급격기압강하시의 생리학적 변화에 관한 실험적 연구

Abstract

[한글]

[영문]

The effects of a decreased barometric pressure on a living body have long been a

main problem in the field of aero-space medicine along with the problems associated

with hypoxia and G-force. At present, aircrafts fly at an altitude higher than

40,000 feet which is the critical limit to produce decompression sickness should

the cabin pressurization fail. Thus, in case of either any mechanical failure in

cabin pressurization system or a sudden canopy loss due to the enemy gunfire or to

any other causes, the pilots and air crews become exposed to the rapid lowering of

ambient pressure, known as "rapid decompression". Therefore, the investigation on

the physiological effects of rapid decompression and the establishment of proper

preventive and protective measures are of great importance in the field of

aero-space medicine.

A series of experiments reported here were conducted upon 109 unanesthetized male

rabbits(approximately 2.0kg). Rapid decompression was achieved by puncturing an

acrylic diaphragm separating a parasite chamber (3 cu.ft) from a large low pressure

chamber (360 cu.ft). Decompression was made from the sea levee to an altitude of

approximately 53,070 feet. The pressure change took place in a matter of

approximately 0.9 seconds. The duration required to produce the desired rate of

rapid decompression was calculated by Haber-Clamann equation. The animals were

provided with the equipment for a continuous supply of oxygen. Recompression to the

sea level was started approximately 1 minute and 30 seconds following decompression

and was accomplished in 5 minutes.

Blood samples were obtained by punctures of the left heart before and after the

exposure. White and red blood cell counts were carried out by using improved

Neubauer chambers and eosinophils by Fuchs-Rosenthal chamber and Hinklemann's

solution. Hematocrit ratios were determined by the capillary tube method and

hemoglobin concentrations by Sahli method.

The frequency of respiration was determined by direct visual observation. For

histopathological examination, various tissue specimens were fixed with 10%

formalin, sectioned by paraffin embedding ailed stained with hematoxylin and eosin.

Electrocardiograms were taken by the standard lead Ⅱ and electroencephalograms by

the left fronto-occipital lead. The heart rate was determined by measuring R-R

intervals on ECG. Contents of O^^2 and CO^^2 of anaerobically drawn arterial blood

samples were determined by Van Slyke manometric blood gas apparatus. Measurements

of plasma Na**+ and K**+ concentrations were done by a Beckmann flame photometer,

and paper electrophoresis was applied to determine the albumin and globulin

contents in plasma.

Ⅰ. Physiological responses in rapid decompression:

In total, 38 animals were used for the observation of physiological responses to

rapid decompression.

A) General behavior of animals:

The reactions of the rabbits that were rapidly decompressed to a barometric

pressure of 75.6mmHg and maintained at that level for a period of 1 minute and 30

seconds were in general as follows: a marked abdominal distension occurred: no

observable respiratory movement existed except a slight movement of nasal area for

the first 30 seconds; the animal then collapsed with occasional convulsions of the

extremities for the next 1 minute and 30 seconds. Urination, defecation and

lacrimation were observed in most of the cases.

Upon gradual recompression to lower altitude. occasional respiratory gasps were

followed by recognizable respiratory movements which usually appeared at 38,000 to

40,000 feet (barometric pressure of 140 mmHg-150 mmHg). However, in fatal cases, no

respiratory movements were regained.

B) Tolerance of animals:

The rabbits usually survived an exposure to an ambient pressure of 75 mmHg(53,000

ft) for 1 minute and 30 seconds while an exposure for 2 minutes and 30 seconds or

longer was usually fatal. The survival rate depended upon both the level of

altitude and the duration of an exposure, and a tolerance curve relating these two

functions has been determined.

C) Body weight was reduced by about 6 per cent during the first 24 hours

following the exposure and then gradual]y returned to the pre-exposure level in 10

days.

D) Cardiovascular system:

Peripheral vascular collapse was so marked that it was impossible to draw blood

samples from peripheral veins for subsequent several hours. Heart rates decreased

to approximately 1/5 of the initial rate within first 10 seconds of exposure, and

then gradually recovered to the pre-exposure level in 8 to 10 minutes.

E) The O^^2 content of the arterial blood showed an initial decrease from 16 vols

% to 12, and then gradually increased to the pre-exposure level in two hours.

F) The CO^^2 content of the arterial blood decreased at 9 minutes from 34 vols %

to 26, and then returned to the control bevel in 2 hours.

G) The red blood cell count, hemoglobin concentration and hematocrit ratio tended

to decrease up to 8 hours following an exposure.

H) Eosinophils and white blood cell counts decreased to 50 per cent at 45 minutes

following an exposure, then increased to a level abode the pre-exposure vague at 5

hours and then returned to the control bevel by 8 hours.

I) The plasma K**+ and Na**+ concentrations tended to decrease but there was no

statistical significance.

J) The plasma albumin and globulin contents remained unchanged.

K) Electrocardiographic changes:

Following a rapid decompression, ECG indicated an appearance of sinus bradycardia

in 10 seconds. Signs of myocardial dysfunction and arrhythmia were also recognized.

In fatal cases, the R wave was diminished or completely disappeared.

L) Electroencephalographic changes:

A slow activity in the EEG was noted at 5 seconds. At 10 to 50 seconds, the wave

became flat and then approximately at 2 minutes slow waves began to reappear Gross

EEG disturbances lasted for nearly 30 minutes.

M) Pathological changes:

All of the animals showed characteristic pulmonary lesions whereas specimens from

other tissues (heart, liver, kidney, small intestine and brain) showed no

recognizable changes. The animals which succumbed during the exposure, the reddish

discoloration of the lung was so severe that it was difficult to distinguish it

from the liver; moreover, pulmonary lesions including atelectasis, petechial

hemorrhage and ruptured intra-alveolar septae were observed microscopically.

Survived animals showed a slight reddish discoloration of small areas in the lungs.

However, after one week following the exposure, the pulmonary lesions were not

noticed. Although there exists a possibility of demonstrating the signs of

infarction secondary to gas emboli which would undoubtedly be formed during the

course of a rapid decompression, no evidence has been found in any tissue specimens

examined.

Ⅱ. The mechanism of bradycardia in rapid decompression:

To investigate the mechanism of dramatic bradycardia observed during a rapid

decompression, the following series of experiments have been performed:

A) Asphyxiation of animals:

7 animals were asphyxiated by covering the nose and mouth for one minute with

electrically insulated hands.

B) Asphyxiation of atropinized animals:

Asphyxiation was induced by the same manner as in (A) on 5 animals which received

atropine sulfate (0.1 mg/kg) subcutaneously 20 minutes before the procedure.

C) Water submersion of nose-mouth area:

A large beaker containing water of 22-24℃ was used to produce water submersion

in 7 animals.

D) Water submersion in atropinized animals:

The same proceduer as in (C) was applied to 6 atropinized animals.

E) Rapid decompression of atropinized animals:

6 animals were exposed to rapid decompression following the injection of atropine

sulfate.

F) Rapid decompression of bilaterally vagotomized animals:

5 animals which had been vagotomized bilaterally in the neck portion 5 hours

prior to the procedure were exposed to rapid decompression.

In this series of experiments, animals showed a bradycardia (1/4-1/8 of the

control rate) throughout the period of asphyxiation and recovered to the normal

rate upon release of asphyxiation. However, in atropinized animals, the extent of

bradycardia was prevented to some extent. In case of water submersion, the extent

of bradycardia was up to 1/8 of the control at 10 to 20 seconds and maintained at

this level throughout the submersion and returned to normal upon release of

submersion. This bradycardia observed in water submersion was also partially

prevented by atropinization. In rapid decompression of atropinized animals, no

severe bradycardia was observed. Bilateral vagotomy almost completely prevented the

appearance of bradycardia. These observations indicate that the characteristic

bradycardia observed during a rapid decompression is shared by a simple

asphyxiation or by a simple water submersion of face. Moreover, this bradycardia

observed under various conditions is equally blocked by atropinization or by

vagotomy. It is, therefore, concluded that the characteristic bradrcardia observed

during a rapid decompression is mast likely due to the breath-holding which takes

place during the decompression phase, and also that this bradycardia is mediated by

the vagus nerve.

Ⅲ. Effects of repeated exposure to rapid decompression:

In order to study the residual erects of exposures to rapid decompression, 15

rabbits were repeatedly exposed to rapid decompression (to 53,000 ft. for 1 min.)

every other day on 5 occasions. Observations were made on the changes in white

blood cell, red blood cell and eosinophil counts, hematocrit ratio and hemoglobin

concentration. The measurements were made before the first exposure and 3 hours

after the last.

The red blood cell count and hematocrit ratio revealed only insignificant

changes. However, both white blood cell and eosinophil counts increased. As for the

tolerance of animals, only 50 per cent of the animals survived and the rest died

during the course of exposure. Pathological findings of the lungs were similar to

those described in "I". These results indicate that there exist certain cumulative

residual effects of a rapid decompression, which would eventually bring the animal

to the termination of life upon repeated exposures.

Ⅳ. Effects of chlorpromazine injection:

As indicated above, the only remarkable pathological finding after an exposure to

a rapid decompression was noted in the lung, as manifested by a marked hemorrhage

and atelectasis. Interestingly enough, these changes are strikingly similar to

those obtained during oxygen poisoning. In the latter case, it has been shown by

Gerschman et al. (1955) that chlorpromazine prevents the occurrence of such changes

in the lung. Hence, attempts have been made to study the effect of chlorpromazine

during a rapid decompression. 20 animals were exposed to rapid decompression 20

minutes after chlorpromazine injection. Similar results as described in "I" were

observed except pathological findings of the lung. Three hours after the rapid

decompression, the lung showed only several petechiae in the upper and middle

lobes, and microscopically atelectasis and hemorrhagic signs of a slight degree.

All animal survived the exposure for 1 minute and 30 ,seconds of rapid

decompression to 54,000 feet. One animal even survived the exposure for 2 minutes

30 seconds to 53,000 feet. Considering the above results, the tolerance seemed to

be increased to some extent by chlorpromazine administration. These results

indicate that chlorpromazine has a definite protective effect to a rapid

decompression in terms of pulmonary pathology as well as of survival. However, the

underlying mechanism for this protective effect is not clear at present.