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Biomedical subjects

P Denoble

Publications and source records attributed to P Denoble.

8 recordsLinked to original sources

Effect of a single air dive on pulmonary diffusing capacity in professional divers.

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

Adult

Flying after diving and decompression sickness.

Reports of 1,159 decompression sickness (DCS) incidents during recreational diving were analyzed by logistic regression for the effects of flying on the occurrence of Type II DCS, complete relief of symptoms after one recompression, and residual symptoms 3 months after treatment. The relevant diver populations were those who: 1) did not fly; 2) had symptoms before flying but flew anyhow; 3) and did not have symptoms before flying but developed symptoms during or after flight. Of the total DCS population, 13.9% had preflight symptoms while 5.6% developed symptoms during or after flight. Symptoms which occurred during or after flight were no more serious and their responses to recompression no less successful than symptoms in nonflying divers. There was a statistically significant association between divers who flew with pre-existing symptoms and Type II DCS, incomplete relief with one recompression, and residual symptoms after 3 months.

Adult

Lung diffusing capacity in a hyperbaric environment: assessment by a rebreathing technique.

A rebreathing method was developed for measuring diffusing lung capacity for carbon monoxide (DLCO) in a hyperbaric environment. Twenty two professional naval divers with normal lung function were included in the study. Significant correlations were found between rebreathing and single breath measurements for DLCO (r = 0.94; p less than 0.001; standard error of the estimate (SEE) = 0.66), alveolar volume (VA) (r = 0.79; p less than 0.005; SEE = 0.51), and DLCO/VA (r = 0.83; p less than 0.001; SEE = 0.11). In 17 divers, rebreathing DLCO (DLCOrb) was also measured at 20 minutes pre-dive, during the first decompression stop of the dive to 45 m for 25 minutes, and at 10 minutes post-dive. Compressed air diving was performed in a dry walk-in chamber and the United States Navy decompression table was followed. The pressure induced decrease in the rate of CO binding to haemoglobin was adjusted to normobaric conditions using a theoretical approach. Also, the presence of venous bubbles post-dive was detected by precordial doppler monitoring. A biphasic change in DLCO was noted: initially, DLCO was increased during the dive (p less than 0.005); this was followed by a post-dive decrease; DLCO/VA changed in a similar manner, as VA was only slightly altered. Only a small post-dive precordial doppler bubble grade was found. In conclusion, rebreathing DLCO measurement is a useful respiratory function test in the hyperbaric environment. It appears that an increase in D(L)CO during the compressed air dive is related predominantly to increased pulmonary capillary blood volume caused by increased negativity of the pleural pressure, hyperoxic pulmonary vasodilatation, and cardiorespiratory centralisation of the blood. The decrease in D(L)CO post-dive was only partially related to the presence of the venous bubbles detectable by doppler.

Adult

Effect of hyperbaric oxygenation on maximal aerobic performance in a normobaric environment.

Eighteen female physical education students, randomly divided into three groups, inhaled 100% O2 for 60 minutes in a hyperbaric chamber. Pressure in the chamber amounted to 2.8 ATA. Three days before the hyperbaric oxygenation (HBO) all the students were subjected to a treadmill test. The first group was retested after 30 minutes, the second after 3 hours and the third 6 hours after the HBO. The first and the second groups of subjects achieved statistically significant maximal oxygen consumption after the HBO (14.4 and 10% respectively) and were capable of sustaining considerably higher exertion on treadmill (12.8%, namely 18.1%, both values were significant on the level of p less than 0.05). The ventilation efficiency parameters (VEO2 and R) did not differ with any of the three groups of subject during the exertion before and after the HBO, although after the HBO the exertion was considerably higher.

Adult

Suppression of rat tumor colonies in the lung by oxygen at high pressure is a local effect.

The effect of hyperbaric oxygen (HBO) on the growth of anaplastic carcinoma colonies in rat lungs after intravenous tumor cell injection was studied. From the first day after tumor cell injection, the rats were exposed to HBO for 16-21 days, 90 min per day. Oxygen at a pressure of 300 kPa (3.0 ATA) significantly decreased the number of lung tumor colonies and increased the survival of tumor-bearing rats, whereas the application of oxygen at a pressure of 100 kPa had no effect. An oxygen-nitrogen normoxic mixture balanced with nitrogen to 300 kPa (3.0 ATA) did not affect the number of colonies, suggesting that the effect was specific for oxygen and not for the increased pressure itself. A 6-day application of oxygen at a 300 kPa pressure suppressed the growth of lung tumor colonies when applied on days 1-6 and 7-12 after intravenous tumor cell injection, but had no effect when applied on days 13-18. In contrast to dramatic effects of HBO on the development of artificial lung metastases, the oxygen at the same 300 kPa pressure had no effect on the growth of tumor cells injected in the hind foot. Thus it appears that the suppression of lung tumor colonies by HBO was due to local oxygen effects in the lungs.

Animals