Elimination of CO through the Lung in CO Poisoned Dog

일산화탄소중독시(一酸化炭素中毒時) 폐(肺)로 부터의 일산화탄소(一酸化炭素) 방산(放散)에 관(關)하여

  • Kang, Bann (Department of Physiology, School of Medicine, Kyungpook National University) ;
  • Kim, Kun-Joo (Department of Physiology, School of Medicine, Kyungpook National University) ;
  • Ryo, Ung-Yun (Department of Physiology, School of Medicine, Kyungpook National University)
  • 강반 (경북대학교 의과대학 생리학교실) ;
  • 김근주 (경북대학교 의과대학 생리학교실) ;
  • 여웅연 (경북대학교 의과대학 생리학교실)
  • Published : 1967.06.01

Abstract

In order to evaluate the elimination of CO through the lung comparing with the decrease of CO content in the blood, authors had induced acute CO poisoning on 9 dogs. Arterial CO-Hb saturation, CO concentration, %, in expired gas and eliminated CO amount through the lung were measured at 1,5,10,30,60, and 120 minutes after acute CO poisoning in 6 dogs breathing room air and 3 dogs breathing room air and oxygen alternately. Results obtained are summarized as follows. In room air breathing group, arterial CO-Hb saturation averaged 50.8% , and 53.67 ml of CO was blew off through the lung during 120 minutes and in alternately air and oBygen breathing group, the arterial CO-Hb saturation averaged 65.6% and 95.6 ml of CO was blew off through the lung. The amount of CO eliminated in expired gas for 120 minute was much less than the amount of decreased CO in arterial blood which was calculated with the decreased CO-Hb content in the estimated circulating blood volume. Such difference between the amount of eliminated CO in expired gas and the decreased CO in blood might be attributed to the oxidation of CO to $CO_2$ in the tissues. Concentration of CO in expired gas was markedly increased and the rate of decrease in arterial CO-Hb saturation is enhanced by oxygen breathing. In early period of recovery from acute CO poisoning, neither the CO concentration in expired gas, nor, the rate of CO elimination (unlit 2 minutes after CO poisoning) showed close correlation with the blood CO-Hb saturation level. The reason seemed to be due to irregularly depressed or unevenly stimulated respiration which were induced by acute CO poisoning.

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