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At least 37 records · Page 2Linked to original sources
PubMed1975

Relationship between saturation exposure pressure and subsequent decompression sickness in mice.

Despite the fact that the pressure reduction is acknowledged to be the single most cogent factor in producing decompression sickness, little has been done to define accurately the allowable limits beyond 2 ATA. This study provides some theoretical guidelines for future manned dives related to this problem. There were 324 albino mice used to define the relationship between saturation exposure pressure and the safe abrupt pressure reduction. The results from both the helium-oxygen and nitrogen-oxygen exposures support the idea of a linear, depth-dependent relationship between the saturation depth and the allowable pressure reduction. Support is presented for the use of a modified decompression ratio P1/P2 (P1 equals saturation pressure and P2 equals pressure following decompression) to account for the observed incidence of decompression sickness. An attempt is made, using the existing human data to relate this empirical relationship to the operational dive setting.

Animals↗
PubMed1994

Effect of atmospheric pressure on hearing in patients with Menière's disease.

Hearing in patients with Menière's disease improved when they were treated in an underpressure chamber. In this study 46 patients with neurotological diseases, including 32 cases of Menière's disease, were tested in an overpressure chamber. As a result, hearing in 32% of the patients with Menière's disease improved, although this was lower than the 50% rate of improvement in Menière's disease patients tested in an underpressure chamber.

Atmosphere Exposure Chambers↗
PubMed1975

Increased susceptibility to pulmonary oxygen toxicity after cholesterol biosynthesis inhibition.

AY-9944, a cholesterol biosynthesis inhibitor, reduces adrenal corticosteroid production and may accelerate pulmonary surfactant production. Divided into four experimental groups were 130 male 100-g, 5-week-old Wistar-Lewis rats. Group 1 received no injections. Group 2 received 0.5 ml N NaCl ip qd times 21 d, and Group 3 received 1.5 mg AY-9944 in 0.5 ml N NaCl ip qd times 21 d. Group 4 animals received 5.0 mg hydrocortisone phosphate in 0.5 ml N NaCl sc qd times 7 d. All injections were done prior to exposing the animals to 98-99 plus % oxygen at 1 atmospheric pressure (OAP) for varying lengths of time. AY-9944 treatment resulted in a significant (p smaller than 0.05) reduction in body growth by Day 7 when compared to saline-injected litter-mates. By Day 21 this difference was highly significant (p equals 0.00002). Lungs from AY-9944 treated rats were heavier than the lungs from the other groups. Surprisingly, there were no differences in lung deflation compliance or area of pressure-volume loop hysteresis between groups before expsoure to O2. Exposure to OAP caused significant increases in lung weights and lung weight/body weight ratios by 48 h in all groups. Lung dry/wet weight ratios decreased in all groups initially but returned to non-OAP levels at 72 h. Lung compliance had decreased significantly from non-OAP levels 56 h in the normal (p equals 0.018), AY-9944 (p equals 0.045) and hydrocortisone (p equals 0.002) groups and after 72 h in the saline group (p equals 0.0015). AY-9944-treated rats had the highest mortality rate from OAP. By 72 h OAP, 40.0% of the normal, 42.9% of the hydrocortisone, 50.0% of the saline, and 100% of the AY-9944 animals were dead. Our study suggests that the effect of AY-9944 on lung lipid metabolism is more detrimental in OAP-exposed rats than the expected benefit of AY-9944's simultaneous reduction in adrenal cortical activity.

Animals↗
PubMed1980

[Functional morphology of myocardial ultrastructure during prolonged adaptation to pressure chamber hypoxia].

The myocardium of the right and left heart ventricles of rats was studied during 2.5-month adaptation to high-pressure chamber hypoxia (at an altitude of 6000 m). During varying time of rats' adaptation to hypoxia, destructive and compensatory-adaptive processes in the cardiomyocytes were seen concurrently. In long-term adaptation to high-pressure chamber hypoxia there developed hypertrophy largely of the heart right ventricle on account of hyperplasia and hypertrophy of individual intracellular organelles, particularly of mitochondria. The animals who adapted to high-pressure chamber hypoxia showed enhanced metabolic processes in the myocardium.

Adaptation, Physiological↗
PubMed1994

Mechanism of hearing disturbance due to alteration in atmospheric pressure.

We used a soundproof pressure chamber to examine how the changes in atmospheric pressure as experienced in daily life reduces bone conduction in a total of 48 normal adults. The subjects were given special ear plugs that connected external auditory canal to the pressure gauge and a small pump located outside the chamber, and were instructed not to swallow, to avoid active opening of the Eustachian tube. The chamber pressure was increased (or decreased) to +/- 500 mmH2O at a rate of 33 mmH2O/s. Then pressure in the external auditory canal was increased (or decreased) gradually after the chamber pressure had reached +/- 500 mmH2O, to equilibrate the pressure across the ear drum. Bone conduction did not recover the level before increase (or decrease) in the chamber pressure. We conclude that at least a minor part of the deterioration in bone conduction after changes in the chamber pressure was caused by displacement of the round window membrane.

Adult↗