Effect of prostacyclin PGI2 on cardiopulmonary bypass-induced lung injury

Lung injury produced by cardiopulmonary bypass (CPB) is clinically characterized as postperfusion pulmonary dysfunction syndrome. The roles of humoral factors, altered perfusion modes and the occurrence of diffuse microembolism have been subjects of a number of studies. This paper presents the effectiveness of a platelet inhibiting drug, PGI2 in preventing occlusive microaggregates in the pulmonary circulation. In a series of experimental dog studies using a PGI2 dosage protocol of 10 ng/kg/minute for 30 minutes prior to the onset of CPB followed by 20 mg/kg/minute during CPB, the following effects have been observed: 1) Preservation of platelet numbers during CPB (p < 0.01 versus controls; n = 16). 2) Significant reduction in platelet aggregation during CPB (p < 0.01; n = 16). 3) Insignificant hypotensive effect at normal levels of peripheral vascular resistance (n = 16). 4) Occlusive fibrin, leucocytes and small platelet-based microaggregates obstructing pulmonary arterioles in six of the seven control dogs but in none of the dogs receiving PGI2 infusion. 5) No evidence of perivascular or intra-alveolar oedema, interstitial inflammatory cell infiltrates or haemorrhage was seen in either group of dogs. The controversy existing in relation to the possible therapeutic role of PGI2 and, in particular, its ability to prevent occlusive microaggregates in the arterioles and capillaries of vital organs should encourage further clinical studies of PGI2 and its derivatives during cardiac surgery.