Comparison of the Effects of Dexmedetomidine on the Induction of Anaesthesia Using
            Marsh and Schnider Pharmacokinetic Models of Propofol Target-Controlled Infusion

Hassan, Wan Mohd Nazaruddin Wan; Hs, Tan; Rh, Mohamed Zaini

doi:10.21315/mjms2018.25.1.4

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…fects without inducing respiratory depression. Also, it reduces anesthetic requirement during intraoperative period and provides hemodynamic stability [14][15][16] . The alpha-2 receptors localized in the blood vessels mediate vasoconstriction and those located at sympathetic terminals play a role in the regulation of the autonomic and cardiovascular system by inhibiting norepinephrine release.…”

Section: Discussionmentioning

confidence: 99%

The effects of dexmedetomidine on hemodynamic parameters and intubation conditions

Ar¹

2018

Haydarpasa Numune Med J

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Introduction: In this study, we aim to investigate the effects of two different preanesthetic doses of dexmedetomidine on the hemodynamic response to endotracheal intubation, intubation conditions and neuromuscular block. Methods: Seventy-five ASAI-II patients, aged 18-70 years, who required tracheal intubation for elective surgery were allocated for this study. Before induction, patients were randomly divided into three groups to receive either saline as placebo (20cc) (GroupC), dexmedetomidine 0.5 μg/kg (Group D0.5) or dexmedetomidine 1 μg/kg (Group D1) in a total volume of 20 cc in 10 min. Heart rate(HR) and mean arterial pressure (MAP) were recorded according to the study's measurement time. Time to achieve 90% and 100% neuromuscular block, time to recovery from neuromuscular block 25% (T25), 50% (T50), 75% (T75) and recovery index values were noted. Results: The increases in HR after laryngoscopy and immediately intubation were lower in both groups D than Group C. Values of MAP during laryngoscopy were lower in both Groups D than Group C Times to achieve 90% and 100% neuromuscular block were found significantly lower in dexmedetomidine groups than Group C. Values of T75 and recovery index in Group D 0.5, T25, T50, T75 and recovery index in Group D1 were longer than Group C. Neuromuscular block properties were similar between dexmedetomidine groups. Discussion and Conclusion: We conclude that dexmedetomidine decreased hemodynamic response to endotracheal intubation, especially heart rate dose-dependently, whereas it decreased time to achieve neuromuscular block and increased time to recovery from the neuromuscular block as independent from dose.

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Section: Discussionmentioning

confidence: 99%

The effects of dexmedetomidine on hemodynamic parameters and intubation conditions

Ar¹

2018

Haydarpasa Numune Med J

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“…General anesthesia is commonly given to patients at the time of surgery because it does not cause pain and is comfortable (Wan Hassan et al, 2018). However, repeated exposure of patients undergoing multiple surgeries to anesthetic compounds leads to harmful side effects such as memory loss and impaired cognition (Anderson, 2018).…”

Section: Introductionmentioning

confidence: 99%

Synthesis of oxymatrine hydrazone and its preventive action against sevoflurane induced neuron damage through ERK pathway up-regulation

Yang

Zhang

et al. 2022

Acta Biochim Pol

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Exposure of patients undergoing multiple surgeries to anesthetic compounds leads to harmful side effects such as memory loss and impaired cognition. The current study was aimed to synthesize and investigate the effect of oxymatrine hydrazone on neuronal toxicity induced by sevoflurane in rats. Incubation with oxymatrine hydrazone was followed by exposure to sevoflurane for 48 h and determination of proliferation by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. Apoptosis was detected by flow cytometry using Annexin V‑FITC and propydium iodide staining. Western blot analysis was used for determination of changes in protein expression. Sevoflurane exposure significantly (P<0.05) reduced proliferation of neurons by activation of cell apoptosis. However, pretreatment of neurons with oxymatrine hydrazone prevented reduction of proliferative potential induced on exposure with sevoflurane. Pre-treatment of neurons with 5.0 µM doses of oxymatrine hydrazone significantly prevented apoptosis induction by sevoflurane. Moreover, oxymatrine hydrazone pretreatment inhibited BCL2 Associated-X (BAX) and cleaved caspase-3 levels induced by sevoflurane exposure in neurons. Phosphorylation of extracellular signal‑regulated protein kinase (ERK1/2) and expression of BCL-2 in neurons exposed to sevoflurane were markedly promoted on pretreatment with oxymatrine hydrazone. Additionally, U0126 (ERK ½ activation inhibitor) treatment of sevoflurane exposed neurons inhibited promotion of ERK1/2 phosphorylation by oxymatrine hydrazone pre-treatment. In summary, cytotoxicity of sevoflurane in neurons was prevented on pretreatment with oxymatrine hydrazone. Pretreatment of sevoflurane exposed neurons with oxymatrine hydrazone inhibited apoptosis, suppressed BAX/caspase-3 and elevated BCL-2. Moreover, oxymatrine hydrazone pre-treatment promoted ERK1/2 phosphorylation in sevoflurane exposed neurons. Therefore, oxymatrine hydrazone has a great potential for prevention of neurotoxicity induced by sevoflurane.

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“…In recent years, with the rapid development of surgical procedures, the proportion of patients who undergo general anesthesia has increased due to its diverse application, safety and comfort (1,2). With this the increase in the number of surgeries anesthetic complications, such as postoperative cognitive dysfunction, have increased annually (3).…”

Section: Introductionmentioning

confidence: 99%

Metformin protects against sevoflurane‑induced neuronal apoptosis through the S1P1 and ERK signaling pathways

Yue

Luo

et al. 2018

Exp Ther Med

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The aim of the current study was to investigate whether metformin could counteract sevoflurane-induced neurotoxicity. In vitro experiments on the sevoflurane-induced nerve injury were performed using hippocampal neurons. Neuronal apoptosis was detected by an MTT assay. Protein expression levels of apoptosis-associated genes, including cleaved-caspase-3, apoptosis regulator BAX and apoptosis regulator Bcl-2 were detected by western blot analysis. The mechanism of the effect of metformin on sevoflurane-induced neuronal apoptosis was investigated using a sphingosine 1-phosphate receptor 1 (S1P1) antagonist (VPC23019) and mitogen-activated protein kinase kinase inhibitor (U0126). The current study revealed that metformin may reduce sevoflurane-induced neuronal apoptosis via activating mitogen-activated protein kinase (ERK)1/2 phosphorylation. VPC23019 and U0126 eliminated the neuroprotective effects of metformin on neuronal apoptosis, which suggests that metformin is able to protect against sevoflurane-induced neurotoxicity via activation of the S1P1-dependent ERK1/2 signaling pathway.

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Comparison of the Effects of Dexmedetomidine on the Induction of Anaesthesia Using Marsh and Schnider Pharmacokinetic Models of Propofol Target-Controlled Infusion

Cited by 6 publications

References 19 publications

The effects of dexmedetomidine on hemodynamic parameters and intubation conditions

The effects of dexmedetomidine on hemodynamic parameters and intubation conditions

Synthesis of oxymatrine hydrazone and its preventive action against sevoflurane induced neuron damage through ERK pathway up-regulation

Metformin protects against sevoflurane‑induced neuronal apoptosis through the S1P1 and ERK signaling pathways

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