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PubMed1966

Experiments on the genesis of bubbles as a result of rapid decompression.

1. The time course of intravascular bubble formation in mice after rapid decompression from 150 Lb/sq. in. has been followed in vivo in a flap preparation of thoracic and abdominal skin.2. Gas appeared first in the arteries, moving distally after a latent period of 3 min or more. Then bubbles appeared, moving centrally, in the venous system.3. The arterial bubbles could not be attributed to air forced into the circulation from the lungs or lumen of the gut.

Abdomen↗
PubMed2003

NOS inhibition increases bubble formation and reduces survival in sedentary but not exercised rats.

Previously we have shown that chronic as well as a single bout of exercise 20 h prior to a simulated dive protects rats from severe decompression illness (DCI) and death. However, the mechanism behind this protection is still not known. The present study determines the effect of inhibiting nitric oxide synthase (NOS) on bubble formation in acutely exercised and sedentary rats exposed to hyperbaric pressure. A total of 45 adult female Sprague-Dawley rats (270-320 g) were randomly assigned into exercise or sedentary control groups, with and without NOS inhibition, using L-NAME (0.05 or 1 mg ml(-1)) (a nonselective NOS inhibitor). Exercising rats ran intervals on a treadmill for 1.5 h, 20 h prior to the simulated dive. Intervals alternated between 8 min at 85-90 % of maximal oxygen uptake, and 2 min at 50-60 %. Rats were compressed (simulated dive) in a pressure chamber, at a rate of 200 kPa min(-1) to a pressure of 700 kPa, and maintained for 45 min breathing air. At the end of the exposure period, rats were decompressed linearly to the "surface" (100 kPa) at a rate of 50 kPa min(-1). Immediately after reaching the surface the animals were anaesthetised and the right ventricle was insonated using ultrasound. The study demonstrated that sedentary rats weighing more than 300 g produced a large amount of bubbles, while those weighing less than 300 g produced few bubbles and most survived the protocol. Prior exercise reduced bubble formation and increased survival in rats weighing more than 300 g, confirming the results from the previous study. During NOS inhibition, the simulated dive induced significantly more bubbles in all sedentary rats weighing less than 300 g. However, this effect could be attenuated by a single bout of exercise 20 h before exposure. The present study demonstrates two previously unreported findings: that administration of L-NAME allows substantial bubble formation and decreased survival in sedentary rats, and that a single bout of exercise protects NOS-inhibited rats from severe bubble formation and death. This is the first report to indicate that biochemical processes are involved in bubble formation, and this information may be important in the search for preventive measures for and treatment of DCI.

Animals↗
PubMed2005

A single air dive reduces arterial endothelial function in man.

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.

Adult↗
PubMed1996

Acoustically enhanced bubble growth at low frequencies and its implications for human diver and marine mammal safety.

Computations are made of the conditions necessary to obtain bubble growth by rectified diffusion under a variety of conditions associated with low-frequency sonar propagation in the ocean. The complex issue of microbubble nuclei stabilization is treated by assuming either a sufficient level of supersaturation to stabilize the initial bubble size, or by examining a microbubble nucleus with zero surface tension. The bubble growth rates and thresholds are obtained for a ranged of sound-pressure levels (re: 1 microPa) from 150-220 dB, for initial bubble radii from 1-10 microns, and for levels of the dissolved gas concentration from 100% to 223% of saturation. It was determined that for the range of conditions examined, it was necessary to utilize three different formulations of the equations for bubble growth. The results of these calculations (and assumptions concerning nuclei stabilization) indicate that for SPL's in excess of 210 dB, significant bubble growth can be expected to occur, and divers and marine mammals exposed to these conditions could be at risk. For SPL's below about 190 dB, however, except under relatively extreme conditions of supersaturation, significant bubble growth is unexpected.

Acoustics↗
PubMed2004

Cumulative sperm whale bone damage and the bends.

Diving mosasaurs, plesiosaurs, and humans develop dysbaric osteonecrosis from end-artery nitrogen embolism ("the bends") in certain bones. Sixteen sperm whales from calves to large adults showed a size-related development of osteonecrosis in chevron and rib bone articulations, deltoid crests, and nasal bones. Occurrence in animals from the Pacific and Atlantic oceans over 111 years made a pathophysiological diagnosis of dysbarism most likely. Decompression avoidance therefore may constrain diving behavior. This suggests why some deep-diving mammals show periodic shallow-depth activity and why gas emboli are found in animals driven to surface precipitously by acoustic stressors such as mid-frequency sonar systems.

Animals↗
PubMed1968

Dysbarism: osmosis caused by dissolved gas?

The pressure in an osmometer, filled with nitrous oxide-saturated water separated from water by a polyurethane polyether membrane 2.5 microns in thickness, rose slowly by 8 to 20 millimeters (of water) in 10 minutes before gradually returning to close to zero within 2 hours. The permeation coefficient of the membrane was approximately 1000 times greater for water than for gases. The osmotic pressure of water saturated with nitrous oxide at 1 atmosphere, derived from the freezing point of the gas solution, was 1.5 atmospheres. It is concluded that dissolved gases exert osmotic pressure. Partial-pressure gradients of dissolved gases in the tissues of animals and man should cause flows of water along osmotic gradients, which may partially account for some of the symptoms and signs of dysbarism.

Decompression Sickness↗
PubMed2004

Aseptic bone necrosis in an amateur scuba diver.

A case is reported that provides further evidence of an old occupational hazard, dysbaric osteonecrosis, presenting in a new population (sports scuba divers) who also appear to be at risk. It highlights the need for an accurate diagnosis of diving related illness.

Adult↗
PubMed1991

Underwater medicine: a neglected area in Accident and Emergency specialist training.

We have evaluated the available medical care to sports divers by a postal questionnaire sent to consultants and senior registrars in Accident and Emergency medicine in the UK, assessing their training in underwater medicine. Replies were received from 60 of 96 consultants (63%) and 32 of 58 (55%) senior registrars. Thirty-two per cent of consultants and 50% of senior registrars had previous personal experience in managing an underwater diving accident. Thirty per cent of consultants and only 19% of senior registrars had prior formal postgraduate training in underwater medicine. Twenty-seven per cent of consultants and 13% of senior registrars replying did not know the pattern of referral for specialist advice nor where the nearest recompression chamber was to be found. We believe that more formal postgraduate training in underwater medicine is needed by A and E medical staff. Furthermore, clear guidelines about emergency management and patterns of referral for diving accidents should be displayed prominently in all A and E departments.

Decompression Sickness↗
PubMed1994

Self-reported long-term effects of diving and decompression illness in recreational scuba divers.

The aim of this study was to examine the long-term effects of neurological decompression illness (NDCI) on recreational divers. Thirty-seven divers who had been treated for neurological decompression illness at least 2 years previously, and a control group of 50 divers with no history of decompression illness, responded to a postal questionnaire. Divers in the accident group reported more symptoms of neurological damage, were more likely to believe that diving had a deleterious effect on their health and were more likely to indicate symptoms of psychiatric morbidity. The quantity of diving in the year preceding the survey was associated with reports of neurological damage in both groups and with symptoms of psychiatric morbidity in the accident group. Although requiring confirmation from a longitudinal study, these results suggest that recreational diving can have negative long-term consequences for health, particularly after decompression illness.

Adult↗
PubMed1996

Late deterioration after decompression illness affecting the spinal cord.

A former amateur diver presented with a progressive paraparesis. Thirteen years previously he had developed acute spinal cord dysfunction immediately after dry hyperbaric exposure. He had completely recovered motor function in the intervening period. No alternative reason for the later decline emerged from detailed investigation.

Adult↗