Does resuscitation produce a reperfusion injury?

Conceptually, shock with resuscitation should produce cellular changes that parallel those observed in a single organ exposed to ischemia with reperfusion, i.e., a transient worsening of the injury pattern after reperfusion with the degree of recovery reflecting the magnitude of the ischemic injury. To test this hypothesis, 74 male Sprague Dawley rats (300-400 g) were randomized into two groups with controls and exposed to 1) hemorrhagic shock (mean arterial pressure < 50 mm Hg) for 2 hours before sacrifice, or 2) shock (2 hours) with reinfusion of shed blood over 1 hour before sacrifice. Mean arterial pressure, blood loss, serum lactate, base excess, and bicarbonate were serially measured to determine the degree of tissue ischemia. At sacrifice, hepatic mitochondrial function was determined by the respiratory control ratio. Our findings were as follows: 1) Hemorrhagic shock produced significant (P < 0.001) tissue ischemia and impairment of mitochondrial function (P < 0.001), 2) resuscitation rapidly corrects the metabolic sequelae of tissue ischemia, and 3) mitochondrial function was unaffected by resuscitation. We conclude that resuscitation rapidly corrects the tissue ischemia associated with hemorrhagic shock, without producing any measurable reperfusion injury at the mitochondrial level.