Abstract
Background. The purpose of this experimental study was to test whether transfusion potentiated physiologic changes associated with fluid resuscitated trauma in controlled conditions.
Methods. Anesthetized and ventilated mongrel pigs were subjected to soft-tissue injury plus 35% hemorrhage and 1 hour shock and then were resuscitated with either autologous (shed) or heterologous (crosstransfused) fresh whole blood. Leukocyte differential counts, T-lymphocyte subsets, neutrophil adherence molecule (CD18) expression, granulocyte oxidative burst, plasma cortisol, and serum chemistries were monitored in awake animals with indwelling catheters on 3 consecutive days. Changes were referenced to preinjury baseline values and to a control group that received heterologous transfusion but no shock. To determine whether these changes might have influenced host defense, a low-dose challenge with Escherichia coli endotoxin (lipopolysaccharide [LPS]; 1 to 2 μg/kgfor 30 minutes) was administered on day 4.
Results. During recovery, neutrophil counts, neutrophil CD18 expression, and granulocyte oxidative burst were generally increased, but the changes were not potentiated by transfusion. Lymphocyte subpopulations remained relatively constant. Serum enzyme markers were elevated with trauma plus shed blood or trauma plus cross-transfusion, but they remained essentially unchanged after heterologous transfusion only. Plasma cortisol, a nonspecific index of stress, peaked at 3 to 6 times higher than baseline. The increases tended to be higher and later with heterologous transfusion only, relative to trauma plus shed blood or trauma plus cross-transfusion. The delayed LPS challenge evoked profound but transient pulmonary hypertension and leukopenia, followed by subsequent hypoxemia; the time courses and magnitude of these changes were similar in all groups.
Conclusions. If these measured variables before and after LPS challenge are a valid index of host defense in this species, then a 35% transfusion does not potentiate the risk for posttrauma immune dysfunction when the magnitude of injury is constant. Thus the predisposition to infection after human trauma might be due to cold storage of blood, separation of blood into components, or other transfusion-related practices rather than to transfusion per se.
