TY - JOUR
AU - Bernard, Gordon R.
AB - Amphotericin therapy in humans has been reported to cause severe pulmonary dysfunction in some patients, and these abnormalities have been reproduced in unanesthetized sheep. To determine the role of cyclooxygenase products in this response, paired, random-order experiments in 11 sheep were done using the cyclooxygenase inhibitor ibuprofen. Ibuprofen blunted increases in pulmonary artery pressure (Ppa) after amphotericin (peak Ppa 38 ± 3 em H20 in amphotericin-alone group vs. 30 ± 1cm H20 in ibuprofen + amphotericin group, P < .05) and reduced peak lung lymph flow to ∼ 170% of baseline compared with 350% of baseline in amphotericin-alone group (P < .05). In addition, the increase in airflow resistance across the lung and the decrease in partial pressure of oxygen seen after amphotericin was blocked by ibuprofen. Therefore, amphotericin-induced lung dysfunction is produced in part through the generation of cyclooxygenase products of arachidonic acid metabolism and can be ameliorated by pretreatment with the cyclooxygenase inhibitor ibuprofen.
TI - Effect of Cyclooxygenase Inhibition on Amphotericin B-Induced Lung Injury in Awake Sheep
JF - The Journal of Infectious Diseases
DO - 10.1093/infdis/166.1.134
DA - 1992-07-01
UR - https://www.deepdyve.com/lp/oxford-university-press/effect-of-cyclooxygenase-inhibition-on-amphotericin-b-induced-lung-efXAeYAxXT
SP - 134
EP - 138
VL - 166
IS - 1
DP - DeepDyve
ER -