scholarly journals Role of Nitric Oxide in Cerebral Blood Flow Abnormalities after Traumatic Brain Injury

2003 ◽  
Vol 23 (5) ◽  
pp. 582-588 ◽  
Author(s):  
Roman Hlatky ◽  
J. Clay Goodman ◽  
Alex B. Valadka ◽  
Claudia S. Robertson
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
No Production ◽  
Critical Reduction ◽  
Nitrate And Nitrite ◽  
Enhanced Computed Tomography

Nitric oxide (NO) has important regulatory functions within the central nervous system. NO is oxidized in vivo to nitrate and nitrite (NOx). Measurement of these products gives an index of NO production. The purpose of this study was to examine the relation between the brain extracellular concentration of NO metabolites and cerebral blood flow (CBF) after severe traumatic brain injury. Using a chemiluminescence method, NOx concentrations were measured in 6,701 microdialysate samples obtained from 60 patients during the first 5 d after severe head injury. Regional and global values of CBF obtained by xenon-enhanced computed tomography were used for analyses. Dialysate NOx values were the highest within the first 24 h after brain trauma and gradually decreased over the 5 postinjury d (time effect, P < 0.001). Mean dialysate concentration of NOx was 15.5 ± 17.6 μmol/L (minimum 0.3, maximum 461 μmol/L) and 65% of samples were between 5 and 20 μmol/L. There was a significant relation between regional CBF and dialysate NOx levels (r2 = 0.316, P < 0.001). Dialysate NOx levels (9.5 ± 2.2 μmol/L) in patients with critical reduction of regional CBF (<18 mL · 100 g−1 · min−1) were significantly lower than in patients with normal CBF (18.6 ± 8.1 μmol/L; P < 0.001). This relation between the dialysate concentration of NOx and regional CBF suggests some role for NO in the abnormalities of CBF that occur after traumatic brain injury.

The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

2001 ◽  
Vol 93 (2) ◽  
pp. 351-353 ◽  
Author(s):  
Monica S. Vavilala ◽  
Joan S. Roberts ◽  
Anne E. Moore ◽  
David W. Newell ◽  
Arthur M. Lam
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Inhaled Nitric Oxide

The Effects of Traumatic Brain Injury on Cerebral Blood Flow and Brain Tissue Nitric Oxide Levels and Cytokine Expression

2004 ◽  
Vol 21 (10) ◽  
pp. 1431-1442 ◽  
Author(s):  
Myung-Ja Ahn ◽  
Edward R. Sherwood ◽  
Donald S. Prough ◽  
Cheng Yie Lin ◽  
Douglas S. DeWitt
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Brain Tissue ◽  
Cytokine Expression

Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates

1996 ◽  
Vol 84 (1) ◽  
pp. 71-78 ◽  
Author(s):  
B. Gregory Thompson ◽  
Ryszard M. Pluta ◽  
Mary E. Girton ◽  
Edward H. Oldfield
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
No Production ◽  
Direct Role ◽  
Content Type ◽  
Continuous Release ◽  
Fine Print

✓ The authors sought to develop a model for assessing in vivo regulation of cerebral vasoregulation by nitric oxide (NO), originally described as endothelial-derived relaxing factor, and to use this model to establish the role of NO in the regulation of cerebral blood flow (CBF) in primates. By using regional intraarterial perfusion, the function of NO in cerebral vasoregulation was examined without producing confounding systemic physiological effects. Issues examined were: whether resting vasomotor tone requires NO; whether NO mediates vasodilation during chemoregulation and autoregulation of CBF; and whether there is a relationship between the degree of hypercapnia and hypotension and NO production. Twelve anesthetized (0.5% isoflurane) cynomolgus monkeys were monitored continuously for cortical CBF, PaCO2, and mean arterial pressure (MAP), which were systematically altered to provide control and experimental curves of chemoregulation (CBF vs. PaCO2) and autoregulation (CBF vs. MAP) during continuous intracarotid infusion of 1) saline and 2) an NO synthase inhibitor (NOSI), either l-n-monomethyl arginine or nitro l-arginine. During basal conditions (PaCO2 of 38–42 mm Hg) NOSI infusion of internal carotid artery (ICA) reduced cortical CBF from 62 (saline) to 53 ml/100 g/per minute (p < 0.01), although there was no effect on MAP. Increased CBF in response to hypercapnia was completely blocked by ICA NOSI. The difference in regional (r)CBF between ICA saline and NOSI infusion increased linearly with PaCO2 when PaCO2 was greater than 40 mm Hg, indicating a graded relationship of NO production, increasing PaCO2, and increasing CBF. Diminution of CBF with NOSI infusion was reversed by simultaneous ICA infusion of l-arginine, indicating a direct role of NO synthesis in the chemoregulation of CBF. Hypotension and hypertension were induced with trimethaphan camsylate (Arfonad) and phenylephrine at constant PaCO2 (40 ± 1 mm Hg). Autoregulation in response to changes in MAP from 50 to 140 mm Hg was unaffected by ICA infusion of NOSI. In primates, cerebral vascular tone is modulated in vivo by NO; continuous release of NO is necessary to maintain homeostatic cerebral vasodilation; vasodilation during chemoregulation of CBF is mediated directly by NO production; autoregulatory vasodilation with hypotension is not mediated by NO; and increasing PaCO2 induces increased NO production.

Amelioration of hypoperfusion after traumatic brain injury by in vivo endothelin-1 knockout

2009 ◽  
Vol 87 (5) ◽  
pp. 379-386 ◽  
Author(s):  
Theodor Petrov
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Sprague Dawley ◽  
Cross Sectional ◽  
Doppler Flowmetry ◽  
Endothelin 1 ◽  
Time Period

Endothelin 1 (ET-1) is one of the most powerful vasoconstrictors in the brain. Its expression is upregulated after traumatic brain injury (TBI) and is a major factor in the ensuing hypoperfusion. Attenuation of ET-1 effects has been mainly achieved by blockade of its receptors. The result of a direct blockade of ET-1 mRNA synthesis is not known. We used the Marmarou’s model to inflict injury to male Sprague–Dawley rats injected with antisense ET-1 oligodeoxynucleotides (ODNs) before injury. Laser Doppler flowmetry in noninjured rats (2 groups, i.e., untreated and animals that received cODNs) revealed a constant cerebral blood flow of approximately 14 mL·min–1·100 g–1, whereas the values from injured animals pretreated with control ODNs (cODNs) or from animals subjected to TBI alone were approximately 8.0 mL·min–1·100 g–1 during the 18–48 h time period post-TBI. After antisense ET-1 ODNs pretreatment, however, cerebral blood flow in injured animals was approximately 17 mL·min–1·100 g–1 during the 6–48 h time period. Antisense ET-1 ODNs-treated animals also had 19%–29% larger microvessel cross-sectional area and approximately one-third less ET-1 immunoreactivity in the 50–75% range after injury than did cODNs-treated animals after TBI. The results indicate that this direct in vivo approach is an effective therapeutic intervention for the restoration of cerebral blood flow after TBI.

scholarly journals Variants of the Endothelial Nitric Oxide Gene and Cerebral Blood Flow after Severe Traumatic Brain Injury

2011 ◽  
Vol 28 (5) ◽  
pp. 727-737 ◽  
Author(s):  
Claudia S. Robertson ◽  
Shankar P. Gopinath ◽  
Alex B. Valadka ◽  
Mai Van ◽  
Paul R. Swank ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Endothelial Nitric Oxide

The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

2001 ◽  
Vol 93 (2) ◽  
pp. 351-353 ◽  
Author(s):  
Monica S. Vavilala ◽  
Joan S. Roberts ◽  
Anne E. Moore ◽  
David W. Newell ◽  
Arthur M. Lam
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Inhaled Nitric Oxide

scholarly journals Quantitative cerebral blood flow using xenon-enhanced CT after decompressive craniectomy in traumatic brain injury

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Clinical Outcome ◽  
Decompressive Craniectomy ◽  
Decompressive Surgery ◽  
Hemodynamic Parameters ◽  
Enhanced Ct ◽  
The Mean

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

Nitric oxide and cerebral blood flow responses to hyperbaric oxygen

2000 ◽  
Vol 88 (4) ◽  
pp. 1381-1389 ◽  
Author(s):  
Ivan T. Demchenko ◽  
Albert E. Boso ◽  
Thomas J. O'Neill ◽  
Peter B. Bennett ◽  
Claude A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Methyl Ester ◽  
No Production ◽  
No Donors ◽  
Mk 801 ◽  
Neuronal Excitation ◽  
Synthase Inhibitor ◽  
Electroencephalogram Eeg

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O2 (HBO2) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O2 exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor ( N ω-nitro-l-arginine methyl ester), l-arginine, NO donors, or the N-methyl-d-aspartate receptor inhibitor MK-801. After 30 min of O2 exposure at 3 and 4 ATA, rCBF decreased by 26–39% and by 37–43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with N ω-nitro-l-arginine methyl ester and exposed to HBO2 at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO2at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO2, but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.

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