Weigand M A, Laipple A, Plaschke K, Eckstein H H, Martin E, Bardenheuer H J
Departments of Anesthesiology and Vascular Surgery (H-H.E.), University of Heidelberg, Heidelberg, Germany.
Stroke. 1999 Feb;30(2):306-11. doi: 10.1161/01.str.30.2.306.
Oxidative stress has been postulated to account for delayed neuronal death due to ischemia/reperfusion. We investigated cerebral formation of malondialdehyde as an index of lipid peroxidation in relation to different sources of reactive oxygen species in patients undergoing carotid endarterectomy.
In 25 patients undergoing carotid endarterectomy, jugular venous-arterial concentration differences of brain metabolites, malondialdehyde, plasma total antioxidant status, and soluble P-selectin and L-selectin were measured. A carotid artery shunt (n=5) was placed only after complete loss of somatosensory evoked potentials, indicating a focal cerebral blood flow <15 mL/min per 100 g.
As an indication of cerebral lipid peroxidation, jugular venous-arterial malondialdehyde concentration differences were significantly enhanced before reperfusion, and an additional rise was observed 15 minutes after reperfusion. Plasma total antioxidant status significantly decreased during carotid artery occlusion only in patients with carotid artery shunt. This decrease was matched by cerebral formation of adenosine, hypoxanthine, and nitrite/nitrate. While jugular venous-arterial concentration differences of soluble P-selectin showed changes similar to those of malondialdehyde, the concentration difference for soluble L-selectin was enhanced exclusively at 15 minutes after reperfusion.
Short-term incomplete cerebral ischemia/reperfusion significantly enhanced cerebral lipid peroxidation, as indicated by malondialdehyde formation. The generation of reactive oxygen species by xanthine oxidase or nitric oxide metabolism might be involved in the induction of lipid peroxidation. The additional rise in cerebral release of malondialdehyde was found to coincide with a significant activation of polymorphonuclear leukocytes across the cerebral circulation.
氧化应激被认为是缺血/再灌注导致迟发性神经元死亡的原因。我们研究了接受颈动脉内膜切除术患者大脑中丙二醛的形成情况，以此作为脂质过氧化的指标，并探讨其与不同活性氧来源的关系。
对25例接受颈动脉内膜切除术的患者，测量其脑代谢产物、丙二醛的颈静脉 - 动脉浓度差、血浆总抗氧化状态以及可溶性P选择素和L选择素。仅在体感诱发电位完全消失后（表明局部脑血流量<每100 g每分钟15 mL）才放置颈动脉分流管（n = 5）。
作为脑脂质过氧化的指标，再灌注前颈静脉 - 动脉丙二醛浓度差显著增加，再灌注15分钟后又出现进一步升高。仅在使用颈动脉分流管的患者中，颈动脉闭塞期间血浆总抗氧化状态显著下降。这种下降与大脑中腺苷、次黄嘌呤和亚硝酸盐/硝酸盐的形成相匹配。虽然可溶性P选择素的颈静脉 - 动脉浓度差变化与丙二醛相似，但可溶性L选择素的浓度差仅在再灌注后15分钟时升高。
短期不完全性脑缺血/再灌注显著增强了脑脂质过氧化，丙二醛的形成表明了这一点。黄嘌呤氧化酶或一氧化氮代谢产生的活性氧可能参与了脂质过氧化的诱导过程。发现脑丙二醛释放的进一步升高与整个脑循环中多形核白细胞的显著活化同时发生。
