Original communication| Volume 83, ISSUE 2, P155-163, February 1978

Platelet and leukocyte lung interactions in patients with respiratory failure

  • Herbert B. Hechtman
    Reprint requests: Herbert B. Hechtman, M.D., Department of Surgery, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, MA 02115.
    From the Department of Surgery, Boston University Medical Center, Boston, Mass. U.S.A.

    From the Department of Cell Biology, Boston University Boston, Mass. U.S.A.
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  • Eileen A. Lonergan
    From the Department of Surgery, Boston University Medical Center, Boston, Mass. U.S.A.

    From the Department of Cell Biology, Boston University Boston, Mass. U.S.A.
    Search for articles by this author
  • David Shepro
    From the Department of Surgery, Boston University Medical Center, Boston, Mass. U.S.A.

    From the Department of Cell Biology, Boston University Boston, Mass. U.S.A.
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      The importance of pulmonary interaction with platelets and leukocytes in inducing acute respiratory failure was studied in a group of 23 severely septic patients and in a second group of 12 patients undergoing abdominal aneurysm surgery. The entrapments of platelets and white blood cells by both groups of patients were significantly correlated. Only the neutrophils were removed consistently by the lungs. Septic patients exhibited severe derangements in physiological shunting (Q̇S/Q̇T), physiological dead space, pulmonary vascular resi These measures of pulmonary function were significantly poorer than in the postoperative aneurysm patients. The thrombocytopenia observed in both patient categories did not relate to the loss of platelets in the lungs. The percentage of platelets or white blood cells in mixed venous blood, which passed through the lungs and appeared in arterial blood was correlated inversely with (Q̇S/Q̇T) in septic patients (p < 0.001) but did not correlate pulmonary function. The aneurysm patients also showed no correlation of platelet and white blood cell entrapment with pulmonary function (save for a surprising relation between increased platelet entrapment and decreased physiological dead space, p < 0.05). The data substantiate a relationship between the pulmonary entrapment of platelets or white blood cells and the hypoxia of sepsis, but fail to relate entrapment to any other functional abnormality associated with acute respiratory failure.
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