TY  - JOUR
T1  - REperfusion pulmonary edema
AU  - Klausner JM, Paterson IS, Mannick JA, Valeri C, Shepro D, Hechtman HB
Y1  - 1989/02/17
N1  - 10.1001/jama.1989.03420070080035
JO  - JAMA
SP  - 1030
EP  - 1035
VL  - 261
IS  - 7
N2  - 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)
SN  - 0098-7484
M3  - doi: 10.1001/jama.1989.03420070080035
UR  - http://dx.doi.org/10.1001/jama.1989.03420070080035
ER  -