2017
DOI: 10.1590/s0102-865020170060000006
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Abstract: Dexmedetomidine is capable of decreasing glutamergic content, and increasing GABAergic content, in order to decrease the injury of the cerebral ultrastructure, following cerebral ischemia-reperfusion injury.

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Cited by 14 publications
(10 citation statements)
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References 23 publications
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“…In light of the information above, we speculated that the potential role of GABA B R might be critical to the development of POCD via mediating the cAMP‐PKA‐CREB signaling pathway. Moreover, Dex has been suggested to be able to reduce the glutamic acid content, increase the GABAergic content, and mitigate injuries to the ultrastructure caused by cerebral ischemia reperfusion . Therefore, we conducted the present study to uncover the potential molecular mechanism concerning Dex in ameliorating the cognitive dysfunction after surgery.…”
Section: Introductionmentioning
confidence: 96%
See 1 more Smart Citation
“…In light of the information above, we speculated that the potential role of GABA B R might be critical to the development of POCD via mediating the cAMP‐PKA‐CREB signaling pathway. Moreover, Dex has been suggested to be able to reduce the glutamic acid content, increase the GABAergic content, and mitigate injuries to the ultrastructure caused by cerebral ischemia reperfusion . Therefore, we conducted the present study to uncover the potential molecular mechanism concerning Dex in ameliorating the cognitive dysfunction after surgery.…”
Section: Introductionmentioning
confidence: 96%
“…Moreover, Dex has been suggested to be able to reduce the glutamic acid content, increase the GABAergic content, and mitigate injuries to the ultrastructure caused by cerebral ischemia reperfusion. 16 Therefore, we conducted the present study to uncover the potential molecular mechanism concerning Dex in ameliorating the cognitive dysfunction after surgery.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, Dex was shown to alleviate acute lung injury in rat pulmonary edema and pleural effusion, inhibiting inflammatory reactions to protect rat lungs (Dong et al, ; Yoshikawa et al, ). Moreover, Dex prevents testicular ischemia‐reperfusion injury in mice with testicular torsion, significantly protects the brain from ischemia‐reperfusion injury in rats, and reduces infarcts in the cerebral cortex and striatum areas (Lin et al, ; Luo et al, ). We speculate that Dex exerts its protective effects by inhibiting neuronal apoptosis.…”
Section: Discussionmentioning
confidence: 99%
“…Recently, it was shown that pretreatment with Dex or post‐conditioning in mouse hippocampal neurons protects hippocampal neurons against ischemic injury, suggesting that Dex exerts its neuroprotective effects in several types of cells in different experimental models of hypoxia or ischemia (Dahmani et al, ). Many studies have shown that Dex exerts protective effects on the heart, brain, lung, and kidney (Dong et al, ; Lin et al, ; Luo et al, ; Yoshikawa et al, ). However, the molecular details of its involvement in hepatic ischemia reperfusion injury, is not known, and needs to be further studied.…”
Section: Introductionmentioning
confidence: 99%
“…The GLU levels in the serum were higher in the model group than the control group. The neurotoxicity of GLU is mainly expressed in the following ways: damaging the cell membrane ion channels and causing cell edema, reducing mitochondrial functions, disturbing energy metabolism, and causing apoptosis in some cells (37). The alleviation of symptoms of tics and anxiety in TS and comorbid anxiety rats treated with JPZDD could be seen by the trend of increases of GABA levels in the striatum and the serum.…”
Section: A B Cmentioning
confidence: 99%