Effects of HBO on the host defence mechanisms

Hamblen47 carried out the first experimental study of the effects of HBO on osteomyelitis in rats. In 1980, in a rabbit model for osteomyelitis, Mader showed how HBO (100 % O2 at 2 ata) improved the bactericidal activity of the PMN's against Staphylococci and how intramedullary PO2 increased from 20 mmHg in normoxia to 104 mmHg at 2 ata48. In an in vitro study carried out at the same time, after increasing pressure of oxygen from 45 to 150 mmHg for two hours, the bactericidal activity of PMN's against Staphylococcus aureus increased from 44 to 71%. The partial pressures of oxygen obtained in the osteomyelitic bone and in vitro before administration of HBO would have inhibited the bactericidal effects of PMN's to a greater extent than they would have inhibited the development of Staphylococcus aureus, which clearly illustrates the impact of HBO on the defence mechanisms of the host. We can therefore conclude that the bactericidal effect of HBO is due to the restoring of the pressure of oxygen required for the oxidative burst to occur.

In a model of subcutaneous infection in rabbits, Hunt (Figure 1.6-2) showed by counting the number of bacteria in the wound exudate that bactericidal activity was greater in animals placed in hyperoxic environments (40 to 45 % O2) than in animals in hypoxia (12 to 14 % O2)38,49,50. Likewise, Knighton showed in a model of skin infection in guinea pigs placed in various oxygen concentrations (hyperoxia : 45 % O2, normoxia : 21 % O2, hypoxia : 12 % O2) that after 24 and 48 hours the diameter of the area of infective necrosis had decreased in the animals placed in hyperoxia as compared to those in hypoxia51.

Number of germs psi (nl <jf exudate {logarithmic scale)

Number of germs psi (nl <jf exudate {logarithmic scale)

Figure 1.6-2. Effects of oxygen on the amount of bacteria in the exudate of experimental wounds on rabbits

In contrast with these studies proving the usefulness of HBO for fighting infection in hypoxic tissues, prolonged exposure to high pressures of oxygen may also have deleterious effects on the functions of PMN's and macrophages. In guinea pigs, prolonged exposure to hyperoxia (85 % O2, 90 hours) induced a decrease in the adhesion, chemotaxis, phagocytosis and bactericidal activity of the PMN's52. In a recent study on 10 healthy volunteers placed in HBO for 136 minutes at 1.8 ata, Labrouche observed an alteration in PMN's functions including a decrease in chemotaxis and in chemokinesis, combined with an increase in oxidative burst and phagocytosis53.

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