Intravenous ibuprofen blocks the hypoxemia of pulmonary glass bead embolism in the dog.
To determine the influence of arachidonic acid metabolites on acute lung injury induced by glass bead embolism, two groups of animals were studied before and after the pulmonary artery pressure was doubled by glass bead embolism. One group represented an untreated time control (n = 6) while the second group (n = 6) was pretreated with 25 mg/kg of iv ibuprofen. Repeat measurements were taken at 30, 60 and 90 min after glass bead embolism. Compared to the untreated group, the pretreated group had only a slightly decreased PaO2 (pretreated, 82% of baseline vs. untreated, 35% of baseline, p less than .05). The initial elevation in pulmonary vascular resistance (PVR) was similar in both groups but in the pretreated group it had returned nearly to baseline values by the end of the study in contrast to the persistent elevation of the PVR observed in the untreated group. We conclude that pretreatment with ibuprofen resulted in improved arterial oxygenation and a reduction in PVR over the time period studied. This implicates a role for arachidonic acid metabolites in the pathophysiology of this injury.
Calvin
J E
JE
Department of Medicine, Ottawa Civic Hospital, University of Ottawa Heart Institute, Ontario, Canada.
Dervin
G
G
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D005898:Glass; D000860:Hypoxia / Q000209:etiology / Q000517:prevention & control*; D007052:Ibuprofen / Q000008:administration & dosage / Q000627:therapeutic use*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011655:Pulmonary Embolism / Q000150:complications* / Q000503:physiopathology; D014655:Vascular Resistance
D010100:Oxygen; D007052:Ibuprofen