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KMID : 0351619690100020069
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Kyungpook Medical Journal
1969 Volume.10 No. 2 p.69 ~ p.80
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CHANGES IN THE CEREBRAL OXYGEN TENSION FOLLOWING CO-POISONING
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Abstract
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Changes in the central nervous system fellowing carbon monoxide(CO) poisoning have been explained to be the result of the anoxemia in which CO fixes the availeble hemoglobin and thus destroys the oxygen carring power of the blood. However, it has not been elucidated clearly whether the effect of CO poisoning on the cerebral oxygen tension is same as that of the simple hypoxia, Gas information in the brain relays information about localized cerebral metabolism which in turn shows cerebral blood flow. To monitor the gas tension in the cerebral tissue, the quantitative oxygen microelectrode is a useful tool, and it opens up a new area in clinical investigation.
The present study attempts to elucidate changes in cerebral oxygen tension at the CO poisoning and the recovery stages, to determine the possible difference in changes of cerebral oxygen tension between the CO poisoning and the simple hypoxia, and to correlate the cerebral oxygen tension with CO and O₂ saturation in arterial blood, arterial blood pressure and central venous pressure. Acute CO poisoing (Group I and Group 2) was induced in anesthetized dog by rebreathing CO gas mixture of 1.4% CO and 50% O₂ at the beginning of the rebreating through closed circuit for 60 minutes. Dogs of the group I were allowed to recover in room air and the group 2 with pure O₂ under 1 atmosphere. Simple hypoxia (Group 3) was induced by rebreathing the gas mixture of 17 ℓ. of room air and 3 ℓ. of O₂ through closed circuit, and racovery was made in the room air. The carebral oxygen tension was measured polarographically by means of Clark oxygen microelectrode.
The results were summerized as follows:
1. The mean value in the cerebral oxygen tension of the control group was 50.3 mm Hg. The cerebral oxygen tension fell progressively following CO rebreathing and the value at the 60th minute was about 7 mmHg, at that time, CO saturation in arterial blood reached about 80%. Cerebral oxygen tension at the recovery stage increased in lineal fashion, but the value did not reach the control value at the 60th minute.
2. In the recovery stage of the group 2, cerebral oxygen tension rose rapidly and reached the control value at the 40th minute.
3. In the group 3, cerebral oxygen tension fell more slowly than those of the CO poisoning groups, and reached 22.4 mm Hg at the 60th minute of low O₂ rebreathing. The cerebral oxygen tension at the recovery stage rose rapidly and returned to the control value at the 20th minute.
4. The possible difference in changes of the cerebral oxygen tension between CO poisoning and simple hypoxia is considered as a result of the shift of the oxygen dissociation curve to the left and some functional damage in the cytochrome enzyme system during CO poisoning.
5. In the group 3, arterial blood pressure rose at the later stage of low O₂ breathing and returned to the control level at the early stage of recovery while the arterial blood pressure declined continuously following CO poisoning.
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