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At least 721 records · Page 40Linked to original sources
PubMed1983

Cardiovascular effects of induced decompression sickness in sheep fetus.

Ten chronically catheterized near-term sheep fetuses were used to study the effect of induced intravascular bubbling on fetal placental vascular dynamics and fetal regional blood flows. Fetal blood pressure and heart rate were measured, and radioactive microspheres were administered to fetuses before and 5, 10, 15, and 20 min after a simulated no-decompression dive to 100 fsw (4 ATA) for 25 min. A decrease in brain blood flow was the only effect observed 5 min after decompression. Fifteen minutes later arterial hypertension was evident. Eight fetuses displayed arrhythmia, but there was no significant change in heart rate, myocardial blood flow, or resistance. There was a reduction in blood flow, and a concomitant increase in vascular resistance, in the gut, kidneys, placental membranes, and skeletal muscle, as well as in the brain. Total placental blood flow was unchanged throughout the postdive period, although placental vascular resistance was elevated 20 min after surfacing. Analysis of the placental blood flow at the cotyledonary level in 6 animals revealed no uniform response to decompression. The results are consistent with the hypothesis that the instrumented fetus suffers widespread vascular embolization and disruption of organ blood flows. We conclude that the observed changes in the fetal cardiovascular system, however, are not precipitated by an initial effect of decompression on the fetal placental circulation.

Animals↗
PubMedDate not supplied

[Prevention of decompression sickness as applied to conditions of multiple space walks].

Six 3-day experiments were carried out in an altitude chamber in which 6 test subjects took part. The experiments simulated repeated extra-vehicular activities--intensive work at an altitude of 10,000 m in a helmet or at an altitude of 40,000 m on a space suit pressurized at 200 mm Hg. It was demonstrated that altitude decompression could be prevented by desaturation--prolonged exposure to the hypobaric atmosphere (430 mm Hg) and 100% O2 or a 40% O2 and 60% N2 mixture. During the 3-day experiment the test subjects made seven 3--4 hour excursions, showing no symptoms of decompression disease.

Adult↗
PubMed1979

Correlation between decompression sickness and circulating bubbles in 232 divers.

Doppler monitoring examinations were carried out during 67 simulated helium-oxygen dives in the pressure chambers of the Centre d'Etudes Hyperbares (CEH) COMEX Marseille, and involved a total of 232 COMEX professional divers. Three to five detections were done in each 24-h period, each consisting of an observation at rest and an observation after deep knee bends. Recordings of the Doppler signals were subsequently analyzed by experienced listeners and graded according to the system described by Spencer and Johanson (1974). The two vestibular decompression accidents in this series were associated with bubble scores of grade 3 at rest; one occurred during the rapid initial phase of a bounce dive decompression and the other after return to the storage depth after an excursion dive. Twenty-five cases of muscular or joint pains were observed. A higher incidence of this type of problem was found with higher bubble grades in general, although it was not possible to predict pain.

Adult↗
PubMed2005

[Experimental study on mechanism of recompression therapy of decompression sickness].

OBJECTIVE: To elucidate that recompression is the most efficient measure in removing the pathogenic factors. METHOD: When rabbits were suffering from severe DCS, their pressure were immediately compressed to 0.5 Mpa. Precordial region was monitored continuously with a Doppler flow meter, micrography of the bulbar conjunctiva was done intermittently and the behaviors of the animals were recorded. RESULT: Effects of therapeutic recompression and elimination of circulating bubbles were correlated to rate and extent of recovery of microvascular function. The animals' DCS with severe dysfunction or failure of blood vessels, DCS became worse owing to progressive impairment of microvascular function during recompression and decompression. CONCLUSION: The pressure could only cancel the tension provoked by supersaturated gas in the blood so as to relieve the spasm of the compensatory blood vessels, which can restore the blood circulation and reverse the developing course of the DCS. The pressure, however, couldn't recover the function of the blood vessels with severe dysfunction or failure, or repair the injured tissues, or eliminate the circulating bubbles directly.

Air Pressure↗
PubMed1995

Effects of physical properties of the breathing gas on decompression-sickness bubbles.

To explore the relative dangers of different inert gases, we developed mathematical relationships concerned with bubble growth, using equations that separate gas properties from other variables. Predictions for saturation exposures were as follows. 1) Peak volume of a bubble is proportional to solubility in tissue when bubble density is high and to the 3/2 power of the ratio of the permeation coefficient to the partition coefficient when density is low. 2) Bubble duration is inversely proportional to the partition coefficient for the inert gas. 3). Sizes and durations of bubbles for one inert gas relative to another depend on whether the tissue is aqueous or lipid but are independent of the magnitude of the decompression and tissue half time. 4). He should give smaller bubbles than N2, except in aqueous tissue with low bubble density; our prediction correlates qualitatively with relative dangers observed with animals but seems to overestimate the safety afforded by He. Numerical simulations illustrate how nonsaturation dives are less predictable because more variables are involved.

Decompression Sickness↗
PubMed1985

Recovery from alpha coma after decompression sickness complicated by spinal cord lesions at cervical and midthoracic levels.

A modified alpha pattern activity occurred in the EEG of a 21-year-old man during recovery from a diving injury. It persisted for 10 days but finally the EEG became normal. There was clinical and neurophysiological evidence of additional separate lesions in the cervical and mid-thoracic spinal cord. The latter resulted in spastic paraplegia but the patient made an otherwise good recovery.

Adult↗
PubMed1974

Bone and joint lesions in decompression sickness.

1 Of 450 divers, 268 (59.5%) has aseptic necrosis of bone; 81 had articular lesions. 2 In proportion to duration of diving experience and maximum depth of diving, incidence of bone necrosis increases. 3 The radiological lesions have been classified by modified Ohta-Matsunaga criteria. 4 Yearly progress of bone changes were mentioned. 5 Pathological appearances of aseptic necrosis of bone in divers are compared with different types of bone necrosis. 6 Experimental studies for aseptic necrosis were mentioned. 7 Etiology of bone necrosis is not yet clear, but some etiological factors were discussed. It was suggested that fat embolism was an important factor, because fat embolisms were seen in our pathological findings of the divers and compressed-air workers. 8 Periodic radiological examination of the bones of divers and compressed-air workers should be carried out. It is important to research the new modified decompression table to prevent bone necrosis. 9 Surgical treatment of bone necrosis was mentioned.

Adolescent↗
PubMed1979

Utilization of a central auditory processing test battery in evaluating residual effects of decompression sickness.

Six professional divers were examined as patients who presented peripheral auditory, vestibular, or central symptoms attributed to incidents which occurred while diving. Each diver received a central auditory processing (CAP) test battery consisting of: (1) a dichotic sentence listening task, (2) a monotic filtered word task, (3) a binaural fusion task, and (4) an alternating speech task. The CAP test results, in all cases substantiated other neurological/vestibular test battery results which we have reported in detail previously.

Adult↗
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↗
PubMed1987

Decompression sickness in women divers.

The comparative incidence of DCS in women has been debated for years. Diving log data from the Naval Diving and Salvage Training Center (NDSTC), Panama City, FL, demonstrate that there is no increased risk of DCS among Navy female divers compared to their male counterparts. Twenty-eight female students were compared to their 487 male classmates on 878 air and helium-oxygen dives between 4.64 and 10.10 ATA (120 to 300 fsw). None of the women experienced DCS while 8 men developed DCS symptoms. The total duration of the dives ranged from 8 min to 2 h and 6 min; bottom times were less than 20 min. Theoretical inert gas supersaturation on these profiles are commensurate with those experienced on 40- to 60-min sport scuba dives.

Adult↗