Resistance to bacterial infection in wounds depends on neutrophils. One component of phagocyte bacterial killing is oxidative killing. Molecular oxygen is converted by the neutrophil to high-energy radicals, such as superoxide, hydroxyl, peroxide, aldehydes, hypochlorite, hypoiodite, and others, all of which are toxic in varying degrees to bacteria (6, Fig. 2). The rate of production of these toxic radicals is directly proportional to oxygen tension (7). Allen et al. showed that superoxide production in neutrophils is half-maximal for oxygen tensions from 45 to 80mmHg and maximal at oxygen tensions greater that 300mmHg. They found that bactericidal activity would rise 3-to 4-fold if mean oxygen tension in a wound increased from 15 to
Figure 1 Oxygen tissue measurements across a healing wound measured in a rabbit ear wound healing chamber. Tissue oxygen tension increases at each capillary. The effect of hyperoxia, hypoxia, and hypovolemia on the oxygen gradient driving diffusion into the dead space of the wound is demonstrated. (From Ref. 21.)
spp, and Klebsiella spp are killed at rates proportional to local oxygen tension (7,9). Hohn et al. measured in vitro leukocyte killing of S. aureus 502A from 0 to 150mmHg. They found a 50% loss of bacterial killing when oxygen tension was reduced to 0mmHg, with the major loss of killing capacity for oxygen tensions below 30mmHg (6,17, Fig. 3).