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Department of Pediatrics, University of Utah, Salt Lake City, Utah 84132
Received 1 October 1996; accepted in final form 9 June 1997.
Carlton, David P., Kurt H. Albertine, Soo Chul Cho, Menno
Lont, and Richard D. Bland. Role of neutrophils in lung vascular injury and edema after premature birth in lambs. J. Appl. Physiol. 83(4): 1307-1317, 1997.
To
investigate the role of neutrophils in the pathogenesis of respiratory
distress after premature birth, we assessed the relationship between
circulating neutrophil concentration and neutrophil accumulation in the
lung, lung lymph and pleural liquid flow, and extravascular lung
water in 10 chronically catheterized preterm lambs (127 ± 1 days gestation) that were mechanically ventilated for 8 h after
birth. Circulating neutrophil concentration transiently decreased
within 2 h after birth and then returned to prenatal values by 6-8
h. The decrease in circulating neutrophil concentration was related
directly to the accumulation of neutrophils in the air spaces, drainage
of liquid and protein from the lung 6-8 h after delivery, and
postmortem extravascular lung water. In additional studies, we
intravenously administered mechlorethamine to 5 fetal lambs to reduce
circulating neutrophils before delivery (neutrophil concentration
before birth: 9 ± 11 cells/µl). Compared with control lambs,
neutrophil-depleted lambs had significantly less drainage of liquid
(7.8 ± 5.9 vs. 2.6 ± 1.9 ml/h, respectively) and protein (116 ± 74 vs. 42 ± 27 mg/h, respectively) from the lung 6-8 h
after birth and significantly less extravascular lung water at
postmortem (6.5 ± 0.8 vs. 4.8 0.6 g/g dry lung,
respectively). Thus neutrophils contribute to the
pathogenesis of respiratory distress after premature birth by
increasing lung vascular protein permeability and promoting lung edema.
pulmonary edema; granulocytes; neutrophil activation; hyaline membrane disease; respiratory distress syndrome
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