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Korean Journal of Otorhinolaryngology-Head and Neck Surgery > Volume 22(1); 1979 > Article
Korean Journal of Otorhinolaryngology-Head and Neck Surgery 1979;22(1): 25-32.
An Experimental Study on the Effect of Hyperbaric Oxygen in the Oxygen Consumption of the Lung Tissue of the Rats
Yun Taik Kim, MD (Director : Prof. Man Kee Paik, MD)
Department of Otolaryngology, College of Medicine, Seoul National University, Korea
급성산소 중독시 흰쥐 폐조직의 산소 소모량의 변화에 관한 실험적연구
김연택 (지도 : 백만기 교수)
서울대학교 의과대학 이비인후과학교실
ABSTRACT

Oxygen inhalation is one of the most prevalent medical procedures and application of the hyperbaric oxygen in various clinical conditions have been popular since last 20 years. In the point of view of physiological and clinical respect, oxygen toxicity presents serious implications in oxygen therapy. Many hypothesis have been proposed since the discovery of oxygen in 1774. There are many chemical agents claimed as the protectants for the oxygen toxicity. Before the application of probable protectants, the exact mechanism of the oxygen toxicity has to be elucidated clearly to justify the effectiveness of the oxygen toxicity protectants. Auther designed this experiment to observe the change of the oxygen consumption in the lung tissue of the rats which were exposed to different level of oxygen consumption in the lung tissue of the rats which were exposed to different level of oxygen concentration and oxygen tension to clarify the validity of the potent enzyme inactivation hypothesis. The findings observed are as follows : 1) The QO2 of the lung tissue stayed stable in 42% and 64% O2, but in 100% O2, QO2, was reduced compared to the control. 2) The QO2 of the lung tissue exposed to hyperbaric oxygen showed marked reduction of in 4 atmosphere O2, the QO2 was reduced almost to half value of the control, Generally under hyperbaric oxygen, the QO2 was inversely proportional to the level of the atmospheric pressure. This results made possible such a extrapolation that the oxygen inactivated enzyme, especially oxidative systems and the decrease in the carbohydrate metabolism ensued in the reduction of the oxygen consumption of the lung tissue. It seems to be possible that this kind of changes in the functional level will act as the precusor of the clinical lung oxygen toxicity.

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