Nitrogen tensions in brachial vein blood of Korean ama divers

1992 ◽  
Vol 73 (6) ◽  
pp. 2592-2595 ◽  
Author(s):  
P. Radermacher ◽  
K. J. Falke ◽  
Y. S. Park ◽  
D. W. Ahn ◽  
S. K. Hong ◽  
...  
Keyword(s):  
Decompression Sickness ◽  
Bubble Formation ◽  
Compartment Model ◽  
Breath Hold ◽  
Computer Assisted ◽  
Half Time ◽  
Single Compartment ◽  
Single Compartment Model ◽  
Effective Depth ◽  
Forearm Muscle

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.

Analysis of Species Characteristics of Laboratory Animals in Reaction to Hyperbaric Environmental Conditions

2019 ◽  
Vol 68 (3) ◽  
pp. 119-138
Author(s):  
Wojciech Giermaziak ◽  
Tadeusz Doboszyński
Keyword(s):  
Decompression Sickness ◽  
Nitrogen Saturation ◽  
Small Animal ◽  
Compartment Model ◽  
Laboratory Animals ◽  
Single Compartment ◽  
Single Compartment Model ◽  
Basic Parameters ◽  
Species Characteristics ◽  
Hyperbaric Exposure

Abstract The aim of this work is to determine the dynamics of nitrogen saturation in small laboratory animals. Nitrogen was chosen as a model gas in this study because of its availability and characteristics, as it is not metabolised and is subject to passive diffusion. By subjecting different species of animals to hyperbaric exposures of increasing time and pressure, the study aimed to identify how rapid a decompression was possible to achieve an outcome that saw 50% of the animals surviving the ensuing acute decompression sickness. The basic parameters of hyperbaric exposure - pressure and time - made it possible to describe the saturation phenomena on the basis of partial saturation periods and to show whether a small animal organism can be considered as a single compartment model.

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

A single compartment model of pacemaking in dissasociated Substantia nigra neurons

2013 ◽  
Vol 35 (3) ◽  
pp. 295-316 ◽  
Author(s):  
Febe Francis ◽  
Míriam R. García ◽  
Richard H. Middleton
Keyword(s):  
Substantia Nigra ◽  
Compartment Model ◽  
Single Compartment ◽  
Single Compartment Model

scholarly journals Deadly diving? Physiological and behavioural management of decompression stress in diving mammals

2011 ◽  
Vol 279 (1731) ◽  
pp. 1041-1050 ◽  
Author(s):  
S. K. Hooker ◽  
A. Fahlman ◽  
M. J. Moore ◽  
N. Aguilar de Soto ◽  
Y. Bernaldo de Quirós ◽  
...  
Keyword(s):  
Marine Mammal ◽  
Marine Mammals ◽  
Multiple Stressors ◽  
Decompression Sickness ◽  
Tissue Injury ◽  
Bubble Formation ◽  
Gas Bubbles ◽  
Breath Hold ◽  
Technological Advances ◽  
Measured Time

Decompression sickness (DCS; ‘the bends’) is a disease associated with gas uptake at pressure. The basic pathology and cause are relatively well known to human divers. Breath-hold diving marine mammals were thought to be relatively immune to DCS owing to multiple anatomical, physiological and behavioural adaptations that reduce nitrogen gas (N 2 ) loading during dives. However, recent observations have shown that gas bubbles may form and tissue injury may occur in marine mammals under certain circumstances. Gas kinetic models based on measured time-depth profiles further suggest the potential occurrence of high blood and tissue N 2 tensions. We review evidence for gas-bubble incidence in marine mammal tissues and discuss the theory behind gas loading and bubble formation. We suggest that diving mammals vary their physiological responses according to multiple stressors, and that the perspective on marine mammal diving physiology should change from simply minimizing N 2 loading to management of the N 2 load . This suggests several avenues for further study, ranging from the effects of gas bubbles at molecular, cellular and organ function levels, to comparative studies relating the presence/absence of gas bubbles to diving behaviour. Technological advances in imaging and remote instrumentation are likely to advance this field in coming years.

scholarly journals Quantitative analysis of flux along the gluconeogenic, glycolytic and pentose phosphate pathways under reducing conditions in hepatocytes isolated from fed rats

1983 ◽  
Vol 212 (3) ◽  
pp. 585-598 ◽  
Author(s):  
J M Crawford ◽  
J J Blum
Keyword(s):  
Compartment Model ◽  
Pentose Phosphate ◽  
Improved Method ◽  
Single Compartment ◽  
Reducing Conditions ◽  
Single Compartment Model ◽  
Net Flux ◽  
Pentose Phosphate Pathways ◽  
Fructose 1,6 Bisphosphate ◽  
Hexose Phosphates

Hepatocytes were isolated from the livers of fed rats and incubated with a mixture of glucose (10 mM), ribose (1 mM), mannose (4 mM), glycerol (3 mM), acetate (1.25 mM), and ethanol (5 mM) with one substrate labelled with 14C in any given incubation. Incorporation of label into CO2, glucose, glycogen, lipid glycerol and fatty acids, acetate and C-1 of glucose was measured at 20 and 40 min after the start of the incubation. The data (about 48 measurements for each interval) were used in conjunction with a single-compartment model of the reactions of the gluconeogenic, glycolytic and pentose phosphate pathways and a simplified model of the relevant mitochondrial reactions. An improved method of computer analysis of the equations describing the flow of label through each carbon atom of each metabolite under steady-state conditions was used to compute values for the 34 independent flux parameters in this model. A good fit to the data was obtained, thereby permitting good estimates of most of the fluxes in the pathways under consideration. The data show that: net flux above the level of the triose phosphates is gluconeogenic; label in the hexose phosphates is fully equilibrated by the second 20 min interval; the triose phosphate isomerase step does not equilibrate label between the triose phosphates; substrate cycles are operating at the glucose-glucose 6-phosphate, fructose 6-phosphate-fructose 1,6-bisphosphate and phosphoenolpyruvate-pyruvate-oxaloacetate cycles; and, although net flux through the enzymes catalysing the non-oxidative steps of the pentose phosphate pathway is small, bidirectional fluxes are large.

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