Hydrogen peroxide (H2O2) production in exhaled air was measured in ventilated preterm newborns at 5, 24 and 48 hours after delivery, using originally designed method of exhaled breath condensate (EBC) collection. H2O2 production in expired gas was 812±34 pmol/20 min during the first measurement and then declined to 389±21 at 24 hours and 259±26 pmol/20 min at 48 hours.
We tested the effect of perinatal (one week prenatal and one week postnatal) normobaric hypoxia on the immune response of rats in their 9th week of life. We found that perinatally hypoxic rats produced less serum antibodies after sequential immunization with ovalbumin and sheep red blood cells. Also phagocytosis of HEMA microparticles by neutrophil leukocytes from perinatally hypoxic rats was depressed as well as the oxidative burst of their peritoneal macrophages and neutrophils. These results demonstrate that perinatal hypoxia has an important effect on the immune system of the rat.
Hydrogen peroxide production was measured in non-elicited rat peritoneal macrophages using luminol-dependent chemiluminescence (LDCL). Isolated cells were activated by a chemotactic peptide (FMLP) or by a phorbol ester (PMA) or by the combination of both. A hundred-fold higher LDCL intensity was achieved with PMA relative to FMLP. However, when FMLP was added subsequently to PMA it produced approximately the same response as did PMA. These measurements were carried out with cells isolated from controls and from animals exposed to normobaric hypoxia (10 % O2) for 3 hours, 3 days, or 21 days. Hypoxia had a dual effect. Acutely (within 3 hours) it attenuated the production of hydrogen peroxide triggered by PMA, whilst during longer exposure (3 or 21 days) it increased the response induced by FMLP. Hypoxia can thus modulate the capacity of respiratory burst in peritoneal macrophages.