Diving seals, ischemia-reperfusion and oxygen radicals

The cardiovascular adaptations of seals that contribute to their ability to tolerate long periods of diving asphyxial hypoxia result in episodic regional ischemia during diving and abrupt reperfusion upon termination of the dive. These conditions might be expected to result in production of oxygen-derived free radicals and other forms of highly reactive oxygen species. Seal organs vary during dives with respect to the degree and persistence of ischemia. Myocardial perfusion is reduced and intermittent; kidney circulation is vigorously vasoconstricted. Heart and kidney tissues from ringed seals (Phoca hispida) and domestic pigs (Sus scrofa) were compared in reactions to experimental ischemia. Resulting production of hypoxanthine, indicative of ATP degradation, was higher in pig than in seal tissues. Activity of superoxide dismutase (SOD), an oxygen radical scavenger, was higher in seal heart. We suggest that these results indicate enhanced protective cellular mechanisms in seals against the potential hazard of highly reactive oxygen forms. SOD activity was unexpectedly higher in pig kidney.     

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.     

Diving: barometric pressure and neurochemical mechanisms

The studies of Paul Bert, presented in his book "La Pression Barométrique" in 1878, were at the origin of the modern hyperbaric physiology. Indeed his research demonstrated the effects of oxygen at high pressure, that compression effects must be dissociated from decompression effects, and that neurological troubles and death of divers during or after decompression were due to the fast rate of decompression. However, it is only in 1935 that the work of Behnke et al. attributed the complaints reported at 3 bars and above in compressed air or nitrogen-oxygen mixture to the increase in partial pressure of nitrogen which induces nitrogen narcosis. Little is known about the origins and mechanisms of this narcosis. The traditional view was that anaesthesia or narcosis occurred when the volume of a hydrophobic membrane site was caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect during general anaesthesia has long supported this lipid theory. However, recently, protein theories have met with increasing recognition since results with gaseous anaesthetics have been interpreted as evidence for a direct gas-protein interaction. The question is to know whether inert gases, that disrupt dopamine and GABA neurotransmissions and probably glutamatergic neurotransmission, act by binding to neurotransmitter protein receptors.