[Operating the Irtysh-2MT atmosphere exposure chamber].
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1,3-butadiene, which is used extensively in the synthetic rubber industry, is a highly reactive, potentially explosive compound, presenting particular problems for the design and execution of inhalation toxicity studies. Before undertaking inhalation studies with butadiene, it was necessary to develop safe systems for the generation and control of stable exposure chamber atmospheres. Infrared and gas chromatographic analytical methods were adapted for monitoring the concentration and distribution of butadiene in exposure chambers, and for analysis of known impurities, particularly, t-butyl catechol and 4-vinyl-1-cyclohexene, in atmospheres generated for inhalation tests.
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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.
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.
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An environmentally-controlled extended-use small animal hypobaric chamber has been designed to study small laboratory animals at low barometric pressures for long periods of exposure. The rectangular chamber (91.4 X 71.1 X 50.8 cm) is constructed of aluminum plate and acrylic resin with a volume of 3.3 X 10(5) cm3. A computer/data acquisition control unit provides for controlling and collecting data on pressure, temperature, and relative humidity (RH) for sustained operations. Altitude simulation is achieved using a two-stage, air-cooled vacuum pump with a displacement of 30 cm3 X min-1. The pressure within the chamber is controlled by an incremental throttling valve in the vacuum line. Temperature (0-100 degrees C) is accomplished by using a remote-controlled constant temperature circulating bath. RH (20-80%) is regulated by pre-conditioning the ventilation purge air prior to entering the chamber. Acceptable levels of oxygen and carbon dioxide gases are maintained by purging with sufficient volumes of fresh air.
The effects of decompression on various blood-cell types in chinook salmon (Oncorhynchus tshawytscha) were investigated using a 4-liter hyperbaric chamber. Thrombocytes (platelets) were found to decrease significantly in numbers following lethal and nonlethal decompressions. The response was highly dependent on depth, gas solubility, and rate of decompression, whereby increasing depth or gas solubility caused greater and faster declines of thrombocyte levels. Return of thrombocyte numbers to normal values usually occurred within 48 hours, except after the more severe decompressions where recovery was never fully attained during the sampling period. Erythrocyte levels increased significantly 1 day after a severe decompression, suggesting hemoconcentration. Leucocytes appeared not to respond to decompression; they were not decreased compared to normal levels, although they were significantly decreased compared to levels of the chamber controls in the nonpressurized chamber. The results are discussed in relation to possible involvement of the fish's blood-coagulation system after decompression.
The dive (Hana Kai II) described in these papers was designed to determine the effects on man of a prolonged exposure to a dry helium-oxygen hyperbaric environment. Comprehensive studies on energy balance, body fluid balance, cardiorespiratory functions, maximal oxygen uptake, psychological performance, and physiological responses to cold were performed at a simulated depth of 580 ft (18.6 ATA) over a 30-day period in March-April 1975. Following a 3-day predive control period at 1 ATA air (period 1), 5 male divers spent 17 days at 18.6 ATA in a helium-oxygen environment (periods 2-6), and returned to 1 ATA air after 7 days of decompression (periods 7-8). They stayed an additional 3 days inside the chamber for postdive control measurements (period 9). The chamber temperature was maintained at 25-27 degrees C during periods 1 and 9, 30-31 degrees C during periods 2-5, and 27-28 degrees C during period 6. At 18.6 ATA, the PO2 and PCO2 of the chamber gas were maintained at approximately 225 and 2 mmHg, respectively. In this introductory paper, physical and physiological characteristics of individual subjects, the major daily activity schedule, and the scope of investigation are presented.
Lowering of the ambient pressure has been reported to have a positive effect on the symptoms in Menière's disease. In order to further investigate this hypothesis the symptoms in the long-term span were studied in 54 Menière patients who had undergone low-pressure chamber tests. Lowering of the ambient pressure can induce a temporary but not a permanent hearing improvement in patients with Menière's disease. The results also indicate positive effects on other symptoms in Menière's disease, but this could not be statistically proven.
An interrupted compression profile technique was used to develop data to separate the effects of time and pressure factors governing increase of high-pressure neurological syndrome (HPNS) convulsion threshold pressures (the compression rate effect) during different compression profiles. A single differential equation fits all data available to date for compression rate effect on convulsion thresholds of CD-1 mice (three distinct types of compression profile; mean compression rates 12-1,000 atm/h). The process leading to increase in HPNS convulsion pressure is initiated at the very beginning of compression, proceeds at increasingly rapid rates as higher pressures are attained, and approaches a limiting upper convulsion pressure. The convulsion threshold pressure in any given experiment is independent of the compression rate prevailing during the time immediately preceding onset of the seizure. The magnitude of the compression rate effect in the CD-1 mouse is independent of chamber temperature over a range of 27-36 degrees C, and rectal temperatures of 29.2-37.5 degrees C. The bearing of these results on the design of optimal compression schedules and on the analysis of the neurological mechanisms underlying the HPNS is discussed.