CO and O2 saturated water at body temperature. In none of these tests was the amount of CO2 (determined as carbonate) significantly increased by X-ray exposures of 500-2,000 γ . Actual differences in cc of standardized HC1 used were 0.4-0.55; 0.45-0.5; 0.07-0.27; 0.35-0.3; 0.45-0.42; 0.4-0.25; 0.18-0.1; 0.1-0.15; 0.2-0.25; 0.1-0.05; 0.2-0.15; 0.3-0.41, an average of 0.09 when a difference of 0.2 might be significant. Dr. Daniel Mazia and Dr. Lloyd B. Thomas kindly advised me in this work. Dr. L. J. Stadler, of the U. S. D. A. and the Department of Field Crops, University of Missouri, generously provided the X-ray services for the work discussed here.
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