Search PubMed⌕ Search

Biomedical subjects

B G D'Aoust

Publications and source records attributed to B G D'Aoust.

At least 19 recordsLinked to original sources

Factors determining temporal pattern of isobaric supersaturation.

It is possible to produce a transient supersaturation or undersaturation in tissues and blood by sequentially breathing gases with different equilibration rates. If the ambient gas pressure is sufficiently high, the induced supersaturation can produce vascular bubbles. By means of the classical perfusion-dependent model of inert gas elimination, which assumes that the effects of diffusion are minimal, the magnitude of the total inert gas pressure can be predicted. If, however, the effects of diffusion cannot be ignored, the supersaturation could be substantially larger. This paper estimates the effects of diffusion in a Krogh cylinder on the supersaturation produced by suddenly changing the inert gas partial pressure in the blood. The results of these estimates indicate that diffusion plays a role in this transient supersaturation only in long Krogh cylinders with high blood flows. The effects of diffusion are further reduced by the finite time necessary to switch the inert gases in arterial blood. The conclusions are supported by experiments that measure vascular bubble production after a switch of the inert portion of the inspired gas. These experiments further show that the formation of vascular bubbles after such a switch cannot be entirely explained by the different diffusion constants of the gases used.

Animals↗

Central venous bubbles and mixed venous nitrogen in goats following decompression.

Decompression of awake goats from saturation at 1, 2, and 3 ATA of air has been carried out using ultrasonic Doppler bubble detection, central venous blood inert gas measurement, and cardiac output measurement. The results of these experiments indicate that the decrease in nitrogen elimination rate as an apparent result of decompression cannot be due to excessive cardiac output or mass transport of a large amount of inert gas to the lungs as bubbles. Rather, the rapid drop in mixed venous nitrogen content is consistent with a generalized decrease in tissue-to-blood nitrogen elimination. This in turn appears to be due to a cardiovascular response to the decompression insult as was previously reported for dogs (D'Aoust et al., J. Appl. Physiol. 41: 348--355, 1976) at 1, 2, and 3 ATA; addition of ultrasonic Doppler monitoring and cardiac output in the present studies allowed measurement of the degree of latency in the appearance of bubbles at a central venous location. This time period includes that required for bubble formation, growth, and vascular transport of the bubbles to the Doppler detector. All results of these studies are consistent with the interpretation that due to a decompression insult, which probably includes bubble formation, some degree of hemostasis, and other hematologic sequelae, the transport of tissue inert gas to the capillary venous blood is retarded, thus providing the rapid apparent decrease in mixed venous blood inert gas content. These results demonstrate what is most likely a general response to a severe but not crucial decompression by the cardiovascular system.

Animals↗

Hematologic response of fish to changes in gas or hydrostatic pressure.

Hematologic changes were studied in fingering salmon after rapid decompression from combined or independent exposure to gas and hydrostatic pressure. After decompression, fingerling salmon saturated with excess gas under pressure (10.1-40.6 m of seawater) suffered a decrease in thrombocyte counts and fibrinogen, prolonged prothrombin (PT) times, and increased fibrinolytic activity, plasma proteins, and erythrocyte counts in proportion to severity of the dive. After decompression, fingerling salmon exposed to increased pressure experienced an increase in thrombocyte counts and available fibrinogen, shortened PT times, increased erythrocyte counts, and decreased plasma protein levels. It appeared that pressure causes activation of the blood coagulation system of fish. This activation may predispose the fish to increased susceptibility to bubble-induced diffuse intravascular coagulation after rapid decompression. Furthermore, hemoconcentration after decompression may be a pressure-related phenomenon and not a response to bubble-induced anoxia.

Animals↗

Separation of basic parameters of decompression using fingerling salmon.

The experimental limitations inherent in use of air-breathing vertebrates for studies of decompression are chiefly due to the difficulty in estimating supersaturation levels associated with both symptoms of decompression sickness and bubble formation. The difficulty is because gas elimination begins upon reduction of pressure and therefore complicates any estimates of the supersaturations that promoted the bubbles or symptoms, or both, in the first place. Use of physostomatous fish such as salmonid fingerlings easily available from hatcheries allows decompression of both fish and surrounding water, thereby minimizing gas tension gradients from the fish to the water and the water to the fish. Depending upon the experimental conditions imposed, the important physical properties such as diffusivity and solubility of different diving gases, H2, Ne, He, and N2, can be separated or combined parametrically. Results of these studies indicate that initial bubble formation in vivo is relatively independent of solubility, whereas the bubble growth phase is more dependent on gas concentration.

Animals↗

Prlonged bubble production by transient isobaric counter-equilibration of helium against nitrogen.

The production of systemic gas bubbles by isobaric counter-equilibration of helium against 5 atmospheres saturated nitrox (0.3 ATA O2 in both mixes) in awake goats was demonstrated. Sixteen animal exposures (8 dives, 2 animals per dive) to a sudden isobaric gas switch from saturation on N2 to He were conducted; 8 saturations occurred at 132 fsw and 8 at 198 fsw. Central venous bubbles were detected acoustically by means of a Doppler ultrasonic cuff surgically implanted around the inferior vena cava of each animal. Bubbles occurred from 20 to 60 min after the switch in both the 132 fsw and 198 fsw exposures, but were not always present in the 132 fsw exposure, and did not persist for as long. Bubbles or other Doppler events were often detected for the entire isobaric period-12 h-following the gas switch in the 198 fsw exposures. Decompressions were conducted according to the USN saturation tables and were uneventful, with only occasional bubbles. Supersaturation ratios calculated to have occurred for a considerable period after the gas switch were approximately 1.15 (tissue gas tension pi, divided by ambient hydrostatic pressure, P) with maxima at 1.26 for the faster tissues. These values are limiting ones in USN decompression only for the slower tissues. In general, therefore, these results argue for reducing the permissible ascent criteria for the faster tissues-assuming bubbles are to be avoided-and allowing more time at stops for non-saturation decompression. Gas switches from a more soluble to a less soluble and/or more rapidly diffusing gas should therefore be avoided until physiological limits are well worked out.

Animals↗

Venous gas bubbles: production by transient, deep isobaric counterdiffusion of helium against nitrogen.

When awake goats were subjected to isobaric gas switching from saturation (17 hours) on 4.7 atmospheres of nitrogen (0.3 atmosphere of oxygen) to 4.7 atmospheres of helium (0.3 atmosphere of oxygen), bubbles detected by 5-megahertz Doppler ultrasound in the posterior vena cava 20 to 60 minutes after the switch continued for 4 hours. Similar experiments carried out at 6.7 atmospheres of inert gas and 0.3 atmosphere of oxygen produced more bubbles for as long as 12 hours after the gas switch. This is believed to be the first objective demonstration of the phenomenon of deep isobaric supersaturation under transient operational diving conditions at relatively shallow diving depths. Detection of bubbles by Doppler ultrasound confirms the potential importance of the phenomenon to shallow saturation diving and holds promise for better quantitification of its effects as well as those of its counterpart, isobaric undersaturation, which can confer a decompression advantage.

Animals↗

Effects of intermittent hyperbaric oxygen on guinea pig lung elastin and collagen.

The effect of high oxygen pressure on collagen and elastin turnover in lung parenchyma tissue was studied in guinea pigs. Three groups of animals was used. One group (I) was given a clinically excessive exposure of 3 h daily for 9 days of 3 ATA oxygen. A second group (II) was given 3 ATA compressed air on the same schedule, and a third (III), a control, was given the same handling conditions only. Collagen and elastin which amounted to 10.45 and 4.62 mg, respectively, per 100 mg dry defatted parenchymal tissue was labeled with [14C]proline injected ip. Connective tissue protein turnover was estimated by labeling half of each group before exposure (a); effects on biosynthesis were determined by labeling the other half postexposure (b). No differences in hydroxyproline specific activity of collagen fractions or elastin were found with respect to either biosynthesis or turnover. Alveolar wall length-tension measurements were not changed. Since exposures were in excess of those used for treatment of gas gangrene, ischemic burns or wound healing, these results suggest that the metabolism of lung connective tissue is unaffected by the short-term exposure to hyperbaric oxygen.

Animals↗

Decompression-induced decrease in nitrogen elimination rate in awake dogs.

Formulation of safe decompression procedures still requires unproven assumptions regarding both gas equilibration rates and the associated ascent criteria. Although the assumption of symmetry of uptake and elimination rates has been suspect for several years, few data are available. Measurements of actual mixed venous blood nitrogen content [vN2] during compression and following decompression in chronically catheterized awake dogs have clearly demonstrated that desaturation is markedly slower than saturation, and that this effect can be imposed by decompression. The disappearance of arteriovenous nitrogen concentration differences during desaturation following a decompression that produced decompression sickness indicates that cardiopulmonary and cardiovascular changes induced by mechanisms associated with decompression per se can potentiate its deleterious effects. Current US practices do not provide for such asymmetry, while those used in the UK have incorporated this in their models for the last decade.

Animals↗

Decompression-induced bubble formation in salmonids: comparison to gas bubble disease.

The relationship of gas bubble disease (GBD) in fish to decompression-induced bubble formation was investigated with salmonids. Acute bioassays were used to determine equilibration times for critical effects in fish decompressed from depths to 200 fsw. It was found that equilibration of critical tissues was complete in 60-90 min. Salmonids and air-breathers are sensitive to decompressions at similar levels of supersaturation if elimination of excess gas following decompression is unrestricted. However, if elimination is restricted, bubble formation and growth increase accordingly. Tests with mixtures of He-O2, Ar-O2, N2-O2 (80% inert gas: 20% O2) and pure oxygen demonstrated that gas solubility as well as supersaturation (delta P), pressure ratio (initial pressure: final pressure), and absolute pressure must be considered in setting tolerance limits for any decompression. Gases with higher solubility are more likely to produce bubbles upon decompression. Oxygen, however, does not follow this relationship until higher pressures are reached, probably owing to its function in metabolism and in binding with hemoglobin. Tissue responses observed in both GBD and decompressed fish involved similar pathological effects at acute exposures. The circulatory system was consistently affected by bubbles that occluded vessels and blocked flow through the heart.

Animals↗

Coral-algal associations: capacity for producing and sustaining elevated oxygen tensions in situ.

Net oxygen production during photosynthesis by all plants requires adaptation to intracellular O2 tensions in excess of 0.21 ATA. The symbiotic association of zooxanthellae (algae) in the tissues of many actinozoans and hydrozoans (corals and anemones) suggests such an adaptation in these tissues as well, and raises the question as to degree. Oxygen production by zooxanthellae in a single coral head of Montastrea cavernosum was monitored daily in situ in a closed, recirculating 15-liter system. The net photosynthetic activity repeatedly raised the PO2 to more than 0.5 ATA, indicating that even higher tensions existed in the coral's tissues in order to cause this increase and suggesting that coral tissue may represent another example of an oxygen-adapted tissue.

Adaptation, Biological↗

The response of fish blood cells, particularly thrombocytes, to decompression.

The effects of decompression on various blood-cell types in chinook salmon (Oncorhynchus tshawytscha) were investigated using a 4-liter hyperbaric chamber. Thrombocytes (platelets) were found to decrease significantly in numbers following lethal and nonlethal decompressions. The response was highly dependent on depth, gas solubility, and rate of decompression, whereby increasing depth or gas solubility caused greater and faster declines of thrombocyte levels. Return of thrombocyte numbers to normal values usually occurred within 48 hours, except after the more severe decompressions where recovery was never fully attained during the sampling period. Erythrocyte levels increased significantly 1 day after a severe decompression, suggesting hemoconcentration. Leucocytes appeared not to respond to decompression; they were not decreased compared to normal levels, although they were significantly decreased compared to levels of the chamber controls in the nonpressurized chamber. The results are discussed in relation to possible involvement of the fish's blood-coagulation system after decompression.

Animals↗

Changes in hemostatic parameters in fish following rapid decompression.

The effect of rapid decompression on the stress-accelerated blood coagulation system of male and fingerling coho salmon (Oncorhynchus kisutch) was examined after simulated 100- and 200-fsw dives. Blood samples taken either through a dorsal aorta cannula or from a severed caudal peduncle were analyzed for total plasma protein and fibrinogen concentrations, prothrombin times (PT), and partial thromboplastin times (PTT). The effect of mild decompression (100-fsw) on the hemostatic mechanism of both adult and fingerling coho salmon indicated an alternating fibrinogen concentration, declining from normal levels 1 min after decompression, followed by an increase 10 to 15 min later with an eventual loss of fibrinogen to one half the original level an hour after decompression. Partial thromboplastin times were found to increase 10 to 15 min after decompression occurred. Prothrombin times showed an increase 1 hour after decompression in adult salmon, whereas in fingerlings, prothrombin times increased almost immediately from normal levels. The effect of severe decompression (200-fsw) showed similar trends, but at an accelerated rate. It was concluded that both mild and severe decompression activates the hemostatic mechanism of fish which may eventually result in consumption coagulopathy at a greater rate than reported for experimental mammals.

Age Factors↗

Bends in fish.

Explore the source record for details and available documents.

Air↗

Hyperbaric oxygen.

Explore the source record for details and available documents.

Atmospheric Pressure↗