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Clinical Trials/NCT03190252
NCT03190252CompletedNot Applicable

Biokemiska förändringar Vid förhöjt Partialtryck för Syrgas

Sahlgrenska University Hospital, Sweden1 site in 1 country10 target enrollmentStarted: June 12, 2017Last updated:
Conditions

Trial Snapshot

Phase
Not Applicable
Status
Completed
Sponsor
Enrollment
10
Locations
1
Primary Endpoint
Concentration of cerebrospinal and inflammatory biochemical markers in blood

Study Overview

Brief Summary

Research hypothesis

  • Diving to depths up to 90msw with an oxygen partial pressure of 130kPa in the breathing gas will affect the central nervous system.
  • Diving to depths up to 90msw with an oxygen partial pressure of 130kPa in the breathing gas will induce inflammatory changes.

Objectives:

  • To investigate the presence of cerebrospinal biochemical markers in blood after diving to depths up to 90msw with an oxygen partial pressure of 130kPa in the breathing gas.
  • To investigate the presence of inflammatory markers in blood after diving to depths up to 90msw with an oxygen partial pressure of 130kPa in the breathing gas.
  • To investigate the presence of venous gas emboli (VGE) in blood after diving to depths up to 90msw with an oxygen partial pressure of 130kPa in the breathing gas.

Detailed Description

When diving with compressed air as breathing gas, a continuous accumulation of nitrogen will take place in the body. The total uptake of nitrogen by the tissues is dependent on the duration and depth of the performed dive. Decompression at the end of a dive can cause accumulated nitrogen to form intravascular bubbles.

Furthermore, at depths greater than 30 meters seawater (msw) the elevated partial pressure of nitrogen in the breathing gas will exert a direct effect on the nervous system. This is known as nitrogen narcosis and can cause altered cognitive function, confusion, behavioural disturbance and altered level of consciousness. The effect of nitrogen narcosis gets more pronounced with increasing diving depth. To avert nitrogen narcosis it is common to reduce the amount of nitrogen in the breathing gas being used. At the same time the amount of oxygen must also be reduced, as partial pressures of oxygen above 1,6kPa could induce seizures. Usually a breathing gas mixture containing helium, nitrogen and oxygen (TriMix) is used.

It has long been considered that decompression sickness (DCS) is caused by bubble formation when dissolved nitrogen at the end of diving comes out of solution. Doppler ultrasound techniques have shown that intravascular gas bubbles could exist even after uneventful dives. Therefore, additional pathophysiological factors must be sought.

There is evidence of an increased inflammatory activity in blood after diving. Signs of neutrophil activation is a common finding. It is not known if hyperbaric exposure in itself is enough to elicit these biochemical changes or if the presence of intravascular nitrogen bubbles is needed.

Studies have shown that biochemical markers of central nervous system (CNS) injury can be detected in blood samples obtained from patients with DCS, metabolic and neurologic disease, during cardiac surgery and after traumatic brain injuries. Such markers can also be seen in blood after sport activities like boxing and breath hold diving. If biochemical markers of CNS injury will be present in blood after hyperbaric exposure is not known.

Study Design

Study Type
Observational
Observational Model
Cohort
Time Perspective
Prospective

Eligibility Criteria

Ages
18 Years to 60 Years (Adult)
Sex
All
Accepts Healthy Volunteers
Yes

Inclusion Criteria

  • Military diver or individual approved by the Swedish navy to dive or perform work in hyperbaric environments

Exclusion Criteria

  • As this is a highly selected population there is no exclusion criteria

Outcomes

Primary Outcomes

Concentration of cerebrospinal and inflammatory biochemical markers in blood

Time Frame: Three months

E.g. GFAP, Tau, NfL, JCHL-1, VCAM-1, ICAM-1

Secondary Outcomes

  • Decompression Sickness (DCS)(Five days)
  • Presence of Venous Gas Emboli (VGE)(Five days)

Investigators

Sponsor
Sahlgrenska University Hospital, Sweden
Sponsor Class
Other
Responsible Party
Principal Investigator
Principal Investigator

Anders Rosén

MD PhD student

Sahlgrenska University Hospital, Sweden

Study Sites (1)

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