cascade, which triggers DNA fragmentation and cellular apoptosis (Endres, 1998; Szabó, 1998; Virág et al., 1998; Yaoita et al., 1998).
Clearly, hemorrhagic shock produces local and whole-body ischemia; and fluid resuscitation, regardless of the type of fluid administered, increases perfusion of previously ischemic or hypoperfused tissues, triggering the production of numerous free radicals and likely contributing to cellular injury.
In addition to the generation of free radicals by reperfusion of hemorrhage-induced ischemia, recent attention has focused on the role of activated neutrophils in resuscitation-mediated cellular injury. Intracellular adhesion molecules 1 and 2 (ICAM-1 and ICAM-2, respectively) have been shown to be upregulated by lactated Ringer's fluid resuscitation from hemorrhagic shock (Rhee, 1998). These adhesion molecules are instrumental in binding leukocytes to the