"Primed" human neutrophils on a standard peripheral blood smear.

Abstract

In the two-event model of end organ injury the first event is the priming of circulating neutrophils (PMNs); the second stressor activates these primed PMNs with subsequent indiscriminate release of cytotoxic reactive oxygen metabolites and proteases into the PMNendothelial microenvironment. After both trauma and cardiopulmonary bypass, circulating PMNs are primed for superoxide release. The first “priming” event in the development of multiple organ failure can be detected with standard light microscopic (100 ) evaluation of routine peripheral blood smears (Wright-Giemsa stain). The resting neutrophil (A) exhibits a smooth, round cell shape with uniform cytoplasmic granularity. After priming (B), with 2 M platelet activating factor, PMNs lose their resting morphology and exhibit an irregular cell shape and membrane, toxic granulation with polarized granularity (white arrowhead), and cytoplasmic vacuolization (black arrowhead).