Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage

Citation
A. Khaldi et al., Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage, NEUROSURGER, 49(1), 2001, pp. 33-38
Citations number
45
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROSURGERY
ISSN journal
0148396X → ACNP
Volume
49
Issue
1
Year of publication
2001
Pages
33 - 38
Database
ISI
SICI code
0148-396X(200107)49:1<33:MONOAB>2.0.ZU;2-M
Abstract
OBJECTIVE: Nitric oxide (NO), one of the most powerful endogenous vasodilat ors, is thought to play a major role in the development of delayed vasospas m in patients with subarachnoid hemorrhage (SAH). However, the role of the production of cerebral NO in patients with SAH is not known. In other SAH s tudies, NO metabolites such as nitrite and nitrate have been demonstrated t o be decreased in cerebrospinal fluid and in plasma. METHODS: In this study, a microdialysis probe was used, along with a multip arameter sensor, to measure NO metabolites, brain tissue oxygen tension, br ain tissue carbon dioxide tension, and pH in the cortex of patients with se vere SAH who were at risk for developing secondary brain damage and vasospa sm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interre lationship between the analytes and clinical variables. RESULTS: Brain tissue oxygen tension was strongly correlated to dialysate n itrate and nitrite (r(2) = 0.326; P < 0.001); however, no correlation was n oted between brain tissue oxygen tension and NO metabolites in cerebrospina l fluid (r(2) = 0.018; P = 0.734). No significant correlation between NO pr oduction, brain tissue carbon dioxide tension, and dialysate glucose and la ctate was observed. CONCLUSION: Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relat ionship between brain tissue oxygen and cerebral NO metabolites that we dem onstrate suggests that substrate delivery and NO are linked in the pathophy siology of vasospasm after SAH.