[A device for treatment in Kravchenko's 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.
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.
The complex investigation of immune and nonspecific reactivity of 30 aquanauts was carried out during five experimental saturation divings up to 350-500 m accompanied by an increase of microbic contamination in water of the hyperbaric chamber. Peculiarities of humoral immune response and phagocyte functions were found to depend on the inflammatory disease of aquanauts. It is concluded that the situational transitory immune deficiency development under the influence of hyperbaric factors is possible and changes in the microbe spectrum are real.
The effects of high altitude (3000 m, low-pressure chamber) on maximum exercise and maximum oxygen uptake were studied in four normal subjects. In order to separate the effects of hypobaria and of hypoxia, exercise testing was performed under normoxic, hypobaric conditions and compared with the results under normoxic, normobaric conditions. There was no significant difference in performance, nor in the effects of exercise on the measured cardiovascular parameters.
The RSAF two-pressure flying suit system to protect the pilot at high altitude has been tested from different medical safety aspects. To secure adequate alveolar oxygen pressure, the suit admits up to 70 mm Hg (9.3 kPa) positive pressure breathing by counter-pressure against the thorax and by a 3.2 times higher pressure in the anti-G suit. After 1 h of oxygen breathing, subjects were exposed to explosive decompression from an altitude of 9,000 m to 17,500 or 20,000 m in 0.5 s in a hypobaric chamber. No symptoms of decompression sickness or of alveolar rupture with gas embolism to the central nervous system were seen. Pulmonary X-rays after the test did not reveal any signs of lung rupture with extrapulmonary gas leakage. With the precordial Doppler ultrasound technique, intracardial gas bubbles (silent bubbles) could be detected only in one subject after explosive decompression to a 20,000-m altitude in the 10 experiments.
The first results on the dynamic behaviour of middle ear impedenzometric variations starting from an altitude of 3,000 mt and descending constantly by about 1,500 mt/min to sea level, are reported. The research was carried out in a hypobaric chamber, under simulated flight conditions, using the equipment of the Aeronautics and Space Medicine Studies and Research Centre of the Air Force. Evaluation of the results obtained in subjects trained for rapid descents and in others not so trained suggests that the technique used is a useful aid in the diagnosis of the tubal conditions of subjects who are to be subjected to rapid ascents and descents.
A complex evaluation of energy metabolism, oxygen-transport function of blood and physical work capacity of aquanauts has been performed during three imitation divings at depths of 400, 450 and 500 m in heliox as a breathing medium. These experiments have shown that optimal levels of partial oxygen pressure in artificial chamber environment are 30-33 kPa at 4.1 MPa, 32-35 kPa at 4.6 MPa and 33-34 kPa at 5.1 MPa. It is established that 24-days exposure of aquanautes to 4.6 MPa and 10-days exposure to 5.1 MPa yield no unfavourable changes of the examined organism functions. The activated lipid exchange in combination with stable carbohydrate catabolism, the elevated levels of oxygen consumption and its partial pressure in blood and transient fluctuations of erythropoiesis activity are interpreted as compensatory responses of diverse organisms under the influence of hyperbaric factors.
As many as 20 patients with coronary heart disease (CHD) were examined for the efficacy of oxygen pressure chamber therapy (OPCT) combined with drugs. Optimal modes of OPCT were elaborated. The treatment consisted of 10-15 daily sessions with the partial oxygen pressure 0.25 MPa and the exposition 50-60 minutes. The treatment with compressed oxygen arrested or decreased heart pain, improved sleep. OPCT ameliorated the ECG readings, raised exercise tolerance, and made lipid metabolism return to normal. Satisfactory long-term results have also been obtained.
Forty altitude chamber experiments were carried out in which 18 test subjects participated. The purpose of the experiments was to prevent decompression sickness in a pilot using an altitude compensatory suit and oxygen mask. It was demonstrated that oxygen breathing on the ground and at an altitude of 8 km for 20 and 50-60 min eliminated severe symptoms and lowered the frequency of occurrence of mild symptoms of decompression sickness during the subsequent 10-20 and 60-120 min exposures to altitudes of 40,000 and 11,000 m respectively. An increase in the absolute pressure to 240-290 mm Hg in the altitude garment prevented decompression sickness of altitudes of 11,000-15,000 m and eliminated it if it occurred at lower barometric pressure.
The method of the study of medical agent influence and biological active substances on duration of small laboratory animals swimming has been worked out excluding the air. For this purpose the animals were placed into altitude chamber, filled with water by 1/3 (one-third) of its volume being in antiorthostatic position on dipping into water. It has been established that at the altitude of 4000 (four thousand) meters high the rat swimming duration became shorter in comparison with their work under normal pressure in 2.5-4 times. Bemitil stimulating work in hypobaric hypoxia depresses it sharply. Bemitil stimulating influence on the rat efficiency did not appear with rising. Antioxidant substance ionol increased efficiency in normal conditions and in hypoxia AKS-85 adaptogenic compound increased swimming in the height duration to a greater degree, mildronat substance for efficiency restoration produced actoprotective influence.