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Biomedical subjects

J Conkin

Publications and source records attributed to J Conkin.

8 recordsLinked to original sources
PubMed1992

Failure of the straight-line DCS boundary when extrapolated to the hypobaric realm.

The lowest pressure (P2) to which a diver can ascend without developing decompression sickness (DCS) after becoming equilibrated at some higher pressure (P1) is described by a straight line with a negative y-intercept. We tested whether extrapolation of such a line also predicts safe decompression to altitude. We substituted tissue nitrogen pressure (P1N2) calculated for a compartment with a 360-min half-time for P1 values; this allows data from hypobaric exposures to be plotted on a P2 vs. P1N2 graph, even if the subject breathes oxygen before ascent. In literature sources, we found 40 reports of human exposures in hypobaric chambers that fell in the region of a P2 vs. P1N2 plot where the extrapolation from hyperbaric data predicted that the decompression should be free of DCS. Of 4,576 exposures, 785 persons suffered decompression sickness (17%), indicating that extrapolation of the diver line to altitude is not valid. Over the pressure range spanned by human hypobaric exposures and hyperbaric air exposures, the best separation between no DCS and DCS on a P2 vs. P1N2 plot seems to be a curve which approximates a straight line in the hyperbaric region but bends toward the origin in the hypobaric region.

Altitude↗
PubMed1992

A computerized databank of decompression sickness incidence in altitude chambers.

This report describes a hypobaric decompression sickness databank (HDSD) for use with personal computers. The databank consolidates some of the decompression sickness (DCS) information that has accumulated from altitude chamber tests from 1942 to the present. The information was transcribed to a data collection form, screened for accuracy and duplication, and then added to the databank through a computer keyboard. The databank consists of two files; 63 fields contain details of the test conditions in the altitude chamber, the outcome of the test in terms of DCS and venous gas emboli, the physical characteristics of the group of subjects who underwent the test, and the denitrogenation procedures prior to decompression. The HDSD currently contains 378 records that represent 130,012 altitude exposures from 80 sources: scientific journal articles, government and contractor reports, and chapters from books.

Atmosphere Exposure Chambers↗
PubMed1989

Pulmonary hemodynamics, extravascular lung water and residual gas bubbles following low dose venous gas embolism in dogs.

Pulmonary hemodynamic responses, extravascular lung water and bubble longevity times were studied in halothane anesthetized dogs receiving low dose venous gas infusions. Dogs in one group (23.3 +/- 4.3 kg, n = 6) were embolized with air (0.05 ml.kg-1.min -1) for 60 min followed by a recovery period lasting 70 min. During the recovery the ventilatory gases were intermittently switched from nitrogen (68-69%)/oxygen (30%) to nitrous oxide (68-69%)/oxygen (30%) to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure, pulmonary vascular resistance, end-tidal carbon dioxide and arterial carbon dioxide tensions were used to indicate the presence of remaining bubbles that would have expanded in volume with the nitrous oxide ventilation. This embolization sequence was repeated three times to simulate repetitive exposure of the pulmonary circulation to venous gas emboli. In a second group of dogs (20.2 +/- 2.7 kg, n = 8) the venous gas infusions (0.05 ml.kg-1.min-1) were continuous for 180 min, followed by recovery with intermittent nitrous oxide/oxygen challenges to determine bubble longevity. Pulmonary hemodynamic and carbon dioxide data were significantly changed from baseline following each embolization. These differences as well as the development of extravascular lung water (edema formulation) were not significant when comparisons were made between the Repetitive gas embolism group after 180 min. Residual pulmonary vascular bubbles were indicated (mean +/- S.E.M.) 26.9 +/- 2.3 min following the 180 min Continuous venous gas infusion and 39.5 +/- 5.3, 46.4 +/- 5.0 and 55.5 +/- 4.4 min, respectively, following the three 60 min Repetitive venous gas infusions.

Animals↗
PubMed1987

The effect of extended O2 prebreathing on altitude decompression sickness and venous gas bubbles.

The purpose of this study was to determine the effect of extended O2 prebreathing on symptom and bubble incidence during decompressions simulating extravehicular activity. The 38 subjects breathed O2 for a 6-h period prior to decompression to 4.3 psi. The subjects performed upper body exercise for 6 h. Subjects were monitored with a Doppler bubble detector and were encouraged to report all symptoms. Eight subjects were exposed to the same protocol after an 8-h prebreathe. Venous bubbles were detected in 18 of 38 subjects decompressed after the 6-h prebreathe. Four of these subjects reported symptoms of altitude decompression sickness. No symptoms or bubbles were detected in the eight subjects who had prebreathed 8 h. The incidence of symptoms and bubbles when combined with prior data on 3.5- and 4.0-hour prebreathes showed an inverse correlation to pre-breathing time. The incidence of symptoms was higher than has been reported for subjects exposed to decompression of shorter duration with less activity.

Adult↗
PubMed1986

Blood biochemical factors in humans resistant and susceptible to formation of venous gas emboli during decompression.

Blood biochemical parameters were measured in 12 male human subjects before and after exposure to a staged decompression protocol, with simulated extravehicular activity, during 3 days. Following the exposure, significant changes occurred in several parameters, including increases in blood urea nitrogen, inorganic phosphate, potassium, and osmolality, and decreases in uric acid and creatinine. Pre-exposure blood samples from subjects who were susceptible to formation of venous gas emboli (VGE) during decompression exhibited significantly greater levels of total cholesterol, high density lipoprotein cholesterol, potassium, inorganic phosphate, calcium, and magnesium. The results indicate that, following this decompression profile, small but significant (P less than 0.05) changes occur in several blood biochemical parameters, and that levels of certain blood factors may be related to susceptibility to VGE formation during decompression.

Adult↗
PubMed1983

Decrease of ether induction time after exposure to dysbaric conditions in rat.

In 22 adult male albino rats (means = 565 g) it was consistently observed that the time required to anesthetize them with 5 ml of diethyl ether after a hyperbaric exposure of 6 ATA using compressed air decreased depending on the severity of the animals' post-decompression reaction to the compression-decompression exposure. Monitoring the time required to lightly anesthetize adult male rats with diethyl ether to a point of losing the righting reflex after a particular compression-decompression exposure provided an indication of the rats' post-exposure state of health. This technique aided in correctly establishing if a rat developed a degree of decompression sickness that may have otherwise gone unnoticed. The loss of resistance to ether induction as a result of decompression sickness may be related to alterations in the blood-brain barrier, blood perfusion inequities, or changes in cardiopulmonary mechanics due to the presence of gaseous emboli. Rats that survived the compression-decompression exposures showed a marked resistance to ether induction after 24 h of recovery.

Animals↗
PubMed1982

Investigation of the combined effects of bedrest and mild hypoxia.

Subjects were exposed to an 8-h mild hypoxia exposure (8000 ft. equivalent, 2438 m) with and without a 28-h period of 6 degrees headdown bedrest. Anticipated responses to the bedrest and the hypoxia were observed. There was no indication that bedrest affected the arterial oxygenation or the oxygen gradient across the lungs of the subjects undergoing mild hypoxia. It is concluded that there is no evidence that would preclude an alveolar O2 pressure as low as 69 torr during contingency spacecraft operation.

Adult↗