Concentration changes of malondialdehyde across the cerebral vascular bed and shedding of L-selectin during carotid endarterectomy.

Concentration changes of malondialdehyde across the cerebral vascular bed and shedding of L-selectin during carotid endarterectomy.
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颈动脉内膜切除术期间脑血管床中丙二醛的浓度变化和 L-选择素的脱落。

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发表时间:
1999
期刊:
影响因子:
8.3
通讯作者:
H. Bardenheuer
H. Bardenheuer
中科院分区:
医学1区
文献类型:
--
作者:
Markus A. Weigand;Andreas Laipple;K. Plaschke;Hans;Eike Martin;H. Bardenheuer

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背景和目的 氧化应激被认为是缺血/再灌注引起的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的患者脑内丙二醛的形成,作为脂质过氧化反应与不同来源的活性氧相关的指标。 方法 在25例接受颈动脉内膜切除术的患者中,测量了脑代谢物、丙二醛、血浆总抗氧化状态和可溶性P-选择素和L-选择素的颈静脉-动脉浓度差异。只有在体感诱发电位完全丧失后才放置颈动脉分流术(n=5),表明局灶性脑血流量<15 mL/min/100 g。 结果 作为脑脂质过氧化反应的指标,颈静脉-动脉丙二醛浓度差异在再灌注前显著增强,再灌注后15分钟观察到额外的上升。血浆总抗氧化状态显着下降,在颈动脉闭塞只有颈动脉分流患者。这种减少与腺苷、次黄嘌呤和亚硝酸盐/硝酸盐的大脑形成相匹配。而颈静脉-动脉浓度差异的可溶性P-选择素显示类似的变化,丙二醛,浓度差异可溶性L-选择素的增强只在15分钟后再灌注。 结论 短期不完全脑缺血/再灌注显着增强脑脂质过氧化反应,丙二醛的形成。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反应的诱导。额外的上升,大脑释放的丙二醛被认为是符合一个显着激活的多形核白细胞在整个脑循环。
BACKGROUND AND PURPOSE 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. METHODS 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. RESULTS 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. CONCLUSIONS 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.
DOI: 10.1073/pnas.88.14.6368
发表时间: 1991-07-01
影响因子: 11.1
作者:
DAWSON, VL;DAWSON, TM;SNYDER, SH
通讯作者: SNYDER, SH
DOI: 10.1016/s0006-3495(93)81195-0
发表时间: 1993-10-01
影响因子: 3.4
作者:
JONES, DA;ABBASSI, O;SMITH, CW
通讯作者: SMITH, CW
DOI: 10.1073/pnas.92.11.5057
发表时间: 1995-05-23
影响因子: 11.1
作者:
FOLBERGROVA, J;ZHAO, Q;SIESJO, BK
通讯作者: SIESJO, BK