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
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.