Prostacyclin (PGI2) is a commonly used protective agent against pulmonary ischemia-reperfusion injury. In this study, it was postulated that the protective effect of PGI2 on pulmonary ischemia-reperfusion injury would differ according to the state of pulmonary expansion during ischemic injury.
MethodsUnder general anesthesia, left pulmonary ischemia was induced by occluding the left hilum in 40 New Zealand white rabbits. They were allocated to four groups (n = 10 in each group). In groups I and II, ischemia was started with lungs inflated, and in groups III and IV, ischemia was started with lungs collapsed. PGI2 was infused only in groups II and IV at 250 ng/kg/min for 20 minutes just before and after the ischemic period. After 60 minutes of ischemia, reperfusion was maintained for 2 hours, and then the left lung was resected. ABGA and lung water fraction were measured to assess the severity of the ischemia-reperfusion injury.
ResultsCompared to groups I and II, PaO2 decreased markedly in group III and moderately in group IV (P < 0.05). The PaCO2 of groups III and IV significantly differed from those of groups I and II (P < 0.05). The percent changes in lung water fraction were significantly higher in group III than in the other groups (P < 0.05).
ConclusionsPGI2 infused before and after pulmonary ischemia produced a significant protective effect on ischemia-reperfusion injury in the collapsed lung group. In the expanded lung group, however, the effect of PGI2 was masked by lung expansion, which itself led to excellent pulmonary preservation against ischemia-reperfusion injury.