There are differences in individual cardiovascular responses to the administration of dexmedetomidine,a highly selective α2A-adrenergic receptor(ADRA2A) agonist.The aim of this study was to investigate ADRA2A gene po...There are differences in individual cardiovascular responses to the administration of dexmedetomidine,a highly selective α2A-adrenergic receptor(ADRA2A) agonist.The aim of this study was to investigate ADRA2A gene polymorphisms in the Chinese Han population and their association with the cardiovascular response to intravenous dexmedetomidine infusion.Sixty elective surgery patients of Chinese Han nationality were administered 1 μg/kg dexmedetomidine intravenously over 10 min as a premedication.ADRA2A C-1291G and A1780G polymorphism status was determined in these patients,and their relationships to changes in blood pressure and heart rate after dexmedetomidine administration were analyzed.There were neither significant differences in systolic or diastolic blood pressure changes in individuals with different A1780G and C-1291G genotypes after dexmedetomidine administration,nor in heart rates among the different A1780G genotypes.However,there were significant differences in changes in heart rates in patients with different C-1291G genotypes.There were no significant differences in the sedative effects of dexmedetomidine among different A1780G and C-1291G genotypes.Logistic regression revealed that the C-1291G polymorphism was associated with differential decreases in heart rate after intravenous infusion of dexmedetomidine.These findings indicate that the ADRA2A C-1291G polymorphism can affect heart rate changes in patients after in-utravenous infusion of dexmedetomidine.展开更多
The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell v...The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt(p-Akt), Bad, phospho-Bad(p-Bad), and Bcl-x L were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-x L/Bad. Dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.展开更多
文摘There are differences in individual cardiovascular responses to the administration of dexmedetomidine,a highly selective α2A-adrenergic receptor(ADRA2A) agonist.The aim of this study was to investigate ADRA2A gene polymorphisms in the Chinese Han population and their association with the cardiovascular response to intravenous dexmedetomidine infusion.Sixty elective surgery patients of Chinese Han nationality were administered 1 μg/kg dexmedetomidine intravenously over 10 min as a premedication.ADRA2A C-1291G and A1780G polymorphism status was determined in these patients,and their relationships to changes in blood pressure and heart rate after dexmedetomidine administration were analyzed.There were neither significant differences in systolic or diastolic blood pressure changes in individuals with different A1780G and C-1291G genotypes after dexmedetomidine administration,nor in heart rates among the different A1780G genotypes.However,there were significant differences in changes in heart rates in patients with different C-1291G genotypes.There were no significant differences in the sedative effects of dexmedetomidine among different A1780G and C-1291G genotypes.Logistic regression revealed that the C-1291G polymorphism was associated with differential decreases in heart rate after intravenous infusion of dexmedetomidine.These findings indicate that the ADRA2A C-1291G polymorphism can affect heart rate changes in patients after in-utravenous infusion of dexmedetomidine.
基金supported by the Medical and Health Technology Development Program in Shandong Province(No.2015WSA13033)the National Natural Science Foundation of China(No.81301114)
文摘The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt(p-Akt), Bad, phospho-Bad(p-Bad), and Bcl-x L were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-x L/Bad. Dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.
