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At least 19 recordsLinked to original sources
PubMed1979

Adrenal function and the incidence of bends after decompression in mice: effect of adrenalectomy, corticosteroids, decompression intensity, and time of day.

The adrenocortical endocrine subsystem has been demonstrated to enhance mammalian tolerance to harsh environmental conditions, including hypoxia and temperature extremes. In a series of factorial experiments, mice were exposed to one of three elevated hydrostatic pressures for 30 min and then decompressed (0.75 atm/s). It was demonstrated that 1) tolerance to decompression does not differ significantly (P greater than 0.3) in surgically intact, sham adrenalectomized, or in adrenalectomized animals; 2) intraperitoneal administration of pharmacologic doses (0.4, 1.0, and 2.0 mg/mouse) or corticosterone or deoxycorticosterone acetate does not significantly enhance (P greater than 0.1) survivorship when compared to vehicle-injected controls; and 3) the incidence of decompression sickness (DS) does not fluctuate with time of day (P greater than 0.4). In a fourth study, the plasma concentration of corticosterone was quantitated in 1) colony control mice, 2) mice exposed to the 1-ATA chamber environment (chamber control), or 3) mice compressed to 3, 5, 7, 9, or 11 ATA and then decompressed. In general, plasma corticosterone in symptom-free mice was elevated approximately threefold (P less than 0.05) by exposure to the 1-ATA chamber environment and by decompression from 3 to 11 ATA. At 11 ATA, plasma corticosterone levels in decompressed mice exhibiting decompression sickness symptoms were significantly elevated (P less than 0.05) compared to the levels observed in decompressed symptom-free mice. These studies indicate that adrenocortical function does not enhance tolerance to decompression in mice.

Adrenal Cortex Hormones↗
PubMed1976

Intracardial bubbles during decompression to altitude in relation to decompression sickness in man.

Doppler ultrasound was used in five subjects to detect intracardial gas bubbles during decompressions to altitude. At a simulated altitude of 8,000 m, neither intracardial bubbles nor symptoms of decompression sickness occurred. At 9,000 m, bubbles were registered in two subjects, one of which had questionable bends. At 11,500 m, bubbles were registered in all but one subject and two had bends. The three subjects who had not gotten bends were exposed to an air-breathing period of 30 min or, in one case, even 45 min at 2 ATA, for extra nitrogen loading, followed by decompression to 11,500 m. These subjects had heavy showers of bubbles followed by bends. In all cases with decompression sickness during the decompressions to altitude, intracardial bubbles were registered prior to the appearance of symptoms. The technique may be used in studies of decompression sickness without provoking actual symptoms, thus making the studies safer.

Brain Diseases↗
PubMed1976

Hematologic changes in man during decompression: relations to overt decompression sickness and bubble scores.

In order to determine whether asymtomatic gas phase separation causes hematologic abnormalities, studies were carried out following two dive series, one to 210 feet of sea water (FSW) for 50 min and the other to 132 FSW for 30 min. Studies included white and red cell count, red cell indices, platelet count, ESR, fibrinogen, fibrin split products, prothrombin time, partial thromboplastin time, coagulation factors II, V, VII, VIII, and X, clot retraction, platelet aggregation and adhesion, euglobulin lysis time, and platelet factor III. Changes were seen in platelet and white cell count, prothrombin time and partial thrombo-plastin time. White cell count was the only variable which correlated with total bubble score. The results are presented and implications of the findings discussed.

Adult↗
PubMed1979

Species differences in decompression.

In an effort to bring together the diverse laboratory-animal decompression studies, a literature review and statistical evaluation were undertaken. Although 22 different species that had been used in decompression studies were identified, systematic data were available for only 7 of these species: man, goat, dog, guinea-pig, rat, hamster, and mouse. Mathematical functions using physiological data on these seven species were developed to estimate 1) saturation time (the time for the body to equilibrate after an increase in hydrostatic pressure), and 2) no-decompression saturation-exposure limits (the maximum saturation-exposure pressure from which an abrupt return to 1 ATA can be tolerated). Data from man, rat, and mouse were used to develop physiological relationships for two additional decompression variables: change in pressure-reduction limits associated with increased exposure pressure and time to onset of decompression symptoms. Finally, data on rats for two other decompression variables, gas elimination time and optimum decompression stop time, are discussed in the hope that this will stimulate additional animal laboratory research in other mammalians. The general functional relationships developed in this paper provide a preliminary and rough means for extrapolating among species the decompression results obtained during animal laboratory experiments.

Animals↗
PubMed1975

Blood flow during 2-Torr exposures at different decompression rates.

Central and peripheral blood flow of denitrogenated dogs, measured in the femoral artery and aorta, declined rapidly and ceased within mean times of 28, 35, 70, or 90 s after 1-, 10-, 30-, or 60-s decompressions from 258 Torr to 2 Torr, respectively. Neither arterial nor venous hypoxemia was seen after 1-s decompressions since the hypoxic blood did not reach the aorta. In contrast, arterial and venous O2 saturation levels dropped as low as 12 or 6% following 10- to 60-s decompressions since circulation continued. A severe and transient decerebratelike rigidity and subsequent temporary flaccid paralysis of the hind legs was seen during recovery from decompressions slower than 1 s, whereas only a mild temporary flaccid paralysis was frequently present after 1-s decompression. The more severe responses following 10- to 60-s decompressions are associated with the greater hypoxemia after slow decompressions, indicating tissue hypoxia is more severe when decompression rate is slow.

Animals↗
PubMed1975

Factors in 171 navy diving decompression accidents occurring between 1960-1969.

Comparisons were made between the incidence of specific factors in U.S. Navy decompression accidents and the incidence of these factors in routine (nonexperimental) U.S. Navy operational dives. It was found that decompression accidents are disproportionately high among a) air dives less than 140 ft which have bottom times of 30 min or less and air dives greater than 140 ft which have bottom times of more than 15 min, b) Divers First Class, c) older divers, and d) dives which do not involve work or divers which require heavy work. Repetitive dives have a lower decompression accident rate than expected. Decompression accidents were not disproportionately high for any category of body build. These results indicate that the present U.S. Navy decompression tables are extremely safe (5 decompression accidents/10,000 dives), and do not appear to require modification. Future decompression research may be directed toward analyzing the relationship of work and aging to physiological processes involved in decompression. In addition, the present findings should be cross-validated using more recent accident and operational diving data.

Accidents↗
PubMed1975

Changes in hemostatic parameters in fish following rapid decompression.

The effect of rapid decompression on the stress-accelerated blood coagulation system of male and fingerling coho salmon (Oncorhynchus kisutch) was examined after simulated 100- and 200-fsw dives. Blood samples taken either through a dorsal aorta cannula or from a severed caudal peduncle were analyzed for total plasma protein and fibrinogen concentrations, prothrombin times (PT), and partial thromboplastin times (PTT). The effect of mild decompression (100-fsw) on the hemostatic mechanism of both adult and fingerling coho salmon indicated an alternating fibrinogen concentration, declining from normal levels 1 min after decompression, followed by an increase 10 to 15 min later with an eventual loss of fibrinogen to one half the original level an hour after decompression. Partial thromboplastin times were found to increase 10 to 15 min after decompression occurred. Prothrombin times showed an increase 1 hour after decompression in adult salmon, whereas in fingerlings, prothrombin times increased almost immediately from normal levels. The effect of severe decompression (200-fsw) showed similar trends, but at an accelerated rate. It was concluded that both mild and severe decompression activates the hemostatic mechanism of fish which may eventually result in consumption coagulopathy at a greater rate than reported for experimental mammals.

Age Factors↗
PubMed1978

Relationship between CO2 levels and decompression sickness: implications for disease prevention.

Extensive data concerning the incidence of decompression sickness among workers participating in the deepest caisson operation in Japan to date have been collected and analyzed for the period April through August, 1976. When the bottom pressure was between 3.0 and 3.2 ATA, the incidence of decompression sickness was 3.05%; subsequently, the incidence was only 0.96% between 3.2 and 3.4 ATA. The man lock (i.e., decompression chamber) had never been ventilated during the former group of decompressions and the level of CO2 had ranged between 1.8 and 2.3% (v/v); in the latter group of decompressions, the CO2 level ranged between 0.3 and 0.8% with ventilation. All other conditions, including the decompression table used, were the same. Moreover, based upon the nature of the muscular activity required of the caisson workers just prior to decompression, their most common site of affliction was found to lie within the body region where the highest tissue tensions of CO2 would be expected during decompression.

Adult↗
PubMed1979

Evaluation of standard decompression schedule by agarose gel method.

The Standard Decompression Schedule was evaluated by the method of bubble formation in agarose gel, the result of which can be summarized as follows: 1) The number of bubbles formed in agarose gel corresponded well with the exposed pressure. 2) The technique of this method was simple and the number of bubbles was accurately counted. 3) Eventually, this method was useful for examining the decompression schedules. 4) It is not always safe to follow the Standard Decompression Schedule in some pressure conditions. 5) As to the period of time that a person is able to tolerate a high pressure condition, the prescription of the Standard Decompression Schedule is not necessarily correct. 6) The number of bubbles was small by the proper decompression schedule, for example, in the cases of exposure above the 60-meter depth of water. 7) This method can be applied for the prevention of decompression sickness when the agarose gel samples are attached to the workers during the compressed air work. 8) The number of bubbles was inconsistent with the coefficient of body pressure (1. N2 in the body), therefore it is not necessarily safe to rely only on the coefficient of body pressure. 9) To prevent osteonecrosis, the Standard Decompression Schedule is not proper, a deeper first stop and slower ascent being recommended.

Decompression↗
PubMed1976

The response of fish blood cells, particularly thrombocytes, to decompression.

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.

Animals↗
PubMed1976

Decompression-induced decrease in nitrogen elimination rate in awake dogs.

Formulation of safe decompression procedures still requires unproven assumptions regarding both gas equilibration rates and the associated ascent criteria. Although the assumption of symmetry of uptake and elimination rates has been suspect for several years, few data are available. Measurements of actual mixed venous blood nitrogen content [vN2] during compression and following decompression in chronically catheterized awake dogs have clearly demonstrated that desaturation is markedly slower than saturation, and that this effect can be imposed by decompression. The disappearance of arteriovenous nitrogen concentration differences during desaturation following a decompression that produced decompression sickness indicates that cardiopulmonary and cardiovascular changes induced by mechanisms associated with decompression per se can potentiate its deleterious effects. Current US practices do not provide for such asymmetry, while those used in the UK have incorporated this in their models for the last decade.

Animals↗
PubMed1978

Movement by helicopter of patients with decompression sickness.

Rapid movement of a patient with decompression sickness sometimes poses problems when the site of the hyperbaric treatment facility is located a considerable distance away. Six cases of aviator decompression sickness were diagnosed in altitude chamber participants during an 18-month period. Five cases were uncomplicated decompression sickness and the sixth case was of central nervous system decompression sickness. All cases were transferred by low-level helicopter flight. No complications were noted when the helicopter stayed within 200 ft (61 m) AGL of the take-off point. Symptoms of decompression sickness did worsen however, when this altitude was exceeded. This study shows that movement of patients with decompression sickness by low-level helicopter flight is both safe and effective, especially when pressurized aircraft is neither available nor practical.

Adult↗
PubMed1976

Gas phase separation during decompression in man: ultrasound monitoring.

During two dive series, one to 132 fsw and one to 210 fsw, Doppler ultrasonic bubble detectors were used to monitor venous gas bubbles in divers during decompression and for 30 min thereafter. Various decompression schedules were used. Bubble scores were evaluated by independent listerners to tape recordings in a blind manner. A significant increase in bubble scores throughout the stages of decompression and postdecompression was demonstrated as well as a statistically significant relationship between bubble score and decompression sickness. A reduction in mean bubble score was found in divers who made an additional deep decompression stop that was unrelated to the extension of the decompression time. The implications of these findings are discussed.

Adult↗
PubMed1979

Transmastoid decompression of the facial nerve in Bell's palsy.

We describe the technique of decompression of the facial nerve from the geniculate ganglion to the stylomastoid foramen. The decompression was made on 51 patients with Bell's palsy, and the results of follow-up study were compared with those of 77 patients in whom the pyramidal and vertical segments were decompressed. The decompressions were indicated when a severe denervation of the nerve was confirmed by electrodiagnostic examinations. Incidences of notable residual palsy and of pronounced sequelae were always lower in the former group of patients regardless of the operational timing. In either group, a more desirable result was obtained by the decompression within 30 days, but a favorable effect of the decompression was recognizable even when the surgery was performed between 31 and 90 days after the onset.

Adolescent↗
PubMed1976

Influence of long-term intermittent exposures to hypoxia on decompression-induced pulmonary haemorrhage.

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.

Acclimatization↗
PubMed1975

[Indication and prognosis of the transethmoidal decompression of the optical nerve in posttraumatic amaurosis (author's transl)].

In 8 patients with unilateral posttraumatic amaurosis a transethmoidal decompression of the optical nerve was performed. In 4 patients the vision returned completely after operation, 1 patient showed only a partial improvement and in 3 cases the amaurosis remained unchanged. These results agree with those reported by Japanese authors (Sugita et al., 1965; Fukado, 1968) and suggest, that opposite to the neurosurgical transfrontal-intradural resection of the roof of the optical canal the rhinosurgical transethmoidal decompression of the optical nerve may improve the prognosis of the posttraumatic amaurosis, espcially, if the decompression can be done as soon after trauma as possible. Further advantages of this surgical method are the smaller risk, the shorter operation time and the preservation of olfaction. It is emphasized that the rhinologist cannot indicate the decompression of the optical nerve without consulting the ophthalmologist and the neurologist. Contraindications are lesions of the bulbus oculi and the fundus, lesions of the chiasma opticum and a posttraumatic amaurosis caused by a sinus-cavernosus-fistula. Regarding the experiences gained by rhinosurgeons so far the early transethmoidal decompression seems to be indicated, if a unilateral impairment of vision exists right after the trauma or develops within the next 24-48 hrs and if there is no damage to the bulbus and the fundus.

Adult↗