Vascular endothelium viability and function after total cardiopulmonary bypass in neonatal piglets

Endothelium dysfunction with severe pulmonary hypertension may occur after total cardiopulmonary bypass (CPB) in infants as a result of a widespread i nflammatory response. The aim of this study was to separate out the effects of lung ischemia-reperfusion from membrane oxygenator-induced activation o f leukocytes on the function and viability of the pulmonary and systemic en dothelia in neonatal piglets submitted to 90-min total CPB followed by 60-m in reperfusion or in sham animals. Hemodynamics, gas exchange, endothelial- dependent relaxation in pulmonary and femoral arteries, and lung and skelet al muscle myeloperoxidase activity were assessed before, during, and after CPB, i.e., after reperfusion. Pulmonary and aortic endothelial cells and ci rculating leukocytes were harvested to assess reperfusion-induced changes i n endothelial cells' viability and proliferation, and leukocyte-endothelial cell adhesion and cytotoxicity. Cas exchange worsened after reperfusion wi th pulmonary hypertension, increase in lung but not skeletal myeloperoxidas e, and reduction of endothelial-dependent relaxation in pulmonary but not f emoral arteries. After reperfusion, viabilities of pulmonary and aortic end othelial cells were reduced to 50%, endothelial cell growths were faster in pulmonary arteries than aorta, and leukocyte-pulmonary endothelial cell ad hesion and cytotoxicity increased. These results suggest that in total CPB lung ischemia-reperfusion aggravates the inflammatory response and predispo ses the lung endothelium to leukocyte-mediated injury.