Measuring the accuracy of propofol target-controlled infusion (TCI) before and after surgery with major blood loss

Mohler, Thomas; Welter, JoEllen; Steurer, Martina A.; Neumann, Luis; Zueger, Max; Kræmer, Thomas; Dullenkopf, Alexander

doi:10.1007/s10877-019-00261-8

Cited by 11 publications

(7 citation statements)

References 17 publications

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“…Previous research indicated that propofol could reduce hippocampal neuronal apoptosis after ischemia-reperfusion in rats, which may be related to the activation of the PI3K/AKT signaling pathway and upregulation of Bcl-2 protein expression, exerting neuroprotective effects (32). Since the prior maximum plasma concentration of propofol used clinically is 56 µM, we selected 100 µM as the highest experimental concentration in our assessments (33). We examined the effects of propofol-induced oxidative stress injuries on reactive oxygen species (ROS) and ATP levels, and apoptosis in hippocampal neurons.…”

Section: Discussionmentioning

confidence: 99%

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

et al. 2022

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Propofol is a fast and short-acting intravenous anesthetic widely used in clinical anesthesia and intensive care unit sedation. However, its use can cause abnormal effects on the central nervous system. Thus, the purpose of this study was to investigate the mechanism of propofol on primary hippocampal neuron injury. In addition, we aimed to determine whether a correlation exists between propofol and mitochondrial apoptosis-induced neurotoxicity. Hippocampal neurons cultured for 4 days were exposed to different drugs. The treatment groups were divided according to drug exposure into propofol, a rotenone inhibitor, and a coenzyme Q10 agonist groups. The final concentrations of propofol were 1, 10 and 100 µM. The content of ATP and reactive oxygen species (ROS) in the neurons of each group were detected using commercial kits in the culture supernatant after 3 h of drug exposure. Western blotting was used to analyze the expression of apoptosis-related proteins. The JC-1 kit was used to detect the mitochondrial membrane potential. The results revealed that, compared with the non-propofol treatment groups, the expression of apoptosis-related proteins, ATP content, and mitochondrial membrane potential were significantly decreased while the ROS content was markedly increased in the propofol treatment group. In conclusion, propofol treatment promoted damage to hippocampal neuronal mitochondria in a dose-dependent manner. This damage may lead to neuronal apoptosis and neurotoxicity by inducing the inhibition of mitochondrial respiratory chain complex I.

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Section: Discussionmentioning

confidence: 99%

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

et al. 2022

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“…This is supported by the statistically significant correlation of performance error at the end of surgery with the calculated fluid balance. In a similar set-up with surgery involving major blood loss, we were unable to demonstrate an association, which was most likely due to the difficulty of calculating a reliable fluid balance in these cases [16].…”

Section: Discussionmentioning

confidence: 68%

propofol-target-controlled-infusion-performance-of-the-schnider-model-in-the-clinical-setting-for-major-surgical-procedures

Neumann¹,

Mohler²,

Steurer³

et al. 2019

Clin Res Trial

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Background: Limited data are available about the difference in propofol plasma levels estimated by target controlled infusion models (TCI) and measured plasma levels during prolonged operations. We hypothesized the difference to be greater at the end of surgery than at the beginning.Methods: For this prospective observational study, adult patients were enrolled (elective surgery, estimated operating time of ≥ 3 hours, eligible to receive propofol using TCI (Schnider model)). Blood was sampled in steady state after anesthesia induction (propofol dosed to achieve BIS values of 40-60; T 1 ) and at the end of the procedure (T 2 ). Fluid balance was recorded. Bias and limits of agreement of actual plasma levels (C blood ) to TCI values (C TCI ) were calculated, hemodynamics assessed, and performance error (PE) measured (PE(%) = ((C blood -C TCI )/C TCI )*100) and assessed for correlations.Results: Thirty patients were included. Mean duration of procedure was 250 min (± 136.7), fluid balance 2066 ml (± 1017), and all patients were hemodynamically stable. Mean C TCI was 2.0 µ/ml (± 0.3) and 1.8 µ/ml

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“…17 In addition, the pharmacokinetics of propofol is significantly influenced by hemodynamics. 18 Intraoperative blood loss, fluid replacement, 19 and vasoactive drugs 20 can all result in changes in propofol volume and velocity distribution. The effect of body mass index (BMI) on TCI propofol has not, to the best of our knowledge, been evaluated before in the clinical setting, excluding combined medications and surgical procedures.…”

Section: What Is K Nown and Objec Tivementioning

confidence: 99%

Body mass index and pharmacodynamics of target‐controlled infusion of propofol: A prospective non‐randomized controlled study

Gong

et al. 2022

Clinical Pharmacy Therapeu

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What is known and objective: In our preliminary study, there were large individual variations at sedation levels during propofol target-controlled infusion (TCI). The present study aimed to assess the effects of body mass index (BMI) on the pharmacodynamic index of propofol TCI. Methods:This prospective, non-randomized controlled trial evaluated 175 female patients undergoing breast lumpectomy. Anesthesia was induced with propofol using the TCI system embedded Schnider model. The effect compartment concentration was set to 3 μg/ml, and the start time of infusion was recorded. When the target concentration reached 3 μg/ml, the patient could not be awakened (Ramsay sedation score ≥4), and when the Bispectral Index (BIS) was <60, the infusion was discontinued, and the time point was recorded. The observation end-point was set at the Observer's Assessment of Alertness/Sedation (OAA/S) score of <4. The correlation between the BMI and the pharmacodynamic index of propofol was evaluated.Results and discussion: Propofol induction time was significantly correlated with the BMI (p < 0.001). The induction time of the underweight subjects was 10.14 ± 2.19 min, which was remarkably higher than that of normal weight (6.48 ± 3.44 min) and overweight (4.75 ± 2.53 min) individuals (p < 0.001). There were still significant differences after multivariable-adjusted regressions (p < 0.001). There were no significant differences in recovery time and sedative effect indicators, such as Ramsay score, BIS value, and effect compartment concentration, between the three groups (p > 0.05 for all).What is new and conclusion: These results suggest that the BMI is one of the critical factors affecting the pharmacodynamic index of propofol TCI, and the induction time decreased progressively with increasing BMI. The Schnider model might underpredict doses of propofol for underweight individuals.

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Measuring the accuracy of propofol target-controlled infusion (TCI) before and after surgery with major blood loss

Cited by 11 publications

References 17 publications

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

propofol-target-controlled-infusion-performance-of-the-schnider-model-in-the-clinical-setting-for-major-surgical-procedures

Body mass index and pharmacodynamics of target‐controlled infusion of propofol: A prospective non‐randomized controlled study

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