The appearance of pulmonary hemorrhage following explosive decompression in rabbits.
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Biomedical subjects
Publications and source records attributed to H S Fang.
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Gold thioglucose-induced hypothalamic obesity caused a higher altitude convulsion threshold and a decrease in the time to altitude convulsion. The average altitude convulsion threshold for the obese mice was 151 torr (38,500 ft). In contrast, the average value for the controls was 131 torr (41,500 ft). It was also observed that at 206 torr (32,000 ft), the average time until altitude convulsion of the obese mice was 69 s; at 179 torr (35,000 ft), 27 s; at 141 torr (40,000 ft), 17 s; at 111 torr (45,000 ft), 10 s; at 87 torr (50,000 ft), 9 s; and at 69 torr (55,000 ft), 8 s. On the other hand, the average control time until altitude convulsion at the above-mentioned altitudes was 97, 37, 26, 11, 9, and 8 s, respectively. Moreover, the average accumulation of fat between pleura and lungs in obese mice was 154 (Table I) or 181 mg (Table II), while the value of the control group was only 72 to 67 mg. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The altitude convulsion threshold and the time until altitude convulsion might thus be changed. The time until altitude convulsion may be regarded as a convenient objective measure of altitude tolerance in mice.
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Altitude convulsion threshold was used for determining the maximal hypoxic tolerance of the mouse during whole-body transverse vibration. Elevation of the lung weight-body weight ratio was taken as evidence of lung edema. It was observed that vibration of 8 cps at 2 mm displacement (peak to peak) or 4 cps at 4 mm displacement did not affect the altitude convulsion threshold and the said ratio. On the other hand, vibration of 12 cps at 2 mm displacement, or 8 and 12 cps at 4 mm displacement caused an increase in a altitude convulsion threshold as well as lung edema. The possible mechanism of these changes is discussed.
Seventeen young rats (40-52 days of age) and 17 old rats (545-702 days of age) were decompressed from one atmospheric pressure to an ambient pressure of 30 mmHg in 0.25 second. It was found that 11 of 34 young lungs (32%) and 23 of 34 old lungs (68%) showed decompression-induced pulmonary haemorrhage. The difference was statistically significant. The pulmonary haemorrhage of the old rats was markedly more severe than that of the young rats.
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Healthy male rats were acclimatized by being placed in a decompression chamber at a simulated altitude of 18 000 feet (5486 m) for three hours daily for 84 days. The altitude acclimatized rats paired with unacclimatized rats were rapidly decompressed together. The range of decompression was performed from on atmospheric pressure to an ambient pressure of 30 mmHg in 0-2 seconds. It was found that in control rats, 14 of 20 lung (70%) exhibited pulmonary haemorrhage following rapid decompression. In altitude acclimatized rats, however, only 6 of 20 (30%) revealed decompression-induced haemorrhage. The difference was statistically significant. The present findings indicate that long-term intermittent exposures to hypoxia might increase the resistance of pulmonary tissue to rapid decompression, resulting in a decrease in frequency and severity of pulmonary haemorrhage. The possible mechanism of such a phenomenon is discussed.
Two hundred suckling mice from 20 litters were used for determining their functional development of the hyperoxic convulsion mechanism. It was found that 1 to 12-day-old mice did not develop convulsion when they were subjected to oxygen under high pressure. The hyperoxic convulsion was observed in 1 of 10 13-day-old (10%), 3 of 10 14-day-old (30%), 16 of 20 15-day-old (80%) and all of 16-day-old mice (100%). This finding indicates that the hyperoxic convulsion mechanism of the young mice takes 13-16 days for functional maturation. Besides, it was shown that hyperoxia could cause pulmonary damage, the incidence of which also increased with age of suckling mice.
Repeated determinations of blood volume and body density were made on 34 Chinese subjects (28 men and 6 women) in Taiwan over a period of 12 yr, as the mean age increased from 31 to 43 yr. Essential body mass calculated from body density and body weight showed no significant change over the 12-yr period. Changes in body weight (mean gain equals 6.0 kg) were attributable to alterations in adipose tissue weight, the density of which was found to be 0.948 g/cm3. In two-thirds of the subjects the second blood volume increased by more than 5% over the first determination, and the mean blood volume for all subjects increased by 7.5% (P less than 0.01). Correlation of the blood volume data with the findings on essential body mass and adipose tissue mass suggests that blood content per unit tissue mass increased in the second determination. This interpretation is supported by the increase in nutrient availability in Taiwan over the 12-yr period, and it may explain the lack of blood volume increase in an earlier longitudinal study on American subjects with stable nutrient availability.
On 27 men and 6 women, total body density and 10 skinfolds were measured 12 yr apart, with the mean age increasing from 31 to 43 yr. The increase in skinfold thickness was found to be related to the increase in total body adiposity, calculated from hydrostatic weighing. The external adipose tissue was calculated from the mean skinfold thickness and body surface area. Variations in total adiposity among the population studied as well as changes in total adiposity with age showed a characteristic distribution with approximately two-thirds on the surface and one-third in the interior. The essential body mass or total adipose mass determined by hydrostatic weighing was compared with the values obtained by water-immersion volumetry, total body potassium counting, and skinfold measurements. Teh volumetric and skinfold determinations gave better estimates of these parameters than total body potassium counting.
A study was made of the effect of hypothalamic hyperphagia on the tolerance of lung to explosive decompression in male Long-Evans rats. The control and hypothalamic hyperphagic rats were explosively decompressed together from 1 atm to an ambient pressure of 30 min Hg in 0.04s. The hypothalamic-lesiones rats gained from 252 g average weight to 460 g, a 82% gain. The respective figures for the controls. were from 248 g to 336 g and 36%. It was also observed that a considerable amount of fat was accumulated between pleura and lungs in experimental animals. The average accumulation of fat between pleura and lungs in experimental rats was 3.23 g, while the value of the control group was only 0.42 g. The difference was statistically significant. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The severity of decompression-induced pulmonary hemorrages might thus be decreased. On the other hand, it also seems possible that the soft fat cushion between pleura and lungs might damp the bruising of the pulmonary tissue against the resistant thoracic wall to a certain extent, thus resulting in a decreased susceptibility to decompression-induced lung damage. Besides , the mortality in obese rats undergoing explosive decompression was also significantly lower than that of the controls
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