급성 일산화탄소 중독의 생리학적 연구

Abstract

[한글]

[영문]

In view of the frequent incidence of acute carbon monoxide(CO) poisoning among

air crews as well as among those who are daily using briquette, the author

undertook in past a series of stuides concerning (1) the tolerance of mice to CO,

and (2) changes in erythrocyte counts and hematocrit ratios in the CO intoxication.

In these investigations the author derived a formula which would enable us to

compute the appearance time of the respiratory arrest when one breathes various

concentrations of CO. Moreover, it was pointed out that there is a considerable

individual difference in the appearance time of the respiratory arrest for a given

CO concentration. Although it has been previously stated by various investigators

that an increase in the hemoglobin concentration during CO exposure is one of the

most important factors which increase the tolerance of animals to CO intoxication,

there was no obvious correlation between the degree of increase in the hemoglobin

concentration and the apperince time of the respiratory arrest during the acute CO

exposure.

These observations led the author to undertake more systematic studies on this

problem of individual difference in order that one can understand what factors are

involved in determining the tolerance of each animal to a given CO enviroment.

Experiments were carried out on 24 anesthetized dogs. Various measurements were

made on the following 5 experimental groups:

Group A: 0.45% CO in air Group B: 0.45% CO in O^^2

Group C: 0.35% CO in air Group D: 0.12% CO in air

Group E: o.12% CO in air, but anemic(hemoglobin concentration of 6.5gm%)

The following items were determined in each group before and during the exposure

of each animal to a given CO gas mixture:

a. Changes in blood composition such as O^^2, CO^^2, CO, glucose, lactic acid,

hydrogen ion and potassium ion.

b. Changes in blood cells.

c. Changes in various cardio-pulmonary functions such as the alveolar gas

exchange, the pulmonary ventilation, the arterial blood pressure, the pulse rate

and the cardiac output.

Unless the animal died in the middle of experiment as in Groups A, C and E, the

observation was made until 280 minutes after the start of breathing CO gas mixture.

The results may be summarized as follows:

(a) Changes in blood composition;

1. Upon exposure to CO, the arterial O^^2 content of blood decreased while the CO

content increased as expected. However, the CO^^2 content was also reduced

significantly and this is attributable to the hyperventilation which takes place

during CO exposure.

In those groups in which the animal died, the arterial O^^2 content was reduced

to approximately 2 vols %.

2. The arterial blood pH was reduced significantly during CO exposure.

3. Both the blood sugar level and the lactic acid concentrationincreased during

the exposure.

4. The plasma concentration of potassium ion was not altered significiantly

during CO exposure.

(b) Changes in blood cells:

1. The erythroyte count, the hemoglobin concentration and the hematocrit ratio

increased in parallel during the exposure to CO.

2. The leucocyte count also increased significiantly during CO exposure. However,

there was a simultaneous eosinopenia.

(c) Changes in various cardio-pulmonary functions;

1. The minute volume as well as the O^^2 consumption and the CO^^2 output were

increased significantly during CO exposrue. The value of alveolar gas exchange

ratio increased temporarily at the beginning but subsequently returned to the

resting level.

2. The blood pressure and the pulse rate somewhat increased at the very

beginning, but were soon reduced to subnormal level.

3. The cardiac output was increased variably during Co exposure.

In general, these changes were more distinct in Groups A, C and E than in Groups

B and D. In other words, when the concentration of CO is the same as in Groups A

and B or in Groups D and E, the animal with either higher O^^2 concentration (i.e.

Group B) or with higher hemoglobin concentration(i.e. Group D) has the greater

tolerance than that of the raspective control. On the basis of the above

observations, the overall sequence of acute Co poisoning may be summarized as

follows: As oon as the animal is exposed to CO, the arterial O^^2 content is

lowered as the result of formation of carboxyhemoglobin and this reduction in blood

O^^2 content stimulates the anaerobic glycolytic process which would in turn

increase the lactic acid concentration and the hydrogen ion concentration. The

increase in hydrogen ion of blood would induce hyperventilation by stimulating the

chemoreceptors. On the other hand, a sudden exposure to CO may also release

adrenaline as indicated by the increased blood sugar, the pulse rate and the blood

pressure. the increase in the hematocrit ratio may also be attributed to the

splenic contraction due to adrenaline released. However, as the arterial O^^2

ontent drops further, the central nervous system may be suppressed as a result of

which the vasomotor center and the cardiac center become less active and thus the

pulse rate and the blood pressure decrease to a subnormal level. As long as

hyperventilation lasts, the respiratory muscles have to work harder and this would

bring about the increase in O^^2 consumption. Although the greater CO^^2 output was

observed, this could be best attributed to hyperventilation as well as to the

oxidation of CO to CO^^2.

The observed increase in the cardiac output is very difficult to be interpreted

in view of the above statement that the activity of the cardiac center may be

suppressed as a result of the reduction in arterial O^^2, although this elevated

cardiac output would be of great help in prolonging the survival time of the

animal. In other words many changes take place upon exposure to CO and some(e.g.,

increases in the hematorit ratio, in the blood sugar level and in the cardiac

output) of these may undoubtedly increase the tolerance of the animal to CO while

some(e.g., increases in O^62 consumption and in hydrogen ion concentration, and in

blood pressure) may be actually detrimental to the maintenance of life in cO

environment. Hence, it is virtually impossible to single out a factor which is most

important in determining the tolerance of animal to CO.