RT Journal
A1 Klausner JM, Paterson IS, Mannick JA, Valeri C, Shepro D, Hechtman HB
T1 REperfusion pulmonary edema
JF JAMA
JO JAMA
YR 1989
FD February 17
VO 261
IS 7
SP 1030
OP 1035
DO 10.1001/jama.1989.03420070080035
UL http://dx.doi.org/10.1001/jama.1989.03420070080035
AB 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)