Editorial: Physiological telemonitoring and interventional telemedicine in extreme environments

One of the possible risks incurred while diving is inert gas narcosis (IGN), yet its mechanism of action remains a matter of controversy. Although providing insights in the basic mechanisms of IGN, research has been primarily limited to animal studies. A human study, in real diving conditions, was needed. Twenty volunteers within strict biometrical criteria (male, age 30-40 years, BMI 20-23, non smoker) were selected. They performed a no-decompression dive to a depth of 33 mfw for 20 min and were assessed by the means of critical flicker fusion frequency (CFFF) measurement before the dive, during the dive upon arriving at the bottom, 5 min before the ascent, and 30 min after surfacing. After this late measurement, divers breathed oxygen for 15 min and were assessed a final time. Compared to the pre-dive value the mean value of each measurement was significantly different (p < 0.001). An increase of CFFF to 104 ± 5.1 % upon arriving to the bottom is followed by a decrease to 93.5 ± 4.3 %. This impairment of CFFF persisted 30 min after surfacing, still decreased to 96.3 ± 8.2 % compared to pre-dive CFFF. Post-dive measures made after 15 min of oxygen were not different from control (without nitrogen supersaturation), 124.4 ± 10.8 versus 124.2 ± 3.9 %. This simple study suggests that IGN (at least partially) depends on gas-protein interactions and that the cerebral impairment persists for at least 30 min after surfacing. This could be an important consideration in situations where precise and accurate judgment or actions are essential.

Saturation diving allows divers to reduce the risk of decompression sickness while working at depth for prolonged periods but may increase reactive oxygen species (ROS) production. Such modifications can affect endothelial function by exacerbating oxidative stress. This study investigated the effects of saturation diving on oxidative stress damage. Redox status was evaluated through: ROS production; total antioxidant capacity (TAC); nitric oxide metabolites (NOx); nitrotyrosine (3-NT); and lipid peroxidation (8-iso-PGF2α) assessment. Creatinine and neopterin were analyzed as markers of renal function and damage. Measurements were performed on saliva and urine samples obtained at four time points: pre; deep; post; and 24 h post. Four divers were included in the study. After the saturation dive (post), significant (p < 0.05) increases in ROS (0.12 ± 0.03 vs. 0.36 ± 0.06 µmol.min−1), TAC (1.88 ± 0.03 vs. 2.01 ± 0.08 mM), NOx (207.0 ± 103.3 vs. 441.8 ± 97.3 µM), 3-NT (43.32 ± 18.03 vs. 18.64 ± 7.45 nM·L−1), and 8-iso-PGF2α (249.7 ± 45.1 vs. 371.9 ± 54.9 pg·mg−1 creatinine) were detected. Markers of renal damage were increased as well after the end of the saturation dive (creatinine 0.54 ± 0.22 vs. 2.72 ± 1.12 g-L−1; neopterin 73.3 ± 27.9 vs. 174.3 ± 20.53 μmol·mol−1 creatinine). These results could ameliorate commercial or military diving protocols or improve the understanding of symptoms caused by oxygen level elevation.

Underwater divers face several potential neurological hazards when breathing compressed gas mixtures including nitrogen narcosis which can impact diver's safety. Various human studies have clearly demonstrated brain impairment due to nitrogen narcosis in divers at 4 ATA using critical flicker fusion frequency (CFFF) as a cortical performance indicator. However, recently some authors have proposed a probable adaptive phenomenon during repetitive exposure to high nitrogen pressure in rats, where they found a reversal effect on dopamine release.