Candinas D, Koyamada N, Miyatake T, Siegel J, Hancock W W, Bach F H, Robson S C
Sandoz Center for Immunobiology, Department of Medicine, Massachusetts 02215, USA.
Thromb Haemost. 1996 Nov;76(5):807-12.
Endothelial cell ATP diphosphohydrolases or ATPDases degrade extracellular inflammatory mediators ATP and ADP, thus inhibiting the formation of platelet thrombi, but the modulation of these ecto-enzymes during vascular injury remains largely undetermined. Renal glomerular ATPDase levels were determined in the rat following ischemia-reperfusion or systemic complement activation, by direct biochemical methods and histochemistry. Ischemia followed by reperfusion times over 30 min were associated with loss of glomerular ATPDase activity. Cobra Venom Factor (CVF) inhibited ATPDase activity and potentiated the deleterious effects of reperfusion. Treatment with either soluble complement receptor type 1 (sCR1), an inhibitor of complement activation, or antioxidants prior to the ischemia-reperfusion was largely protective. Expression of rat glomerular ATPDase activity appears susceptible to the inflammatory injury associated with systemic complement activation and ischemia/reperfusion processes. Oxidative stress could, at least in part, result in the loss of ATPDase activity and thus thrombotic consequences of vascular injury.
内皮细胞ATP二磷酸水解酶或ATP酶可降解细胞外炎症介质ATP和ADP，从而抑制血小板血栓的形成，但在血管损伤过程中这些外切酶的调节作用仍很大程度上未明确。通过直接生化方法和组织化学测定了大鼠在缺血再灌注或全身补体激活后的肾小球ATP酶水平。缺血后再灌注时间超过30分钟与肾小球ATP酶活性丧失有关。眼镜蛇毒因子（CVF）抑制ATP酶活性并增强再灌注的有害作用。在缺血再灌注前用可溶性1型补体受体（sCR1）（一种补体激活抑制剂）或抗氧化剂进行治疗在很大程度上具有保护作用。大鼠肾小球ATP酶活性的表达似乎易受与全身补体激活和缺血/再灌注过程相关的炎症损伤影响。氧化应激可能至少部分导致ATP酶活性丧失，从而导致血管损伤的血栓形成后果。
