The median effective concentration (EC50) of propofol with different doses of fentanyl during colonoscopy in elderly patients

Li, Shiyang; Fang, Yu; Zhu, Haiqin; Yang, Yuting; Yang, Liqun; Lian, Jianfeng

doi:10.1186/s12871-016-0189-y

Cited by 20 publications

(36 citation statements)

References 23 publications

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“…Fentanyl was shown to cause and promote hypotension [ 1 , 2 ]. On the other hand, the addition of fentanyl prior to propofol induction is used to decrease propofol dose and hypertensive response to tracheal intubation [ 30 – 32 ]. In our study, 1.3 μg/kg of fentanyl for the stable group (MAP change < 30%) and 1.2 μg/kg for the unstable group (MAP change ≥30%) were administered for anesthetic induction ( P < 0.001).…”

Section: Discussionmentioning

confidence: 99%

Prediction of hemodynamic fluctuations after induction of general anesthesia using propofol in non-cardiac surgery: a retrospective cohort study

et al. 2018

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BackgroundAlthough propofol is a common anesthetic agent for the induction of general anesthesia, hemodynamic fluctuations are occasionally prominent during induction/intubation. The aims of this study were to determine the influential factors on enhanced hemodynamic fluctuation and to establish a prediction formula to quickly determine the dose of propofol to protect against hemodynamic fluctuations.MethodsThis retrospective cohort study patients (n = 2097) were 18 years or older. They underwent general anesthesia induction using propofol and orotracheal intubation for non-cardiac surgery at Kyushu University Hospital during April 2015 to March 2016. Preoperative patient clinical information was collected from anesthesia preoperative evaluation records. Intraoperative data were obtained from computerized anesthesia records. If patients’ post-induction mean arterial blood pressure (MAP) decreased or increased 30% or more from their pre-induction MAP, they were determined to have enhanced hemodynamic fluctuations. Unconditional logistic regression was used to assess the adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Structural equation modeling (SEM) was conducted to simultaneously examine the direct and indirect effect (path coefficient = r) of potential variables.ResultsIn the SEM analysis, age was significantly associated with enhanced hemodynamic fluctuations (adjusted odds ratio = 1.008, 95% CI = 1.001–1.015, P = 0.03). Age (path coefficient (r) = − 0.0113, 95% CI = − 0.0126–0.010, P < 0.001), American Society of Anesthesiologists physical status (ASA-PS) (r = − 0.0788, 95% CI = − 0.1431–0.0145, P = 0.02), sex (r = 0.057, 95% CI = 0.0149–0.9906, P = 0.01), and fentanyl dose (r = 0.1087, 95% CI = 0.0707–0.1467, P < 0.001) influenced the dose of propofol in induction. The prediction formula of “Propofol dose (mg) = [2.374 – 0.0113 × age (year) – 0.0788 (if ASA-PS 3 or 4) + 0.057 (if female) + 0.1087 × fentanyl dose (μg/kg)] × body weight (kg)” was derived.ConclusionsAge was associated with hemodynamic fluctuations in induction. Although the prediction formula is considered to be acceptable, future studies validating whether it can decrease patients’ risk of enhanced hemodynamic fluctuations in clinical situations are necessary.

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Section: Discussionmentioning

confidence: 99%

Prediction of hemodynamic fluctuations after induction of general anesthesia using propofol in non-cardiac surgery: a retrospective cohort study

et al. 2018

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“…One must use caution in interpreting the results of in vitro cell culture experiments. Most of the studies cited in this review used concentrations of propofol in the range of clinical doses (2 to 4 μg/mL [ 29 – 31 ]). However, propofol binds extensively to erythrocytes (50%) and serum proteins almost exclusively albumin (48%) [ 32 ].…”

Section: Effects Of Propofol On Breast Cancer Cellsmentioning

confidence: 99%

Effect of Propofol on breast Cancer cell, the immune system, and patient outcome

Liu

Dilger

et al. 2018

BMC Anesthesiol

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Breast cancer is the second leading cause of cancer death in women. Surgery is the first line of treatment for breast cancer. Retrospective clinical studies suggest that the type of anesthesia administered during oncological surgery may influence patient outcome. Propofol, the widely used intravenous anesthetic agent, may lead to better outcomes compared to volatile anesthetics. Here we review the literature on the effect of propofol in breast cancer cells, the immune system, pain management, and patient outcomes. Evidence from the study of breast cancer cell lines suggests that high concentrations of propofol have both anti-tumor and pro-tumor effects. Propofol and volatile anesthetics have different effects on the immune system. Propofol has also been shown to reduce the development and severity of acute and chronic pain following surgery. Although a retrospective study that included many types of cancer indicated that propofol increases the long-term survival of patients following surgery, the evidence for this in breast cancer is weak. It has been shown that Propofol combined with paravertebral block led to change of serum composition that affects the breast cancer cell behaviors and natural killer cell activity. Prospective studies are in progress and will be finished within 5 years. The existing evidence is not sufficient to warrant changes to current anesthetic management. Further research is needed to clarify the mechanisms by which propofol affects cancer cells and the immune system.

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“…In our electrophysiology experiments, propofol was observed to cause left shift activation, increasing with concentrations of 0.3-3 µM, and decreasing with concentrations from 3-30 µM, while inactivation increased with concentrations (Figure 2). According to clinical studies, the EC 50 of propofol in human plasma is around 15 µM (Li et al, 2015), and maintenance is around 30 µM (Casati et al, 1999). Hence, We conclude that light anesthesia primarily accelerates Na V activation, while deep anesthesia enhances Na V inactivation.…”

Section: Mammalian Na V and Nachbacmentioning

confidence: 75%

“…It has been reported that the EC 50 of propofol in human plasma is 11-17 µM (2.0-3.14 µg/mL) (Kodaka et al, 2004;Li et al, 2015) and deep anesthesia requires 28-34 µM (5-6 µg/mL) (Casati et al, 1999). To investigate the manner in which different concentrations of propofol affect Na V , we established a concentration gradient with 0.03, 0.1, 0.3, 1, 3, 10, 20, and 30 µM propofol, and measured corresponding activation and inactivation parameters by electrophysiology.…”

Section: The Effects Of Propofol On the Activation And Inactivation Omentioning

confidence: 99%

A Potential Mechanism of Sodium Channel Mediating the General Anesthesia Induced by Propofol

Xiao

Chen

2020

Front. Cell. Neurosci.

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General anesthesia has revolutionized healthcare over the past 200 years and continues to show advancements. However, many phenomena induced by general anesthetics including paradoxical excitation are still poorly understood. Voltage-gated sodium channels (NaV) were believed to be one of the proteins targeted during general anesthesia. Based on electrophysiological measurements before and after propofol treatments of different concentrations, we mathematically modified the Hodgkin–Huxley sodium channel formulations and constructed a thalamocortical model to investigate the potential roles of NaV. The ion channels of individual neurons were modeled using the Hodgkin–Huxley type equations. The enhancement of propofol-induced GABAa current was simulated by increasing the maximal conductance and the time-constant of decay. Electroencephalogram (EEG) was evaluated as the post-synaptic potential from pyramidal (PY) cells. We found that a left shift in activation of NaV was induced primarily by a low concentration of propofol (0.3–10 μM), while a left shift in inactivation of NaV was induced by an increasing concentration (0.3–30 μM). Mathematical simulation indicated that a left shift of NaV activation produced a Hopf bifurcation, leading to cell oscillations. Left shift of NaV activation around a value of 5.5 mV in the thalamocortical models suppressed normal bursting of thalamocortical (TC) cells by triggering its chaotic oscillations. This led to irregular spiking of PY cells and an increased frequency in EEG readings. This observation suggests a mechanism leading to paradoxical excitation during general anesthesia. While a left shift in inactivation led to light hyperpolarization in individual cells, it inhibited the activity of the thalamocortical model after a certain depth of anesthesia. This finding implies that high doses of propofol inhibit the network partly by accelerating NaV toward inactivation. Additionally, this result explains why the application of sodium channel blockers decreases the requirement for general anesthetics. Our study provides an insight into the roles that NaV plays in the mechanism of general anesthesia. Since the activation and inactivation of NaV are structurally independent, it should be possible to avoid side effects by state-dependent binding to the NaV to achieve precision medicine in the future.

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The median effective concentration (EC50) of propofol with different doses of fentanyl during colonoscopy in elderly patients

Cited by 20 publications

References 23 publications

Prediction of hemodynamic fluctuations after induction of general anesthesia using propofol in non-cardiac surgery: a retrospective cohort study

Prediction of hemodynamic fluctuations after induction of general anesthesia using propofol in non-cardiac surgery: a retrospective cohort study

Effect of Propofol on breast Cancer cell, the immune system, and patient outcome

A Potential Mechanism of Sodium Channel Mediating the General Anesthesia Induced by Propofol

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