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KMID : 0383119630110020001
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Journal of Aerospace Medicine
1963 Volume.11 No. 2 p.1 ~ p.15
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PHYSIOLOGICAL EFFECTS OF RAPID DECOMPRSSION IN THE RABBIT
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Abstract
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The effects of a decreased barometric pressure on a living, body have long bean 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 other: 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 serie3 of experiments reported here were conducted upon 38 unane thetized male rabbits (approximately 2.0 kg) Rapid Decompression was achieved by puncturing a acrylic diaphragram separating a parasite chamber ´(3 cu. ft) from a large low pressure chamber(360 cu. ft). Decompression was carried from the sea. level to an altitude of approximately 53,000 _feet. The pressure change took placc in a matter´ of aPP-roximtely 0.9 seconds. The duration required to Produce the desired. rate of rapid decompression was calculated by Haber-clam hnn examination. 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 acomplished in 5.Minutes.
Blood samples were obtained by punctures of the left heart before and after the exposure. Wh.ite and red. blood cell counts were carried out by using improved Neubauer chambers and Eosinophils by Fuchs-Rosenthal chamber: and Ninklemann´s:´solution. Hematocrit ratios were: detemined by the capillary tube method and Hemoglobin concentrations by Sahli method.
The frequency of respiration was deternimined by direct visual observation. For histopathological examination, various tissue specimens were fixed with 10 / formalin, sectioned by Paraffin embedding and stained with hematoxylin and eosin Electorocardiogrms were taken by the standard lead II and electroence phalograms by-the left fronto-ociPital lead. The heart rate was
determined by measuring R-R intervals on ECG. Contents of Og and COQ of anaerobically drawn arterial blood samples were determined by Van Slyke manometric blood gas apparatus. Measurement of plasma Na 4 and K+ concentrations were done by a Beckman flame photometer, and paper electrophoresis Bas applied to determine the albumin and globulin contents in plasma.
Results
A) General behavior of animals:
The reactions of the rabbits that wore rapidly decompresed .to a barometric pressure of 75.6 mmHg. and maintained at that level for a period hof I minute and 30 seconds were in general as =follows: a marked abdominal distension occur: red; no observable respiratory movement existed a slight movement of nasal area for- the first X30 seconds- the animal then- collapsed with goccasional convulsions of the extremities for the "next Immute.´and´30seconds..Urination,. defetion and lacrimation were observed in most if the cases.
Upon gradual ;recompression_ to -´lower altitu e, an .occasional respiratory gasps are , foliowed by recognizable respiratory movements hich usually appeared, at 38, 000 to 40,:000 feet barometric pressure of 140mmHg-150 mmHg). owever, in fatal cases, no respiratory move ants were regained.
B) Tolerance of animals: he rabbits usually survived an exposure to ambient pressure of 75 mmHg(53, 000 ft) for mute ´and 30 seconds while an exposure for´ Inutes.arid 30 seconds orionger was usually fatal, The surival 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 gradually returned to the pre-exposure level in 10 days.
D) Cadiovascular system
Peripheral vascular collapse was so marked that it was impossible to draw blood samplings. from peripheral veins for subsequent several hours. Heart rates were decreased to appr oximately V5 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 02 content of the arterial blood showed an initial decrease from 16 vols / to 12, and then gradually increased to the preexposure level in two hours.
F) The COQ content of the arterial blood
decreased, at 9 minutes, ´from 34 vols % to 26 and then returned to the control level in 2 hours.
G) The red blood cell count, hemoglobin concentration and hematocrit ratio tended to decrease up to 9 hours followng an exposure.
H) Eosinophils and white blood cell. counts were decreased to 50 per- cent at 45 minuts following an exposure, then increased to a)evel, above the ´pre-exposure value at 5 hours and
then returned to the control level 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 .dysfuncsion;and arrhythmia were: also recognized. In fatal
cases, the R wave was dininished or completely disappeared.
L) Electroencephalographic changes:
A slow activity in the EEG wag 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 where as specimens from other tissueg(heart, liver, kidney, small intestine, and brain) showed no recognizable changes. The animals which succumbed during the exposure, the reddish discoloration of the lung wag 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 a week following the exposure, the pulmonary lesions were not noticed. Although thepe exists a possibility of demonstrating the signs of infarction secondary to gas emboli which would undoubtedly be formed during the course of a rapid decompr. ession, no evidence has been found in any tissue specimens examined.
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