Acute asphyxia affects neutrophil number and function in the rat

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Abstract

Design:

Prospective, laboratory study.

Setting:

Research laboratory.

Subjects:

Adult female Wistar rats.

Interventions:

Exposure to CO2 and cold stress.

Measurements and Main Results:

Arterial blood gas, blood glucose, neutrophil number, neutrophil-mediated, complement-dependent bacterial phagocytosis and killing were determined.

Measurements and Main Results:

After a 20-sec exposure to CO2 and cold stress (dry ice vapors), adult rats developed acute respiratory acidosis (pH 6.89 ± 0.26, Paco2 220 ±183 torr [29.3 ± 24.3 kPa]), and mild hypoxia (60 ± 20 torr [8.0 ± 2.7 kPa]) followed by significant metabolic acidosis (base deficit = −12.0 ± 1.5). Neutrophil number slowly increased and reached statistical significance by 72 hrs (5.0 ± 1.5 × 103/ mm3) compared to controls (2.9 ± 1.6 × 103/mm3) (p = .03). Phagocytosis and killing of group B streptococci by neutrophils isolated immediately after asphyxia were significantly impaired (p = .03), and this decrease in function lasted for 24 hrs after asphyxia (p = .04), as measured by two different in vitro complement and antibody-mediated functional assays.

Conclusions:

After brief exposure to CO2 and cold stress, rats developed an acute respiratory acidosis and subsequent metabolic acidosis similar to acute asphyxia. Neutrophil number did not increase until 72 hrs after asphyxia. However, neutrophil-mediated phagocytosis and killing of bacteria were immediately impaired. We speculate that asphyxia may increase the risk for sepsis secondary to altered neutrophil function. (Crit Care Med 1993; 21:1929–1934)

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