Vascular gas emboli (VGE) start forming during the degassing of tissues in the decompression (ascent) phase of the dive when bubble precursors (micronuclei) are triggered to growth. The precise formation mechanism of micronuclei is still debated, with formation sites in facilitating regions with surfactants, hydrophobic surfaces or crevices. Ho wever, significant inter-subject variability to VGE exists for the same diving exposure and VGE may even be reduced with a single pre-dive intervention. The precise link between VGE and endothelial dysfunction observed post dive remains unclear and a nitric oxide (NO) mechanism has been hypothesized.

Bubbles can form in the body during or after decompression from pressure exposures such as those undergone by scuba divers, astronauts, caisson and tunnel workers. Bubble growth and detachment physics then becomes significant in predicting and controlling the probability of these bubbles causing mechanical problems by blocking vessels, displacing tissues, or inducing an inflammatory cascade if they persist for too long in the body before being dissolved...

The sites for formation of microbubbles that are routinely detected precordially by Doppler after a decompression are still a matter of debate. Firstly, microbubbles could form on the endothelial wall of capillaries, at specific nanometric sites, but the release mechanism of such small emerging entities remains puzzling.

OBJECTIVES: Vasodilation of the peripheral arteries during reactive hyperaemia depends in part on release of nitric oxide from endothelial cells. Previous studies mainly employed a fingertip tonometric device to derive pulse wave amplitude (PWA) and PWA hyperaemic changes. An alternative approach is based on photoplethysmography (PPG). We sought to evaluate the correlates of digital PPG PWA hyperaemic responses as a measure of peripheral vascular function...

Hypoxia is the natural trigger for endogenous EPO production but recently the use of intermittent hyperoxia to stimulate EPO has been postulated and this phenomenon has been called the "normobaric oxygen paradox" (NOP). The "NOP" is a mechanism by which oxygen regulates the expression of the Hypoxia Inducible Factor 1 alpha (HIF-1α)...