The clinical application of Hyperbaric Oxygen Therapy (HBOT), although based on sound physiological principles as well as on a logical rationale, has often been characterized by empirical procedures, and the choice of the treatment schedules has been more fortuitous than rational. The indication for HBOT and the treatment protocol are originated by the general and often acritical assumption that a given lesion or malfunction is caused, facilitated or worsened by hypoxia. Furthermore, the increasingly common use of multiplace hyperbaric chambers, where many patients can be treated at the same time, although maximizing the cost benefit ration of HBOT and the performance of the chamber technical and nursing personnel justified the commonly adopted routine of using average treatment pressures and schedules without considering the differences between indications, patients, disease conditions and the evolving physiopathological stages of the healing process in the individual patients. As a consequence, it is quite frequent to witness the very strange paradox that a treatment based on extremely solid physiological grounds is often applied empirically and nonrationally.

Saturation divers are exposed to elevated partial pressure of oxygen (ppO2) in their hyperbaric work environment. Experimental studies indicate that oxygen transport is altered, and we have previously reported a drop in hematocrit and extensive downregulation of genes involved in blood oxygen transport capacity after decompression from professional saturation diving. Here we investigate the initial period of hematological adjustment back to normobaric air after professional saturation diving. Erythropoietin (EPO) and hemoglobin (Hb) were measured in blood from 13 divers at two time-points after saturation assignments lasting up to 4 weeks; first immediately after decompression and again 24 h later. Pre-dive levels defined baselines.

Oxygenation conditions are crucial for growth and tumor progression. Recent data suggests a decrease in cancer cell proliferation occurring after exposure to normobaric hyperoxia. Those changes are associated with fractal dimension. The purpose of this research was to study the impact of hyperoxia on apoptosis and morphology of leukemia cell lines. Two hematopoietic lymphoid cancer cell lines (a T-lymphoblastoid line, JURKAT and a B lymphoid line, CCRF-SB) were tested under conditions of normobaric hyperoxia (FiO2 > 60%, ± 18h) and compared to a standard group (FiO2 = 21%). We tested for apoptosis using a caspase-3 assay.

Scuba divers with patent foramen ovale (PFO) may be at risk for paradoxical nitrogen gas emboli when performing maneuvers that cause a rebound blood loading to the right atrium. We measured the rise and fall in intrathoracic pressure (ITP) during various maneuvers in 15 divers. The tests were standard isometric exercises (control), forceful coughing, knee bend (with and without respiration blocked), and Valsalva maneuver (maximal, gradually increased to reach control ITP, and as performed by divers to equalize middle ear pressure). All the maneuvers, as well as the downward slope of ITP at the release phase, were related to the control value.

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.