Fast hyperbaric decompression after heliox saturation altered the brain proteome in rats.

Better understanding of the physiological mechanisms and neurological symptoms involved in the development of decompression sickness could contribute to improvements of diving procedures. The main objective of the present study was to determine effects on the brain proteome of fast decompression (1 bar/20 s) compared to controls (1 bar/10 min) after heliox saturation diving, using rats in a model system. The protein S100B, considered a biomarker for brain injury, was not significantly different in serum samples from one week before, immediately after, and one week after the dive.

Bubbles Quantified In vivo by Ultrasound Relates to Amount of Gas Detected Post-mortem in Rabbits Decompressed from High Pressure.

The pathophysiological mechanism of decompression sickness is not fully understood but there is evidence that it can be caused by intravascular and autochthonous bubbles. Doppler ultrasound at a given circulatory location is used to detect and quantify the presence of intravascular gas bubbles as an indicator of decompression stress. In this manuscript we studied the relationship between presence and quantity of gas bubbles by echosonography of the pulmonary artery of anesthetized, air-breathing New Zealand White rabbits that were compressed and decompressed.

S100B and NSE serum concentrations after simulated diving in rats.

The purpose of this study was to assess whether one could detect S100 calcium-binding protein B (S100B) and neuron-specific enolase (NSE) in serum of rats after a simulated dive breathing air, with the main hypothesis that the serum concentrations of S100B and NSE in rats will increase above pre-exposure levels following severe decompression stress measured as venous gas emboli (VGE). The dive group was exposed to a simulated air dive to 700 kPa for 45 min. Pulmonary artery was monitored for vascular gas bubbles by ultrasound.

Eccentric exercise 48 h prior to simulated diving has no effect on vascular bubble formation in rats.

Purpose: Decompression sickness (DCS) caused by vascular bubble formation is a major risk when diving. Prior studies have shown that physical exercise has a significant impact in both reducing and increasing bubble formation. There is limited knowledge about the mechanisms, but there are indications that exercise-induced muscle injury prior to diving may cause increased bubble formation.

Simulated dive in rats lead to acute changes in cerebral blood flow on MRI, but no cerebral injuries to grey or white matter.

In this study, the effect of a simulated dive on rat brain was investigated using several magnetic resonance imaging (MRI)-methods and immunohistochemistry. Rats were randomly assigned to a dive- or a control group. The dive group was exposed to a simulated air dive to 600 kPa for 45 min.

Exercise-induced myofibrillar disruption with sarcolemmal integrity prior to simulated diving has no effect on vascular bubble formation in rats.

Decompression sickness is initiated by gas bubbles formed during decompression, and it has been generally accepted that exercise before decompression causes increased bubble formation. There are indications that exercise-induced muscle injury seems to be involved. Trauma-induced skeletal muscle injury and vigorous exercise that could theoretically injure muscle tissues before decompression have each been shown to result in profuse bubble formation.

Doxycycline treatment in a neonatal rat model of hypoxia-ischemia reduces cerebral tissue and white matter injury: a longitudinal magnetic resonance imaging study.

Doxycycline may potentially be a neuroprotective treatment for neonatal hypoxic-ischemic brain injury through its anti-inflammatory effects. The aim of this study was to examine any long-term neuroprotection by doxycycline treatment on cerebral gray and white matter. Hypoxic-ischemic brain injury was induced in 7-day-old rats.

Concentration of circulating autoantibodies against HSP 60 is lowered through diving when compared to non-diving rats.

Objective: Skin and ear infections, primarily caused by Pseudomonas aeruginosa (P. aeruginosa), are recurrent problems for saturation divers, whereas infections caused by P. aeruginosa are seldom observed in healthy people outside saturation chambers.

S100B and its relation to intravascular bubbles following decompression.

Introduction: When neurological damage occurs in divers, it is considered to be caused by gas bubbles. Entrapment of these bubbles may lead to cellular injury and cerebral oedema. S100B is a protein biomarker that is released in CNS injuries and the concentration is related to the amount of brain damage.

Simulated diving after heat stress potentiates the induction of heat shock protein 70 and elevates glutathione in human endothelial cells.

Heat stress prior to diving has been shown to confer protection against endothelial damage due to decompression sickness. Several lines of evidence indicate a relation between such protection and the heat shock protein (HSP)70 and HSP90 and the major cellular red-ox determinant, glutathione (GSH). The present study has used human endothelial cells as a model system to investigate how heat stress and simulated diving affect these central cellular defense molecules.

The effect of two consecutive dives on bubble formation and endothelial function in rats.

Introduction: Gas bubble formation during and after decompression is considered to be the main initiator of decompression sickness (DCS). Compressed-air workers have been reported to acclimatise to the working environment and hence have a reduced risk of DCS, but the exact nature of the adaptation is not known. In the present study, we investigated the effect of two consecutive dives, separated by a 24-hour surface interval, on bubble formation and endothelial damage in rats.