Reperfusion pulmonary edema

Journal Article · Fri Feb 17 00:00:00 EST 1989 · JAMA, Journal of the American Medical Association; (USA)

DOI:https://doi.org/10.1001/jama.261.7.1030· OSTI ID:5640332

Klausner, J M; Paterson, I S; Mannick, J A; Valeri, C R; Shepro, D; Hechtman, H B ^[1]

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1. Harvard Medical School, Boston, MA (USA)

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 B{sub 4} and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. The authors 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.

• OSTI ID: 5640332
• Journal Information: JAMA, Journal of the American Medical Association; (USA), Vol. 261:7; ISSN 0098-7484
• Country of Publication: United States
• Language: English

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HYPERTENSION
ISCHEMIA
LEUKOCYTES
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550602* - Medicine- External Radiation in Diagnostics- (1980-)