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

Citation
Ma. Weigand et al., Concentration changes of malondialdehyde across the cerebral vascular bed and shedding of L-selectin during carotid endarterectomy, STROKE, 30(2), 1999, pp. 306-311
Citations number
37
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
30
Issue
2
Year of publication
1999
Pages
306 - 311
Database
ISI
SICI code
0039-2499(199902)30:2<306:CCOMAT>2.0.ZU;2-Y
Abstract
Background and Purpose - Oxidative stress has been postulated to account fo r delayed neuronal death due to ischemia/reperfusion. We investigated cereb ral formation of malondialdehyde as an index of lipid peroxidation in relat ion 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, p lasma total antioxidant status, and soluble P-selectin and L-selectin were measured. A carotid artery shunt (n = 5) was placed only after complete los s of somatosensory evoked potentials, indicating a focal cerebral blood flo w < 15 mL/min per 100 g. Results - As an indication of cerebral lipid peroxidation, jugular venous-a rterial malondialdehyde concentration differences were significantly enhanc ed before reperfusion, and an additional rise was observed 15 minutes after reperfusion. Plasma total antioxidant status significantly decreased durin g 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 o f soluble P-selectin showed changes similar to these of malondialdehyde, th e concentration difference for soluble L-selectin was enhanced exclusively at 15 minutes after reperfusion. Conclusions - Short-term incomplete cerebral ischemia/reperfusion significa ntly 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 peroxi dation. The additional rise in cerebral release of malondialdehyde was foun d to coincide with a significant activation of polymorphonuclear leukocytes across the cerebral circulation.