Increased Pulmonary Transvascular Protein Flux after Canine Cardiopulmonary Bypass

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Abstract
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 < 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 × 109 cells/L in both sample sites, falling to 3.0 ± 0.5 and 2.9 ± 0.5, respectively, p < 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 < 0.01), but likewise, there was a significant transpulmonary gradient only after reversal of asystole. The thoracotomy control dogs showed no significant changes in neutrophil counts or TBA reactivity. Significant rank correlation was demonstrated between protein flux measured after bypass and both net lung lipid peroxidation and neutrophil sequestration during the time period after pulmonary perfusion recommenced (rs = 0.81, p < 0.05 versus lipid peroxidation; rs = 0.66, p < 0.05 versus neutrophil sequestration). Additionally, correlation was shown between lipid peroxidation and neutrophil sequestration during this period (rs = 0.76, p < 0.05). These associations suggest that tissue oxidants, which may be released by sequestered neutrophils, play a role in causing abnormal pulmonary microvascular integrity after canine CPB.

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