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S100B and its relation to intravascular bubbles following decompression.

Marianne B Havnes¹, Astrid Hjelde, Alf O Brubakk

¹Doctoral student, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Olav Kyrres gt. 9, N-7489 Trondheim, Norway, Phone: +47-(0) 72-828043,

Diving and Hyperbaric Medicine

|November 1, 2012

Summary

Diving-induced neurological damage may be indicated by elevated S100B protein levels. Higher pressure dives correlated with increased S100B and more gas bubbles, suggesting S100B as a potential biomarker for decompression illness.

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Area of Science:

Neurology
Diving Medicine
Biomarkers

Background:

Neurological damage in divers is often attributed to gas bubbles, which can cause cellular injury and cerebral edema.
S100B protein is a known indicator released during central nervous system (CNS) injuries, with its concentration correlating to the extent of brain damage.

Purpose of the Study:

To investigate the relationship between simulated diving pressures, gas bubble formation, and serum S100B protein levels in rats.
To evaluate S100B as a potential biomarker for neurological damage resulting from decompression.

Main Methods:

27 rats were divided into control, 400 kPa simulated dive, and 700 kPa simulated dive groups.
Venous gas bubble scores were assessed via ultrasound post-dive.
Serum S100B concentrations were measured using ELISA and compared against bubble grades.

Main Results:

Rats exposed to 700 kPa showed significantly higher S100B levels compared to controls (P=0.038) and 400 kPa groups (P=0.003).
No significant difference in S100B was observed between control and 400 kPa groups.
Higher bubble grades were observed in the 700 kPa group compared to the 400 kPa group (P=0.001).

Conclusions:

A correlation exists between the severity of gas bubble formation and elevated serum S100B protein levels.
S100B protein shows promise as a biomarker for detecting neurological damage caused by decompression in diving.