Increased synthesis of nitric oxide in rat brain cortex due to halogenated volatile anesthetics confirmed by EPR spectroscopy

Баумане, Л.; Dzintare, Maija; Zvejniece, Liga; Meirena, Dainuvite; Lauberte, Lasma; Sile, V.; Kalvinsh, Ivars; Sjakste, Nikolajs

doi:10.1034/j.1399-6576.2002.460408.x

Cited by 35 publications

(12 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since isoflurane and chloral hydrate have a very similar suppressive effect on systemic blood pressure these findings suggest that isoflurane may have an additional vasodilatatory effect on cerebral vessels, as also suggested by others [37]. The mechanisms responsible for this effect seem to be a selective upregulation of nitric oxide synthesis in the brain by volatile anesthetics [38]. These findings suggest that the use of isoflurane and other volatile anesthetics should be discouraged when studying SAH.…”

Section: Discussionsupporting

confidence: 61%

Impact of anesthesia on pathophysiology and mortality following subarachnoid hemorrhage in rats

Hockel¹,

Trabold

Schöller

et al. 2012

Exp & Trans Stroke Med

View full text Add to dashboard Cite

BackgroundAnesthesia is indispensable for in vivo research but has the intrinsic potential to alter study results. The aim of the current study was to investigate the impact of three common anesthesia protocols on physiological parameters and outcome following the most common experimental model for subarachnoid hemorrhage (SAH), endovascular perforation.MethodsSprague-Dawley rats (n = 38) were randomly assigned to (1) chloral hydrate, (2) isoflurane or (3) midazolam/medetomidine/fentanyl (MMF) anesthesia. Arterial blood gases, intracranial pressure (ICP), mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), and regional cerebral blood flow (rCBF) were monitored before and for 3 hours after SAH. Brain water content, mortality and rate of secondary bleeding were also evaluated.ResultsUnder baseline conditions isoflurane anesthesia resulted in deterioration of respiratory parameters (arterial pCO2 and pO2) and increased brain water content. After SAH, isoflurane and chloral hydrate were associated with reduced MAP, incomplete recovery of post-hemorrhagic rCBF (23 ± 13% and 87 ± 18% of baseline, respectively) and a high anesthesia-related mortality (17 and 50%, respectively). Anesthesia with MMF provided stable hemodynamics (MAP between 100-110 mmHg), high post-hemorrhagic rCBF values, and a high rate of re-bleedings (> 50%), a phenomenon often observed after SAH in humans.ConclusionBased on these findings we recommend anesthesia with MMF for the endovascular perforation model of SAH.

show abstract

Section: Discussionsupporting

confidence: 61%

Impact of anesthesia on pathophysiology and mortality following subarachnoid hemorrhage in rats

Hockel¹,

Trabold

Schöller

et al. 2012

Exp & Trans Stroke Med

View full text Add to dashboard Cite

show abstract

“…These results suggest that the degree of anesthesia may affect the coupling between neuronal activity and blood circulation. The exact mechanism remains unknown, but a number of studies have shown that anesthetics can influence the production of possible mediators, such nitric oxide (NO), involved in AFC (Baumane et al, 2002;Galley et al, 2001;Nakao et al, 2001).…”

Section: Why Do Some Observe the Initial Dip Whereas Others Do Not?mentioning

confidence: 99%

Coupling of Changes in Cerebral Blood Flow with Neural Activity: What Must Initially Dip Must Come Back Up

Ances

2004

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: Activation flow coupling, increases in neuronal activity leading to changes in cerebral blood flow (CBF), is the basis of many neuroimaging methods. An early rise in deoxygenation, the "initial dip," occurs before changes in CBF and cerebral blood volume (CBV) and may provide a better spatial localizer of early neuronal activity compared with subsequent increases in CBF. Imaging modality, anesthetic, degree of oxygenation, and species can influence the magnitude of this initial dip. The observed initial dip may reflect a depletion of mitochondrial oxygen (O 2 ) buffers caused by increased neuronal activity. Changes in CBF mediated by nitric oxide (NO) or other metabolites and not caused by a lack of O 2 or energy depletion most likely lead to an increased delivery of capillary O 2 in an attempt to maintain intracellular O 2 buffers.

show abstract

“…The effects of halogenated volatile anaesthetics on NOS activity and regulation in the brain are multiple and probably depend on the enzyme isoform. An increased synthesis of nitric oxide has been observed in the rat brain cortex during anaesthesia by volatile anaesthetics using paramagnetic resonance spectroscopy (Baumane et al, 2002). Furthermore, the expression of proteins of the NO pathway such as NG,NG-dimethylarginine dimethyaminohydrolase (DDAH) was increased at the end of desflurane anaesthesia and lasted for up to 72 h. These findings support the hypothesis of persisting increased NOS activity, mediated by decreased NOS inhibition and it is likely that halothane changes the activity of a lot of proteins as well (Futterer et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO

Baldauf

Henrich‐Noack

Reymann

2007

Journal of Neuroscience Methods

View full text Add to dashboard Cite

Increased synthesis of nitric oxide in rat brain cortex due to halogenated volatile anesthetics confirmed by EPR spectroscopy

Abstract: The action of volatile anesthetics is coupled with an increase of NO content in the cortex dependent on NOS activity.

Cited by 35 publications

References 27 publications

Impact of anesthesia on pathophysiology and mortality following subarachnoid hemorrhage in rats

Impact of anesthesia on pathophysiology and mortality following subarachnoid hemorrhage in rats

Coupling of Changes in Cerebral Blood Flow with Neural Activity: What Must Initially Dip Must Come Back Up

Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO

Contact Info

Product

Resources

About