Relation of cerebral energy metabolism and extracellular nitrite and nitrate concentrations in patients after aneurysmal subarachnoid hemorrhage

Citation
Ow. Sakowitz et al., Relation of cerebral energy metabolism and extracellular nitrite and nitrate concentrations in patients after aneurysmal subarachnoid hemorrhage, J CEREBR B, 21(9), 2001, pp. 1067-1076
Citations number
58
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
ISSN journal
0271678X → ACNP
Volume
21
Issue
9
Year of publication
2001
Pages
1067 - 1076
Database
ISI
SICI code
0271-678X(200109)21:9<1067:ROCEMA>2.0.ZU;2-V
Abstract
In a prospective clinical investigation on neurochemical intensive care mon itoring, the authors' aim was to elucidate the temporal profile of nitric o xide metabolite concentrations - that is, nitrite and nitrate (NOx) - and c ompounds related to energy-metabolism in the cerebral interstitium of patie nts after aneurysmal subarachnoid hemorrhage (SAH). During aneurysm surgery , microdialysis probes were implanted in cerebral white matter of the vascu lar territory most likely affected by vasospasm. Temporal profiles of NOx w ere analyzed in a subset of 10 patients (7 female. 3 male. mean age = 47 +/ - 14 years). Microdialysis was performed for 152 +/- 63 hours. Extracellula r metabolites (glucose, lactate, pyruvate, glutamate) were recovered from t he extracellular fluid of the cerebral parenchyma. NOx was measured using a fluorometric assay. After early surgery, SAH patients revealed characteris tic decreases of NOx from initial values of 46.2 +/- 34.8 mu mol/L to 23.5 +/- 9.0 mu mol/L on day 7 after SAH (P < 0.05). Decreases in NO, were seen regardless of development of delayed ischemia (DIND). Overall NOx correlate d intraindividually with glucose, lactate, and glutamate (r = 0.58, P < 0.0 5; r = 0.32, P < 0.05; r = 0.28, P < 0.05 respectively). After SAH, cerebra l extracellular concentrations of NO metabolites decrease over time and are associated with concomitant alterations in energy- or damage-related compo unds. This could be related to reduced NO availability, potentially leading to an imbalance of vasodilatory and vasoconstrictive factors. On the basis of the current findings, however, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.