Abstract
Cultured rat aortic endothelial cells were morphologically and immunologically characterized before incubation under anoxic conditions for 120 minutes. Cell samples were reoxygenated for 10, 30, and 60 minutes as a model of anoxia-reperfusion injury. The effects of anoxia-reoxygenation were evaluated by measurements of membrane microviscosity, intracellular Ca2+ content, release of 51Cr, and uptake of trypan blue. Membrane microviscosity decreased from 2.03 ± 0.17 poise before anoxia to 1.72 ± 0.22 poise after 120 minutes of anoxia, with a further decrease to 1.54 ± 0.29 poise after 60 minutes of reoxygenation. Release of 51Cr correlated negatively with the decrease in membrane microviscosity and rose from 7.14% ± 0.4% to 12.16% ± 2.79% after anoxia and to 27.17% ± 2.59% after 60 minutes of reoxygenation. Intracellular Ca2+ content and uptake of trypan blue showed no noticeable change during anoxia but they increased significantly during reoxygenation. Addition of fructose-1,6-diphosphate to the anoxic incubation medium partly prevented the change in microviscosity and significantly reduced the release of 51Cr and the uptake of Ca2+ and trypan blue. Captopril exerted similar but less potent effects to those of fructose-1,6-diphosphate.
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