Neutrophil depletion fails to improve neurologic outcome after cardiac arrest in dogs

We tested the hypothesis that polymorphonuclear leukocytes (neutrophils) contribute to morbidity and mortality in a canine model of cardiac arrest-induced central nervous system ischemia. Circulating neutrophils were depleted by administration of a neutrophil-specific sheep immune serum before a ten-minute cardiac arrest in ten experimental animals. Ischemic damage measured by a neurologic deficit score in these animals was compared with that in 12 animals that received either vehicle control or nonimmune sheep serum. Animals receiving immune serum averaged 89% depletion of neutrophils immediately after resuscitation (neutrophils ± SEM: 703 ± 123/mm³ after antiserum versus 6,384 ± 1,171/mm³ before immune serum) and 70% depletion over the first three hours after resuscitation. Neurologic deficit scores assessed at one, two, six, 12, and 24 hours after arrest did not vary between depleted dogs and controls. Overall survival time in neutrophil-depleted dogs was less than in controls (15.5 ± 1.3 versus 19.5 ± 1.3 hours; P = .04). These results suggest that neutrophils may not contribute to clinically important central nervous system dysfunction after resuscitation from a ten-minute cardiac arrest.