Ma. Mcmillen et al., COMMON PATHWAY OF ENDOTHELIAL-LEUKOCYTE INTERACTION IN SHOCK, ISCHEMIA, AND REPERFUSION, The American journal of surgery, 166(5), 1993, pp. 557-562
Impaired blood flow m shock and ischemia results in significant organ
dysfunction and failure of critical cellular functions. Although some
cellular function can proceed via anaerobic mechanisms, a point is rea
ched at which restoration of blood flow and oxygen delivery does not r
esult in restoration of function (''refractory shock'' or the ''no-ref
low phenomenon''). But even if blood flow is restored after shock or i
schemia, a second mechanism of cellular injury is initiated: monocytes
and neutrophils are activated, resulting in an inflammatory response.
Current evidence suggests that the activation of inflammatory cells i
s triggered by substances from ischemic or injured vascular endotheliu
m that cause leukocyte adherence, activation, and further injury. This
review summarizes the current literature on endothelial cell, monocyt
e, and neutrophil interactions in reperfusion injury after shock or is
chemia and suggests how a recently described peptide from the vascular
endothelium may play an important role in the cascade.