Abstract
Ischemia–reperfusion injury is induced by activation of the arachidonic acid cascade following the induction of cyclooxygenase-2. This study evaluated the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia–reperfusion injury in the lung. Male Wistar rats were divided into two groups. In the FK3311 group (n = 27), FK3311 (4 mg/kg) was administered intravenously 5 min before ischemia, while in the control group (n = 27) only vehicle was injected. Warm ischemia was induced for 1 h by clamping the left hilus. The arterial oxygen pressure (PaO2) and saturation (SaO2) were measured 30 and 120 min after reperfusion. Serum thromboxane B2 and 6-keto-prostaglandin F1α were also measured 30 min after reperfusion. Lung specimens were harvested 120 min after reperfusion for histologic examination and polymorphonuclear counts, and immunostained with cyclooxygenase-2. The 1-week survival rate in the two groups was compared. PaO2 and SaO2 30 and 120 min after reperfusion were significantly (p <. 05) better in the FK3311 group. Serum thromboxane B2 levels were significantly (p <. 05) lower in the FK3311 group. However, there was no significant difference in 6-keto-prostaglandin F1α. Histologically, tissue damage was mild and polymorphonuclear infiltration was reduced in the FK3311 group compared to the control group. The expression of cyclooxygenase-2 in the alveolar epithelium based on immunostaining was suppressed in the FK3311 group. The 1-week survival rate was significantly (p <. 05) higher in the FK3311 group. We conclude that FK3311 has protective effects on pulmonary ischemia–reperfusion injury, and results in improvement in the 1-week survival rate.
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