Improved lung preservation with dextran 40 is not mediated by a superoxide radical scavenging mechanism.

Abstract

Improved lung preservation with a low-potassium dextran-containing solution has been previously demonstrated. In a subsequent study, it was shown that dextran 40 contributes significantly to this improved preservation. In the current in vitro study, human neutrophils suspended in lung preservation solutions (low potassium with dextran and low potassium without dextran) were stimulated to produce superoxide radicals. The presence of dextran in the solution did not significantly alter the amount of superoxide measured in the assay (low potassium with dextran, 4.149 +/- 0.144 nmol/10(6) cells/20 min; low potassium without dextran, 3.896 +/- 0.215; p greater than 0.2). This suggests that dextran 40 did not appreciably scavenge superoxide radicals, nor did it alter the production of superoxide radicals by stimulated neutrophils. Thus the significantly improved lung preservation seen with the use of dextran 40 is probably not mediated by a superoxide radical scavenging process.