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

Ahmad Khaldi, Alois Zauner, Michael Reinert, John J. Woodward, Ross Bullock

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

OBJECTIVE: Nitric oxide (NO), one of the most powerful endogenous vasodilators, is thought to play a major role in the development of delayed vasospasm 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 studies, NO metabolites such as nitrite and nitrate have been demonstrated to be decreased in cerebrospinal fluid and in plasma. METHODS: In this study, a microdialysis probe was used, along with a multiparameter sensor, to measure NO metabolites, brain tissue oxygen tension, brain tissue carbon dioxide tension, and pH in the cortex of patients with severe SAH who were at risk for developing secondary brain damage and vasospasm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interrelationship between the analytes and clinical variables. RESULTS: Brain tissue oxygen tension was strongly correlated to dialysate nitrate and nitrite (r2 = 0.326; P < 0.001); however, no correlation was noted between brain tissue oxygen tension and NO metabolites in cerebrospinal fluid (r2 = 0.018; P = 0.734). No significant correlation between NO production, brain tissue carbon dioxide tension, and dialysate glucose and lactate was observed. CONCLUSION: Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relationship between brain tissue oxygen and cerebral NO metabolites that we demonstrate suggests that substrate delivery and NO are linked in the pathophysiology of vasospasm after SAH.

Original languageEnglish
Pages (from-to)33-40
Number of pages8
JournalNeurosurgery
Volume49
Issue number1
StatePublished - Jul 3 2001
Externally publishedYes

Fingerprint

Subarachnoid Hemorrhage
Nitric Oxide
Oxygen
Brain
Dialysis Solutions
Nitrites
Carbon Dioxide
Nitrates
Cerebrospinal Fluid
Lactic Acid
Glucose
Microdialysis
Brain Ischemia
Vasodilator Agents
Morbidity

Keywords

  • Brain tissue oxygen
  • Carbon dioxide
  • Glucose
  • Lactate
  • Nitric oxide
  • Subarachnoid hemorrhage

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Khaldi, A., Zauner, A., Reinert, M., Woodward, J. J., & Bullock, R. (2001). Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage. Neurosurgery, 49(1), 33-40.

Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage. / Khaldi, Ahmad; Zauner, Alois; Reinert, Michael; Woodward, John J.; Bullock, Ross.

In: Neurosurgery, Vol. 49, No. 1, 03.07.2001, p. 33-40.

Research output: Contribution to journalArticle

Khaldi, A, Zauner, A, Reinert, M, Woodward, JJ & Bullock, R 2001, 'Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage', Neurosurgery, vol. 49, no. 1, pp. 33-40.
Khaldi A, Zauner A, Reinert M, Woodward JJ, Bullock R. Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage. Neurosurgery. 2001 Jul 3;49(1):33-40.
Khaldi, Ahmad ; Zauner, Alois ; Reinert, Michael ; Woodward, John J. ; Bullock, Ross. / Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage. In: Neurosurgery. 2001 ; Vol. 49, No. 1. pp. 33-40.
@article{eb43d2619da043dbadc153994d554824,
title = "Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage",
abstract = "OBJECTIVE: Nitric oxide (NO), one of the most powerful endogenous vasodilators, is thought to play a major role in the development of delayed vasospasm 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 studies, NO metabolites such as nitrite and nitrate have been demonstrated to be decreased in cerebrospinal fluid and in plasma. METHODS: In this study, a microdialysis probe was used, along with a multiparameter sensor, to measure NO metabolites, brain tissue oxygen tension, brain tissue carbon dioxide tension, and pH in the cortex of patients with severe SAH who were at risk for developing secondary brain damage and vasospasm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interrelationship between the analytes and clinical variables. RESULTS: Brain tissue oxygen tension was strongly correlated to dialysate nitrate and nitrite (r2 = 0.326; P < 0.001); however, no correlation was noted between brain tissue oxygen tension and NO metabolites in cerebrospinal fluid (r2 = 0.018; P = 0.734). No significant correlation between NO production, brain tissue carbon dioxide tension, and dialysate glucose and lactate was observed. CONCLUSION: Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relationship between brain tissue oxygen and cerebral NO metabolites that we demonstrate suggests that substrate delivery and NO are linked in the pathophysiology of vasospasm after SAH.",
keywords = "Brain tissue oxygen, Carbon dioxide, Glucose, Lactate, Nitric oxide, Subarachnoid hemorrhage",
author = "Ahmad Khaldi and Alois Zauner and Michael Reinert and Woodward, {John J.} and Ross Bullock",
year = "2001",
month = "7",
day = "3",
language = "English",
volume = "49",
pages = "33--40",
journal = "Neurosurgery",
issn = "0148-396X",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Measurement of nitric oxide and brain tissue oxygen tension in patients after severe subarachnoid hemorrhage

AU - Khaldi, Ahmad

AU - Zauner, Alois

AU - Reinert, Michael

AU - Woodward, John J.

AU - Bullock, Ross

PY - 2001/7/3

Y1 - 2001/7/3

N2 - OBJECTIVE: Nitric oxide (NO), one of the most powerful endogenous vasodilators, is thought to play a major role in the development of delayed vasospasm 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 studies, NO metabolites such as nitrite and nitrate have been demonstrated to be decreased in cerebrospinal fluid and in plasma. METHODS: In this study, a microdialysis probe was used, along with a multiparameter sensor, to measure NO metabolites, brain tissue oxygen tension, brain tissue carbon dioxide tension, and pH in the cortex of patients with severe SAH who were at risk for developing secondary brain damage and vasospasm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interrelationship between the analytes and clinical variables. RESULTS: Brain tissue oxygen tension was strongly correlated to dialysate nitrate and nitrite (r2 = 0.326; P < 0.001); however, no correlation was noted between brain tissue oxygen tension and NO metabolites in cerebrospinal fluid (r2 = 0.018; P = 0.734). No significant correlation between NO production, brain tissue carbon dioxide tension, and dialysate glucose and lactate was observed. CONCLUSION: Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relationship between brain tissue oxygen and cerebral NO metabolites that we demonstrate suggests that substrate delivery and NO are linked in the pathophysiology of vasospasm after SAH.

AB - OBJECTIVE: Nitric oxide (NO), one of the most powerful endogenous vasodilators, is thought to play a major role in the development of delayed vasospasm 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 studies, NO metabolites such as nitrite and nitrate have been demonstrated to be decreased in cerebrospinal fluid and in plasma. METHODS: In this study, a microdialysis probe was used, along with a multiparameter sensor, to measure NO metabolites, brain tissue oxygen tension, brain tissue carbon dioxide tension, and pH in the cortex of patients with severe SAH who were at risk for developing secondary brain damage and vasospasm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interrelationship between the analytes and clinical variables. RESULTS: Brain tissue oxygen tension was strongly correlated to dialysate nitrate and nitrite (r2 = 0.326; P < 0.001); however, no correlation was noted between brain tissue oxygen tension and NO metabolites in cerebrospinal fluid (r2 = 0.018; P = 0.734). No significant correlation between NO production, brain tissue carbon dioxide tension, and dialysate glucose and lactate was observed. CONCLUSION: Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relationship between brain tissue oxygen and cerebral NO metabolites that we demonstrate suggests that substrate delivery and NO are linked in the pathophysiology of vasospasm after SAH.

KW - Brain tissue oxygen

KW - Carbon dioxide

KW - Glucose

KW - Lactate

KW - Nitric oxide

KW - Subarachnoid hemorrhage

UR - http://www.scopus.com/inward/record.url?scp=0034967933&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034967933&partnerID=8YFLogxK

M3 - Article

C2 - 11440457

AN - SCOPUS:0034967933

VL - 49

SP - 33

EP - 40

JO - Neurosurgery

JF - Neurosurgery

SN - 0148-396X

IS - 1

ER -