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Article
February 17, 1989

Reperfusion Pulmonary Edema

Author Affiliations

From the Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston (Drs Klausner, Paterson, Mannick, and Hechtman); the Naval Blood Research Laboratory, Boston University School of Medicine (Dr Valeri); and the Biological Science Center, Boston University (Dr Shepro).

From the Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston (Drs Klausner, Paterson, Mannick, and Hechtman); the Naval Blood Research Laboratory, Boston University School of Medicine (Dr Valeri); and the Biological Science Center, Boston University (Dr Shepro).

JAMA. 1989;261(7):1030-1035. doi:10.1001/jama.1989.03420070080035
Abstract

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

(JAMA 1989;261:1030-1035)

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