Roles of neuronal nitric oxide synthase, oxidative stress, and propofol in N-methyl-d-aspartate-induced dilatation of cerebral arterioles

Hama-Tomioka, Keiko; Kinoshita, Hiroyuki; Nakahata, Katsutoshi; Kondo, Toshikazu; Azma, Toshiharu; Kawahito, Shinji; Hatakeyama, Noboru; Matsuda, Naoyuki

doi:10.1093/bja/aer368

Cited by 17 publications

(16 citation statements)

References 34 publications

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“…Excessive calcium influx caused by hyperactivation of NMDA receptors may cause oxidative stress by increasing calcium entry into the mitochondria (Clay et al, 2010; Gao et al, 2007; Giorgi et al, 2011; Hama-Tomioka et al, 2012; Lemasters et al, 2009). In turn, excessive mitochondrial calcium can disturb the electron transfer process, producing reactive oxygen species (ROS) through leakage of electrons from the electron transport chain (ETC), particularly complexes I and III.…”

Section: Introductionmentioning

confidence: 99%

“…In turn, excessive mitochondrial calcium can disturb the electron transfer process, producing reactive oxygen species (ROS) through leakage of electrons from the electron transport chain (ETC), particularly complexes I and III. Furthermore, excess calcium can cause activation of nitric oxide synthase, resulting in increased production of nitric oxide that can form peroxynitrite, a reactive nitrogen species (RNS) (Girouard et al, 2009; Hama-Tomioka et al, 2012). RNS and ROS produced in this process can react with lipids, proteins and DNA to cause various structural and functional modifications (Barzilai and Yamamoto, 2004; Beal, 2002; Clay et al, 2010; Fariss et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

Kim

Isaacs-Trepanier

Elmi

et al. 2016

Journal of Psychiatric Research

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Chronic N-methyl-d-aspartate (NMDA) administration to rats may be a model to investigate excitotoxicity mediated by glutamatergic hyperactivity, and lithium has been reported to be neuroprotective. We hypothesized that glutamatergic hyperactivity in chronic NMDA injected rats would cause mitochondrial dysfunction and lipid peroxidation in the brain, and that chronic lithium treatment would ameliorate some of these NMDA-induced alterations. Rats treated with lithium for 6 weeks were injected i.p. 25 mg/kg NMDA on a daily basis for the last 21 days of lithium treatment. Brain was removed and frontal cortex was analyzed. Chronic NMDA decreased brain levels of mitochondrial complex I and III, and increased levels of the lipid oxidation products, 8-isoprostane and 4-hydroxynonenal, compared with non-NMDA injected rats. Lithium treatment prevented the NMDA-induced increments in 8-isoprostane and 4-hydroxynonenal. Our findings suggest that increased chronic activation of NMDA receptors can induce alterations in electron transport chain complexes I and III and in lipid peroxidation in brain. The NMDA-induced changes may contribute to glutamate-mediated excitotoxicity, which plays a role in brain diseases such as bipolar disorder. Lithium treatment prevented changes in 8-isoprostane and 4-hydroxynonenal, which may contribute to lithium's reported neuroprotective effect and efficacy in bipolar disorder.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

Kim

Isaacs-Trepanier

Elmi

et al. 2016

Journal of Psychiatric Research

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show abstract

“…Many of these studies lack a scientific rationale, and the pharmacologic interventions often tested do not have a biologic basis. The effects of anesthetics and perioperative stress on NO production have been previously demonstrated [23, 24]. In patients with asthma, corticosteroids reduced the levels of exhaled NO, and dexamethasone inhibited nitrite production in cells from the human joint and lung epithelial cells [12].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Intravenous Dexamethasone and Lidocaine on Propofol-Induced Vascular Pain: A Randomized Double-Blinded Placebo-Controlled Trial

Ahmad

Oliveira

Fitzgerald

et al. 2013

Pain Research and Treatment

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Background. The mechanism for pain associated with intravenous administration of propofol is believed to be related to the release of nitric oxide. We hypothesized that pain following propofol injection would be reduced by pretreatment with dexamethasone. Methods. One hundred fourteen female subjects received 5 mL of preservative-free saline, 0.5 mg·kg−1 of lignocaine hydrochloride 10 mg·mL−1 or 0.25 mg·kg−1 of dexamethasone, intravenously, following exsanguination and occlusion of the veins of the arm. This was followed by a 0.5 mg·kg−1 injection of propofol. Pain scores, facial grimacing, arm withdrawal, and vocalization were recorded prior to and at 15 and 30 seconds following the injection of propofol. Results. The incidence of moderate to severe pain following the injection of propofol was significantly decreased with both lidocaine and dexamethasone. Hand withdrawal was also significantly decreased in comparison to saline. Conclusion. Low dose dexamethasone is commonly used as an antiemetic, and, in larger doses, it has been demonstrated to provide prolonged postoperative analgesia. At higher analgesic doses, dexamethasone may also reduce pain associated with the injection of propofol. This effect is probably related to the effect of the steroid on nitric oxide production associated with intravenous propofol injection.

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“…The specific mechanism underlying the association between anti-NMDAR encephalitis and venous thrombosis remains unknown, but might be partially related to the fact that autoantibodies to NMDAR are associated with a risk of other thrombotic diseases, including stroke, although the causal relationship remains unclear [9,10]. Nevertheless, because NMDAR is expressed in vascular endothelial cells and because its stimulation induces dilation of vessels [11], we speculate that vascular systems are damaged or functionally altered by autoantibodies to NMDAR. Men are at higher risk for idiopathic venous thrombosis than women [12].…”

Section: Discussionmentioning

confidence: 99%

Details of Treatment-Related Difficulties in Men with Anti-N-Methyl-<smlcap>d</smlcap>-Aspartate Receptor Encephalitis

et al. 2012

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Anti-N-methyl-d-aspartate receptor (anti-NMDAR) antibody-associated encephalitis is an immunologic disease characterized by a female preponderance. Males are infrequently affected. The clinical symptoms of affected boys as well as girls have been summarized, and they have some clinical features distinct from those of adults. However, the characteristics of men have been described in only a few reports. We describe in detail four men with anti-NMDAR encephalitis who presented with several clinical features that complicated disease management and recovery, including venous thrombosis, bilateral hippocampal involvement, hypersexuality, and joint contracture. We also report the first detailed clinical information about a male patient who died of this disease. In addition, we summarize the clinical characteristics of five patients previously reported by others.

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Roles of neuronal nitric oxide synthase, oxidative stress, and propofol in N-methyl-d-aspartate-induced dilatation of cerebral arterioles

Abstract: NMDA dilates cerebral parenchymal arterioles possibly via neuronal NOS activation, whereas it produces superoxide via NADPH oxidase. In these arterioles, propofol reduces both the dilatation and superoxide production in response to NMDA.

Cited by 17 publications

References 34 publications

Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

The Effect of Intravenous Dexamethasone and Lidocaine on Propofol-Induced Vascular Pain: A Randomized Double-Blinded Placebo-Controlled Trial

Details of Treatment-Related Difficulties in Men with Anti-N-Methyl-<smlcap>d</smlcap>-Aspartate Receptor Encephalitis

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