ABNORMAL NEUTROPHIL-PULMONARY INTERACTION IN THE ADULT RESPIRATORY-DISTRESS SYNDROME - QUALITATIVE AND QUANTITATIVE ASSESSMENT OF PULMONARY NEUTROPHIL KINETICS IN HUMANS WITH INVIVO IN-111 NEUTROPHIL SCINTIGRAPHY

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  • 1 May 1986
    • journal article
    • research article
    • Vol. 133  (5) , 797-804
Abstract
In the absence of direct toxins, the majority of evidence from animal models suggests that neutrophils (PMN) are necessary for the full expression of the abnormal pulmonary permeability accompanying acute microvascular lung injury. We therefore studied the role of the PMN in the human correlate of this disease, the adult respiratory distress syndrome (ARDS), by assessing the pulmonary retention of infused autologous 111Indium-labeled PMN (PMN-In). We evaluated 79 patients, prospectively categorized as: "active" ARDS (Aa; n = 30), "active" ARDS and concurrent corticosteroid therapy (As; n = 11), "resolving" ARDS (Ar; n = 13), sepsis without pulmonary edema (S; n = 7), and cardiac pulmonary edema (C; n = 18). This clinical separation was confirmed by retrospective analysis of associated measures of hemodynamic and respiratory dysfunction. We found that both analog scintigrams (positive/negative for diffuse pulmonary PMN-In sequestration) and computer-assisted quantitative analysis in 46 patients (T 1/2 of first hour demargination and percentage of peak activity/pixel/second remaining at 17 to 20 h) showed a significant rank order decreased in the pulmonary retention of labeled PMN-In through the Groups Aa .fwdarw. As .fwdarw. Ar .fwdarw. C. Our findings recognized aspects of in vivo PMN-In behavior that implied pathophysiologic differences between groups of critically ill paitents in either the PMN themselves or in PMN-pulmonary endothelial interaction. This demonstrates the possibility of abnormal in vivo PMN-endothelial interaction in ARDS by virtue of the greater pulmonary localization of PMN in active ARDS versus resolving disease, septic non-ARDS states, and cardiac pulmonary edema. Additionally, a significant diminution of lung neutrophil retention in the lungs was apparent in patients with ARDS receiving corticosteroid therapy.