Babbitt D G, Forman M B, Jones R, Bajaj A K, Hoover R L
Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232-2170.
Am J Pathol. 1990 Feb;136(2):451-9.
Myocardial salvage after reperfusion may be limited by neutrophil-mediated microvascular damage. The effect of the perfluorochemical, Fluosol-DA, and its various components on neutrophil adherence, cytotoxicity, and proteolytic enzyme release was examined on sheep large and small vessel endothelial cells in vitro. Cells were studied under normoxic (N) and anoxic conditions (A). Various concentrations of Fluosol (10%, 25%, and 50%) significantly reduced neutrophil adherence under both experimental conditions [mean 22 +/- 3.25% versus 7 +/- 0.8% (N) and 20 +/- 3.2% versus 7.5 +/- 0.9% (A); P less than 0.01]. The perfluorocarbons, perfluorodecalin (PFD), and perfluoro-tripropylamine (PFTP) in a 50 volume/percent concentration exhibited profound effects on adherence, particularly on cells subjected to anoxia (51% and 69% reduction in adherence, respectively; P less than 0.01). No effect on adherence was observed with other components, including the detergent, pluronic F68. A 25% reduction (P less than 0.02) in endothelial cytotoxicity was noted when neutrophils were preincubated with Fluosol. However, pretreatment of endothelial cells with Fluosol did not inhibit neutrophil adherence. Neutrophils stimulated with cytochalasin B and FMLP showed a significant reduction in lysozyme release after incubation with Fluosol (28 +/- 5% versus 17 +/- 4%; P less than 0.01). This study demonstrates that Fluosol significantly attenuates neutrophil adherence, cytotoxicity, and enzyme release in an in vitro model of microvascular injury. It also suggests that prevention of neutrophil-mediated microvascular damage may be an important mechanism whereby Fluosol enhances myocardial salvage after ischemia and reperfusion.
再灌注后的心肌挽救可能会受到中性粒细胞介导的微血管损伤的限制。在体外对绵羊大、小血管内皮细胞研究了全氟化合物氟碳乳剂（Fluosol-DA）及其各种成分对中性粒细胞黏附、细胞毒性和蛋白水解酶释放的影响。在常氧（N）和缺氧条件（A）下对细胞进行研究。各种浓度的氟碳乳剂（10%、25%和50%）在两种实验条件下均显著降低中性粒细胞黏附[平均值：常氧时为22±3.25%对7±0.8%，缺氧时为20±3.2%对7.5±0.9%；P＜0.01]。50体积百分比浓度的全氟碳化合物全氟萘烷（PFD）和全氟三丙胺（PFTP）对黏附表现出显著影响，尤其是对缺氧细胞（黏附分别降低51%和69%；P＜0.01）。包括去污剂普朗尼克F68在内的其他成分对黏附无影响。当中性粒细胞与氟碳乳剂预孵育时，内皮细胞毒性降低了25%（P＜0.02）。然而，用氟碳乳剂对内皮细胞进行预处理并未抑制中性粒细胞黏附。用细胞松弛素B和N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）刺激的中性粒细胞在与氟碳乳剂孵育后溶菌酶释放显著降低（28±5%对17±4%；P＜0.01）。本研究表明，在微血管损伤的体外模型中，氟碳乳剂显著减弱中性粒细胞黏附、细胞毒性和酶释放。这也提示，预防中性粒细胞介导的微血管损伤可能是氟碳乳剂增强缺血再灌注后心肌挽救的重要机制。
