[Participation of platelet activating factor in the pulmonary injury during cardiopulmonary bypass]

Activations of leukocytes and platelets have been considered to be one of the major harmful factors related to Adult Respiratory Distress Syndrome (ARDS). As a hypothesis of the present study, similar events may exaggerate the post perfusion lung syndrome following the cardiopulmonary bypass (BPB). Since platelet activating factor (PAF) is a strong activator of leukocytes and platelets, we measured the kinetics of PAF level, number of leukocytes and platelets in 20 anesthetized dogs. beta-TG and PF4 were also measured in patients with organic heart disease before and after CPB. We also studied the preventive effects of PAF antagonist (CV-3988) on the postperfusion lung injury in dogs. The PAF activities increased twice 5 minutes after the beginning of CPB, then it was progressively increased to a level 4.5 times at the end of CPB. Circulating numbers of leukocytes and platelets depleted sharply after the CPB, and then decreased gradually. Such depletion was not modified by PAF antagonist, CV-3988. Accumulation of leukocytes at the pulmonary circulation, and the microscopic evidence of leukocyte sequestration in pulmonary capillary beds were noted in cases without PAF antagonist. Rapid increases of beta-TG and PF45 minutes after the beginning of CPB also showed that activation of platelets occurs immediately. Adhesion of activated leukocytes or platelets to the pulmonary capillary bed in dog cases may suggest the ensuring damage to the vascular beds by releasing free radicals, lysosomal enzymes, or other chemical mediators. Restriction of inflow rate of activated leukocytes to the lung or the heart before aortic clamping may attenuate harmful effects of leukocytes on the respiratory function related to the CPB.