Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary function was measured before and after a 28-day saturation dive to a pressure of 0.25 MPa in eight subjects. PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa for the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. A 28-day saturation dive with six subjects to a pressure of 0.15 MPa and a PO2 of 21 kPa was used as control. The measurements included static and dynamic lung volumes and flows, transfer factor for carbon monoxide (TLCO), and a cycle ergometer exercise test. There was a significant reduction in TLCO of 9.8 +/- 6.0% (P < 0.001) after the dive when values were corrected for hemoglobin concentration changes. Effective alveolar volume was unchanged. There was a reduction in forced midexpiratory flow rate of 9.8 +/- 7.0% (P < 0.01), but forced vital capacity and forced expired volume in 1 s were unchanged. Peak oxygen uptake was reduced by 10.1 +/- 5.3% (P < 0.001). There were no significant changes in any of the lung function variables after the control dive. Exposure to raised PO2 contributes significantly to the changes in pulmonary function that have been reported after deep saturation dives to pressures of 3.1-4.6 MPa with a similar profile of oxygen exposure. TLCO is apparently a more sensitive index than vital capacity for oxygen toxicity.
The small number of reports concerning blood platelets during deep saturation diving have shown that there may be a decrease in the number of circulating platelets. Gas bubbles are often present in theblood during decompression. In vitro, gas bubbles activate platelets, and alter the shape from discoidto spherical configuration with multiple, blunt spikes. This study was done to investigate if there are changes in the morphology of human blood platelets during deep diving. An 18 day long experimentalon-shore saturation dive to 360 msw was performed at NUTEC 1986. Bloodsamples were obtained from the 6 divers on 6 occations: pre-dive control, at 360 msw, 300 msw, 140 msw, 1 and 3 days after surfacing. Using 18 G Wasserman needles antecubital venous blood samples (3ml) were collected directly into the fixative agent (7 ml of 2% glutardialdehyde in cacodylate buffer) whilestill in the hyperbaric chamber. The samples were then decompressed,and the platelets separated from the blood by centrifugation at roomtemperature for 10 min at 190 g. Preparation to transmission electron microscopy included post-fixation in osmium tetroxide, staining uranyl-en-bloc and eventually lead, dehydration and embedding in Epon.Ultrathin sections were examined by a Philips 300 I electron microscope. The examination revealed alterations in both platelet size and shape in the course of the dive. The mean platelet area was increased during and immidiately after thedive, the greatest increase occuring at 360 msw. There was a high incidence of shape changed plateletswith spherical configuration and multiple, blunt spikes. This form was by far most abundant at 360 msw, and the morphology normalised towards surface. This rises the suspection of a pressure-related rather rhan bubble-related effect and the results indicate that plateletsin circulation can be activated bypressure itself
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