| pubmed-article:3777683 | pubmed:abstractText | We examined the hypothesis that increased pulmonary transvascular protein flux after cardiopulmonary bypass (CPB) is mediated in part by neutrophil-derived, oxygen-free radicals. Measurements of transvascular lung 113mIn-transferrin flux, transpulmonary neutrophil counts, and plasma concentrations of thiobarbituric acid (TBA) reactive substances were made in 8 dogs after CPB and in 6 dogs who underwent thoracotomy alone. The TBA reactivity is indicative of lipid peroxidation and was used as an index of oxygen-free radical release. All 14 dogs had a baseline measurement of lung protein flux 1 wk prior to thoracotomy. In the bypass dogs, lung protein flux was -0.2 +/- 0.3 protein flux units (mean +/- SEM) at baseline and increased significantly after bypass to 3.3 +/- 1.0 (p less than 0.01). The control thoracotomy group had baseline values similar to the baseline studies in the CPB dogs (0.2 +/- 0.3 units), but no significant difference was noted after thoracotomy. The CPB dogs showed initial significant parallel falls in left atrial (LA) and central venous (CV) neutrophil counts during bypass (baseline, 5.3 +/- 0.7 X 10(9) cells/L in both sample sites, falling to 3.0 +/- 0.5 and 2.9 +/- 0.5, respectively, p less than 0.001), but a significant CV-LA transpulmonary gradient existed only when pulmonary perfusion recommenced after a period of total asystole. Concentration of TBA reactive substances increased significantly during the course of bypass (baseline LA, 6.4 +/- 0.5 nmol/L, baseline CV, 6.4 +/- 0.5, increasing to 9.8 +/- 1.0 and 9.4 +/- 1.6 at the end of bypass, respectively, p less than 0.01), but likewise, there was a significant transpulmonary gradient only after reversal of asystole.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
