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

Departments of Anesthesiology and Vascular Surgery (H-H.E.), University of Heidelberg, Heidelberg, Germany.
Stroke (Impact Factor: 6.02). 03/1999; 30(2):306-11. DOI: 10.1161/01.STR.30.2.306
Source: PubMed

ABSTRACT 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.


Available from: Hans-Henning Eckstein, Feb 22, 2014
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to investigate whether postoperative hyperperfusion is associated with preoperative cerebral hemodynamic impairment due to chronic ischemia and with acute cerebral ischemia during clamping of the internal carotid artery (ICA) during carotid endarterectomy (CEA). Transcranial cerebral oxygen saturation (SO2) was monitored intraoperatively using near-infrared spectroscopy in 89 patients undergoing CEA for ipsilateral ICA stenosis (>70%). Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were also measured using single photon emission computed tomography (SPECT) before CEA. In addition, CBF was measured immediately after CEA and on the third postoperative day. Hyperperfusion (CBF increase>100% compared with preoperative values) was observed immediately after CEA in 10 of 18 patients (56%) with reduced preoperative CVR. Also, post-CEA hyperperfusion was observed in nine of 16 patients (56%) whose SO2 during clamping of the ICA decreased to less than 90% of the preclamping value. Logistic regression analysis showed that reduced preoperative CVR and reduced SO2 during ICA clamping were significant independent predictors of the development of hyperperfusion immediately after CEA. In fact, all patients with reduced preoperative CVR and reduced SO2 during ICA clamping developed post-CEA hyperperfusion, and two of these patients developed cerebral hyperperfusion syndrome. These data suggest that development of cerebral hyperperfusion after CEA is associated with preoperative hemodynamic impairment and intraoperative cerebral ischemia.
    Journal of Cerebral Blood Flow & Metabolism 08/2006; 26(7):878-84. DOI:10.1038/sj.jcbfm.9600244 · 5.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Oxidative stress is well believed to play a role in the pathogenesis of acute ischemic stroke. Reports on antioxidant enzyme activities in patients with stroke are conflicting. Therefore, the aim of this study was to investigate serum antioxidant enzyme activities and oxidative stress levels in patients with acute ischemic stroke within 1st, 5th, and 21st day after stroke onset and also the relationship between these results and the clinical status of patients. The current study comprised 45 patients with acute ischemic stroke and 30 healthy controls. Serum malondialdehyde (MDA) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase activities were measured spectrophotometrically. Serum MDA levels were significantly higher in acute ischemic stroke patients within 24 h after stroke onset than controls (p < 0.05), whereas serum catalase activity was significantly lower (p < 0.05). There were no significant differences in GSH-Px and SOD activities. Serum catalase and SOD activities were significantly lower in fifth day than those of controls (both, p < 0.05) but GSH-Px activity and MDA levels did not change (p > 0.05). Serum SOD activity was significantly lower in 21st day compared to SOD activity of controls (p < 0.05) but MDA levels, GSH-Px, and CAT activities did not change significantly. Our study demonstrated that acute ischemic stroke patients have increased oxidative stress and decreased antioxidant enzymes activities. These findings indicated that an imbalance of oxidant and antioxidant status might play a role in the pathogenesis of acute ischemic stroke.
    Wiener klinische Wochenschrift 04/2015; DOI:10.1007/s00508-015-0742-6 · 0.79 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Reactive oxygen species (ROS) are implicated in various pathological conditions. Synthetic antioxidants have adverse health effects, while many medicinal plants have antioxidant components that can prevent the harmful effects of ROS. This study quantitatively determined the total phenolic content (TPC), total flavonoid content (TFC), and antioxidant properties of ethanol extract of the stem bark of Terminalia glaucescens (EESTG). The objectives were achieved based on in vitro assays. Data were analyzed by Sigma Plot (version 11.0). Using gallic acid as the standard compound, TPC value obtained was 596.57 μg GAE/mg extract. TFC content of EESTG, determined as quercetin equivalent was 129.58 μg QE/mg extract. Furthermore, EESTG significantly (P < 0.001) displayed higher reducing power activity than the standard compounds (ascorbic acid and butylated hydroxytoluene [BHT]). Total antioxidant capacity assay, measured by phosphomolybdate method, was 358.33 ± 5.77 μg butylated hydroxytoluene equivalents [BHTE]/mg extract. β-carotene-linoleate bleaching method affirmed the potency of EESTG because of its significantly (P < 0.001) higher anti-oxidant activity when compared with quercetin and BHT. Based on DPPH assay, EESTG displayed significantly (P < 0.001) higher activity than BHT, while the hydroxyl radical scavenging activities of BHT and quercetin significantly (P < 0.001) exceeded that of the extract, although EESTG still displayed a high level of activity obtained as 83.77% in comparison to 92.80% of the standard compounds. Findings from this study indicate the presence of promisingly potent phytoconstituents in EESTG that have the capability to act as antioxidants and free radical scavengers.