Granulocyte adherence in pulmonary and systemic arterial blood samples from patients with adult respiratory distress syndrome.

The accumulation of granulocytes in lung capillaries, caused by increased granulocyte adherence in response to circulating inflammatory mediators, is proposed as one mechanism of pulmonary vascular injury in the adult respiratory distress syndrome (ARDS). The adherence characteristics of granulocytes from humans with this syndrome have, however, not been described. We assayed the granulocyte adherence to nylon fiber columns using whole blood samples collected from the pulmonary artery of 14 patients within 24 h of satisfying criteria for ARDS. The mean value was 83% of that of normal subjects, and granulocyte adherence was less than or equal to control in samples from 10 of 14 patients. Eight of 12 plasma samples, including 7 of 10 from patients with decreased or normal whole blood granulocyte adherence, contained an activity that increased the adherence of granulocytes isolated from normal subjects. These data suggest that granulocytes may become desensitized to a circulating adherence-promoting mediator or that granulocytes with different functional characteristics circulate in some patients with ARDS. Granulocyte adherence varied directly with the circulating platelet number, indicating that adherence may be influenced by cell-cell interactions as well as by humoral mediators. The granulocyte adherence was a mean of 75% of control samples in samples from 3 patients with increased lung uptake of indium-labeled leukocytes, suggesting that granulocyte accumulation in the lung can occur in the absence of markedly enhanced adherence of circulating cells. These data also suggest that alterations in lung endothelial cells, or the local elaboration of inflammatory mediators, may be important determinants of granulocyte accumulation in the pulmonary microvasculature in established ARDS.