High concentrations of glucose reduce the oxidative metabolism of dog neutrophils in vitro

The capacity of the neutrophils to reduce tetrazolium nitroblue decreased significantly in the higher concentration of glucose (15.13 ± 9.73% (8 mmol/L) versus 8.93 ± 5.71% (16 mmol/L)). However, there were no changes in tetrazolium nitroblue reduction at different glucose concentrations when the neutrophils were first activated with phorbol myristate acetate. High concentrations of glucose did not affect the viability and apoptosis rate of canine neutrophils either with or without prior camptothecin stimulation. This study provides the first evidence that high concentrations of glucose inhibit the oxidative metabolism of canine neutrophils in vitro in a manner similar to that which occurs in humans, and that the decrease in superoxide production did not increase the apoptosis rate.A high concentration of glucose reduces the oxidative metabolism of canine neutrophils in vitro. It is likely that glucose at high concentrations rapidly affects membrane receptors responsible for the activation of NADPH oxidase in neutrophils; therefore, the nonspecific immune response can be compromised in dogs with acute and chronic hyperglycemic conditions.Hyperglycemia occurs frequently in critically ill dogs hospitalized in intensive care units (16%), and their morbidity is directly associated with their blood glucose concentration [1]. In humans, functional defects in neutrophils that diminish the microbicidal and phagocytic function of the cells and increase the risk of bacterial infection are attributed to hyperglycemia [2]. The molecular, biochemical and cellular basis of this decrease in immunological defense is not well understood in humans [3], and the relationship between hyperglycemia and neutrophil dysfunction in dogs remains to be adequately investigated.Reactive oxygen species (ROS), including superoxide anion and its derivatives, exert an important bactericidal function in neutrophils and are components of some of the conditions associated with the pathogenesis of diabe