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Impact of fospropofol disodium on lipid metabolism and inflammatory response in patients with hyperlipidemia: a randomized trial

Abstract

Objective

This study aims to assess the impact of intravenous infusion of fospropofol disodium on lipid metabolism and the inflammatory response in individuals with hyperlipidemia.

Methods

A total of 360 preoperative individuals with hyperlipidemia were selected and randomly assigned to either the treatment group or the control group, with 180 participants in each group. The treatment group received an induction dose of fospropofol disodium at 10 mg/kg intravenously, followed by maintenance at a rate of 10 mg/(kg·h). The control group was administered propofol intravenously at 2 mg/kg for induction and maintained at 4 mg/(kg·h). All other medications were consistent between the two groups. Blood samples (3 ml of venous blood) were collected from patients at four-time points: 1 day before surgery (T0), 3 h after anesthesia induction (T1), 4 h post-surgery (T2), and 24 h post-surgery (T3), to measure levels of triglycerides (TG), cholesterol (CHOL), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (ApoA1), and apolipoprotein B (ApoB). C-reactive protein (CRP) and interleukin-6 (IL-6) levels were assessed at T0 and T3. Sedation onset time and adverse reactions were recorded for both groups.

Results

At T0, the control group exhibited increased TG, CHOL, LDL-C, ApoB, and the ApoB/ApoA1 ratio, while the ApoA1 level had decreased. The LDL-C level and the ApoB/ApoA1 ratio showed significant increases (P < 0.01). Both groups showed elevated CRP and IL-6 levels at T3 (P < 0.01). Compared to the control group, the treatment group demonstrated reduced levels of TG, CHOL, LDL-C, ApoB, and the ApoB/ApoA1 ratio at T1-T3, while ApoA1 levels were higher at T1-T2 (P < 0.01 or P < 0.05). The sedation onset time was notably longer in the treatment group, and the incidence of injection-related pain, respiratory depression, hypotension, and other adverse reactions was significantly lower (P < 0.01).

Conclusion

Compared with propofol, intravenous infusion of fospropofol disodium for more than 3 h during anesthesia has lesser impact on lipid metabolism in patients with hyperlipidemia and does not increase inflammatory factors levels.

Peer Review reports

Introduction

In clinical practice, propofol is a widely used intravenous anesthetic. However, since its formulation requires an emulsion as a carrier, prolonged intravenous anesthesia with propofol can lead to elevated blood lipid levels [1]. Studies have shown that continuous use of propofol anesthesia may exacerbate fat accumulation, disrupt lipid metabolism, and contribute to the development of hyperlipidemia [2]. Fospropofol disodium, a class I water-soluble intravenous anesthetic, is primarily metabolized into propofol via alkaline phosphatase in the body and does not rely on a fat emulsion carrier. It is characterized by rapid onset, shorter duration of action, and a lower incidence of injection pain [3]. While it has minimal effects on blood lipids in patients with normal lipid metabolism during anesthesia, its influence on lipid metabolism in patients with hyperlipidemia during the perioperative period requires further investigation.

Other studies have indicated that propofol can inhibit inflammatory activation and the generation of oxygen-free radicals, exhibiting certain anti-inflammatory properties [4]. Currently, research on the anti-inflammatory effects of fospropofol disodium remains limited. Based on the above background, we hypothesized that intravenous infusion of propofol disodium during anesthesia positively affect lipid metabolism and inflammatory responses in patients with hyperlipidemia. Therefore, this study aims to evaluate the impact of prolonged intravenous fospropofol disodium infusion on lipid metabolism and the inflammatory response in patients with hyperlipidemia, providing a basis for its clinical application.

Materials and methods

General information

This study was approved by the Chinese Clinical Trial Registry (registration number: ChiCTR2400088910) and designed as a prospective, multicenter, randomized, single-blind, parallel-group trial. The trial was conducted across seven centers, with the First People’s Hospital of Guangyuan serving as the lead institution. Ethical approval was granted by the ethics committee of the lead institution (Approval Number: GYYYKY20220102901) and by the respective ethics committees of the participating centers. All participants provided signed informed consent. A total of 360 preoperative patients with hyperlipidemia, admitted between January 2023 and March 2024, were enrolled and randomly assigned to either the treatment group or the control group, with 180 patients in each, using a random number table.

Inclusion criteria: (1) Patients aged 18 to 64 years; (2) American Society of Anesthesiologists (ASA) physical status classification of I or II; (3) Anesthesia duration of more than 3 h; (4) Preoperative triglyceride (TG) levels > 1.70 mmol/L and/or cholesterol (CHOL) levels > 5.17 mmol/L (The normal range of TG levels is 0.56–1.70 mmol/L, and that of CHOL is 2.80–5.17 mmol/L).

Exclusion criteria: (1) Patients who had used lipid-altering drugs before surgery; (2) Planned hepatobiliary or pancreatic surgery; (3) Preoperative abnormal liver function or use of hepatotoxic drugs; (4) History of pancreatitis; (5) Long-term alcohol consumption; (6) Severe mental illness; (7) BMI < 18.5 kg/m² or > 29.9 kg/m².

Methods

All enrolled patients were instructed to abstain from drinking liquids for 2 h and to fast for 8 h before surgery. Additionally, 0.3 mg of penehyclidine hydrochloride was administered intravenously before the procedure. Routine monitoring included ECG, heart rate, blood pressure, oxygen saturation, and bispectral index (BIS), with continuous blood pressure monitored through left radial artery puncture.

For anesthesia induction, the treatment group received an intravenous injection of 10 mg/kg fospropofol disodium (Yichang Humanwell Pharmaceutical Co., LTD.), dissolved in 0.9% sodium chloride and prepared at a concentration of 50 mg/mL. The control group was administered propofol (medium/long-chain lipid emulsion) at 2 mg/kg (Yangtze River Pharmaceutical Group). Once the patients had been successfully anesthetized, both groups received intravenous injections of 0.4 µg/kg sufentanil and 0.6 mg/kg rocuronium, followed by mechanical ventilation after tracheal intubation. For anesthesia maintenance, the treatment group was infused with fospropofol disodium at 10 mg/(kg·h) using infusion pumps, while the control group was infused with propofol at 4 mg/(kg·h) using a medium/long-chain lipid emulsion. Both groups also received continuous intravenous remifentanil at 0.1–0.2 µg/(kg·min) and inhaled 1–2% sevoflurane. In the treatment group, fospropofol disodium infusion was stopped 30 min before the operation’s conclusion, and all anesthetic drugs were discontinued at the end of the surgery in both groups.

Observed indicators

The levels of TG, CHOL, HDL-C, LDL-C, ApoA1, and ApoB were measured in 3 mL of venous blood collected from patients at four-time points: 1 day before surgery (T0), 3 h after anesthesia induction (T1), 4 h after surgery (T2), and 24 h after surgery (T3). C-reactive protein (CRP) and interleukin-6 (IL-6) levels were assessed using ELISA at T0 and T3, respectively. The effective sedation time during induction and the incidence of adverse reactions—including injection pain, hypotension, respiratory depression, nausea, and vomiting—were recorded for both groups. The effective sedation time was defined as the duration from the start of anesthetic drug administration to the loss of the eyelash reflex (by verbal response), while hypotension was characterized as a decrease in mean arterial pressure of more than 20% from the baseline level.

Statistical analysis

TG levels at 4 h post-operation were used as the primary evaluation index to calculate the sample size. Oztekin et al. reported that the plasma TG levels at 4 h after anesthesia induction and maintenance with propofol were significantly higher than baseline levels [5]. Assuming that plasma TG levels in the propofol group were 125 ± 34 mg/dl at 4 h post-operation and 94 ± 39 mg/dl in the phosphate propofol disodium group (based on midazolam data), with α = 0.025, β = 0.2, and an optimality cut-off value of 12, the sample size calculation formula indicate that 57 participants are required for each group. Accounting for a 20% dropout rate, the minimum required sample size increases to 71 participants per group, or 142 in the two groups. As this is a multicenter clinical study carried out in 7 hospitals, the sample size is expanded 2.5-fold, resulting in 360 participants, with 180 in each group.

SPSS 25.0 software was utilized for the comparative analysis of the data. Measurement data that followed a normal distribution were expressed as mean ± standard deviation (\(\bar x \pm s\)). For comparing indicators at different time points between the two groups, ANOVA and single-factor tests of repeated measures were employed. Paired t-tests were conducted for pairwise comparisons at different time points within each group, while independent sample t-tests were used for comparisons between groups. Categorical data were analyzed using the Chi-square test, and P < 0.05 was considered statistically significant.

Results

Comparison of general data and types of surgery between the two groups

There were no significant differences in age, sex, BMI, ASA grade, type of surgery, surgical duration, and anesthesia duration between the two groups (P > 0.05). See Table 1.

Table 1 Comparison of general characteristics and types of surgery between the two groups

Main effect test of lipid metabolism indices in both groups

Normality and homogeneity of variance tests were conducted on the lipid metabolism indices in both groups at different time points, and results indicated that all lipid metabolism indices followed a normal distribution with homogeneity of variance (P > 0.05). Mauchly’s test of sphericity revealed that the covariance matrix of the dependent variables was unequal (P < 0.001), necessitating the use of the Greenhouse-Geisser correction. Analysis of the indicators from both groups demonstrated that, except HDL-C, the time effects were statistically significant (P < 0.001), and significant differences in levels of TG, CHOL, ApoB, and the ApoB/ApoA1 ratio were observed between the two groups (P < 0.001). Other interaction effects were also statistically significant (P < 0.001). See Table 2; Fig. 1A-G.

Table 2 Repeated measures of ANOVA for lipid metabolism analysis during anesthesia in both groups
Fig. 1
figure 1

(A) TG levels and group interactions at various time points in both groups; (B) CHOL levels and group interactions at various time points in both groups; (C) HDL-C levels and group interactions at various time points in both groups; (D) LDL-C levels and group interactions at various time points in both groups; (E) ApoA1 levels and group interactions at various time points in both groups; (F) ApoB levels and group interactions at various time points in both groups; (G) ApoB/ApoA1 ratios and group interactions at various time points in both groups

The two groups of lipid metabolism indices were tested separately

Repeated measures of ANOVA revealed that, compared to T0, levels of TG, CHOL, LDL-C, and ApoB in the control group increased, while ApoA1 levels decreased. In the treatment group, LDL-C and the ApoB/ApoA1 ratio also increased (P < 0.01). Multivariate analysis of variance indicated that the levels of TG, CHOL, LDL-C, ApoB, and the ApoB/ApoA1 ratio in the treatment group were significantly lower at T1 − 3 compared to the control group, and ApoA1 levels were significantly higher at T1 − 2 than in the control group (P < 0.01 or < 0.05).

The significance level was corrected to α’ = 0.008 (0.05/6) for a total of 6 comparisons at 4 time points. The results showed that in the treatment group, TG and LDL-C levels exhibited the following pattern: T0 < T1, and T1 > T2 > T3 (P < α’). For CHOL levels, T0 < T3 was observed (P < α’), while ApoA1 levels showed T0 > T1 and T0 > T2 (P < α’). Additionally, ApoB levels and the ApoB/ApoA1 ratio indicated T1 > T0, T2 < T1, and T3 < T1 (P < α’). In the control group, the levels of TG, CHOL, LDL-C, ApoA1, ApoB, and the ApoB/ApoA1 ratio followed the pattern T0 < T1, and T1 > T2 > T3 (P < α’). See Table 3.

Table 3 Comparison of lipid metabolism parameters between the two groups (\(\bar x \pm s\))

Comparison of CRP and IL6 levels in T0 and T3 between the two groups

Compared to T0, levels of CRP and IL-6 were significantly increased at T3 in both groups, with t-values of 9.745 and 30.023, respectively, in the treatment group, and 9.203 and 26.007 in the control group (P < 0.01 for both). See Fig. 2.

Fig. 2
figure 2

(A) Comparison of CRP levels in T0 and T3 between the two groups, compared with T0, aP<0.01; (B) Comparison of IL-6 levels at T0 and T3 between the two groups, compared with T0, aP<0.01

Comparison of sedation onset time and incidence of adverse reactions between the two groups

Compared to the control group, the effective sedation time in the treatment group was significantly prolonged, while the incidence of injection pain, respiratory depression, hypotension, and other adverse reactions was notably reduced (P < 0.01). See Table 4.

Table 4 Comparison of lipid metabolism indicators between the two groups

Discussion

In recent years, the incidence of cardiovascular and cerebrovascular diseases related to hyperlipidemia has been on the rise, and perioperative hyperlipidemia can negatively impact postoperative outcomes. Elevated blood lipid levels can lead to atherosclerosis, subsequently inducing and exacerbating cardiovascular and cerebrovascular diseases [6, 7]. Factors such as perioperative anesthesia, surgical procedures, blood loss, and postoperative pain may intensify the stress response, increasing the body’s release of stress hormones such as catecholamines, thyroid hormones, and glucagon. These hormones can counteract some effects of insulin, thereby enhancing lipolysis [8,9,10]. Additionally, hyperlipidemia can alter the energy supply in patients, potentially leading to insulin resistance during the perioperative period [11]. This can result in decreased glucose metabolism in tissues, leading to hyperinsulinemia, hyperglycemia, and hyperlipidemia.

Propofol has been widely utilized in clinical anesthesia and sedation due to its advantages, including rapid onset, effective sedation, quick recovery, and minimal side effects [12]. As a short-acting intravenous anesthetic, propofol functions by inhibiting calcium channels and reducing calcium ion influx, which can, to some extent, offset the body’s stress response [13]. However, the side effects associated with intravenous infusion are significant. Propofol employs fat emulsion as a carrier, and prolonged infusion can lead to elevated blood lipid levels, with the triglyceride component in the emulsion being a key contributor to this increase. Previous studies have identified ApoA1 as an important anti-atherosclerotic factor, while ApoB is a recognized risk factor for atherosclerosis. The ApoB/ApoA1 ratio reflects the balance between and pro-atherosclerotic and anti-atherosclerotic factors in plasma. It serves as the most specific indicator for all ischemic events, superior the predictive value of ApoAl or ApoB alone [14, 15]. This study demonstrated that levels of TG, CHOL, LDL-C, ApoB, and the ApoB/ApoA1 ratio in the control group significantly increased after 3 h of continuous intravenous propofol infusion compared to preoperative values. Although these lipid metabolism indices showed a decreasing trend over time, they did not return to baseline levels 24 h post-surgery. This may be attributed to alterations in the enzyme system under stress, which can slow fat metabolism. Furthermore, the infusion of propofol exacerbates the body’s fat load, leading to hyperlipidemia [16]. In addition to propofol infusion, patients with hyperlipidemia may experience insulin resistance, which alters their energy supply and subsequently reduces triglyceride metabolism [17]. Clinical studies have indicated that prolonged and continuous infusion of propofol in the ICU can cause hyperlipidemia and impair liver function, aligning with the findings of this study [18, 19].

This study indicates that fospropofol disodium effectively reduces perioperative lipid metabolism disorders in patients with hyperlipidemia. Fospropofol disodium, a phosphate ester of propofol, exhibits good water solubility and does not require fat emulsion as a carrier, resulting in minimal impact on lipid metabolism during the perioperative period for these patients. As a water-soluble drug and a precursor to propofol, it is converted into propofol by alkaline phosphatase in the body, thereby producing its anesthetic effects [20, 21]. Once in the bloodstream, propofol crosses the blood-brain barrier and binds to GABAA receptors, enhancing chloride ion influx while reducing calcium ion flow, which inhibits the sedative effects on postsynaptic neurons [22]. Notably, while levels of TG, CHOL, LDL-C, ApoB, and the ApoB/ApoA1 ratio in the treatment group were elevated compared to preoperative levels, the degree of increase was significantly less pronounced than in the control group, with values largely returning to baseline 24 h post-surgery. These findings suggest that fospropofol disodium has a minimal effect on perioperative lipid metabolism in hyperlipidemic patients and may offer a protective effect.

Propofol is known for its anti-inflammatory and antioxidant stress effects. Research has shown that it can inhibit the expression of interleukins and cyclooxygenase, thereby reducing oxidative stress and inflammation during the perioperative period, demonstrating its anti-inflammatory properties [23]. In this study, CRP and IL-6 levels increased in both groups 24 h post-surgery, but no significant differences were observed between them. This increase may be attributed to factors such as anesthesia, surgical trauma, and postoperative pain.

Fospropofol disodium, which is converted to propofol by alkaline phosphatase in the body, shares a similar mechanism of action with propofol. Although fospropofol disodium has been modified to be a water-soluble preparation without the need for fatty emulsions, the lack of significant difference in inflammatory response between the two suggests that its anti-inflammatory effect is comparable to that of propofol, with minimal influence from its physical and chemical properties.

This study also indicates that fospropofol disodium has a longer onset time for sedation compared to propofol, along with a lower incidence of adverse reactions such as injection pain, hypotension, and respiratory depression. This prolonged sedation effect is likely due to the conversion of fospropofol disodium to propofol by alkaline phosphatase in vivo, which requires time to complete [24, 25]. During this conversion process, the instantaneous concentration of propofol is lower, contributing to the reduced incidence of adverse reactions.

The limitation of this study lies in its focus on immediate complications associated with anesthetic drugs, such as injection pain, respiratory depression, and hypotension. Long-term complications related to hyperlipidemia, including cardiovascular and cerebrovascular diseases or acute pancreatitis, were not assessed. Future research should aim to investigate these long-term outcomes to provide a more comprehensive understanding of the implications of anesthetic choices in patients with hyperlipidemia.

Conclusion

In conclusion, compared with propofol, intravenous infusion of fospropofol disodium for more than 3 h during anesthesia can reduce the impact on lipid metabolism in patients with hyperlipidemia, and does not increase the level of inflammatory factors.

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Abbreviations

TG:

triglyceride

CHOL:

Cholesterol

HDL-C:

High-density lipoprotein cholesterol

LDL-C:

Low-density lipoprotein cholesterol

ApoA1:

Apolipoprotein A1

ApoB:

Apolipoprotein B

CRP:

C-reactive protein

IL6:

Interleukin 6

BM:

Body mass index

GABAA receptor:

A type γ-aminobutyric acid receptor

References

  1. Arnold HM, Hollands JM, Skrupky LP, Mice ST. Optimizing sustained use of sedation in mechanically ventilated patients: focus on safety. Curr Drug Saf. 2010 Jan;5(1):6–12. https://doiorg.publicaciones.saludcastillayleon.es/10.2174/157488610789869102.

  2. Devaud JC, Berger MM, Pannatier A, Marques-Vidal P, Tappy L, Rodondi N, Chiolero R, Voirol P. Hypertriglyceridemia: a potential side effect of propofol sedation in critical illness. Intensive Care Med. 2012;38(12):1990–8. https://doiorg.publicaciones.saludcastillayleon.es/10.1007/s00134-012-2688-8.

    Article  CAS  PubMed  Google Scholar 

  3. Zhao Z, Jin X, Li Y, Wang X, Cui Y, Zhang B, Kang Y, Zhang G, Chu Q, Zhang J. Efficacy and safety of fospropofol disodium sedation for same-day bidirectional endoscopy in elderly patients: protocol for a prospective, single-center, randomized, double-blind, non-inferiority trial. Front Pharmacol. 2024;15:1378081. https://doiorg.publicaciones.saludcastillayleon.es/10.3389/fphar.2024.1378081.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Tomsič K, Nemec Svete A, Nemec A, Domanjko Petrič A, Pirman T, Rezar V, Vovk T, Seliškar A. Antioxidant capacity of lipid- and water-soluble antioxidants in dogs with subclinical myxomatous mitral valve degeneration anaesthetised with propofol or sevoflurane. BMC Vet Res. 2020;16(1):305. https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12917-020-02529-7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Oztekin I, Gökdoğan S, Oztekin DS, Işsever H, Göksel O, Canik S. Effects of propofol and midazolam on lipids, glucose, and plasma osmolality during and in the early postoperative period following coronary artery bypass graft surgery: a randomized trial. Yakugaku Zasshi. 2007;127(1):173–82. https://doiorg.publicaciones.saludcastillayleon.es/10.1248/yakushi.127.173.

    Article  CAS  PubMed  Google Scholar 

  6. Li JN, Wang MY, Tan YR, Wang LL. Multidirectional Intervention of Chinese Herbal Medicine in the Prevention and treatment of atherosclerosis: from endothelial protection to Immunomodulation. Am J Chin Med. 2024;52(4):925–47. https://doiorg.publicaciones.saludcastillayleon.es/10.1142/S0192415X24500381.

    Article  CAS  PubMed  Google Scholar 

  7. Shi C, Liu S, Zheng M, Yan F, Xu D, Wang W, Chen J. Phospholipid and glycerolipid metabolism as potential diagnostic biomarkers for acute pancreatitis. Lipids Health Dis. 2024;23(1):223. https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12944-024-02217-7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Kargı-Gemici E, Şengelen A, Aksüt Y, Akyol O, Şengiz-Erhan S, Bay M, Önay-Uçar E, Selcan A, Demirgan S. Cerium oxide nanoparticles (nanoceria) pretreatment attenuates cell death in the hippocampus and cognitive dysfunction due to repeated isoflurane anesthesia in newborn rats. Neurotoxicology. 2024;105:82–93. https://doiorg.publicaciones.saludcastillayleon.es/10.1016/j.neuro.2024.08.005.

    Article  CAS  PubMed  Google Scholar 

  9. Jing J, Chen S, Wu X, Yang J, Liu X, Wang J, Wang J, Li Y, Zhang P, Tang Z. Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway. Neural Regen Res. 2024 Jul;29. https://doiorg.publicaciones.saludcastillayleon.es/10.4103/NRR.NRR-D-23-01953.

  10. Reysner M, Reysner T, Janusz P, Kowalski G, Shadi M, Daroszewski P, Wieczorowska-Tobis K, Kotwicki T. Dexamethasone as a perineural adjuvant to a ropivacaine popliteal sciatic nerve block for pediatric foot surgery: a randomized, double-blind, placebo-controlled trial. Reg Anesth Pain Med. 2024 Aug;29:rapm–2024. https://doiorg.publicaciones.saludcastillayleon.es/10.1136/rapm-2024-105694.

  11. Chen X, Gu J, Huang Y. High dietary intake of unsaturated fatty acids is associated with improved insulin resistance - a cross-sectional study based on the NHANES database. Lipids Health Dis. 2023;22(1):216. https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12944-023-01982-1.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Jia Z, Cai RZ, Zhao CC, Zhou B, Tan ZM. [Impacts of different anesthetic protocols on the speed and quality of postoperative resuscitation in patients undergoing painless gastroscopy]. Zhonghua Yi Xue Za Zhi. 2024;104(31):2943–8. https://doiorg.publicaciones.saludcastillayleon.es/10.3760/cma.j.cn112137-20240126-00203. Chinese.

    Article  CAS  PubMed  Google Scholar 

  13. Kaushal RP, Vatal A, Pathak R. Effect of etomidate and propofol induction on hemodynamic and endocrine response in patients undergoing coronary artery bypass grafting/mitral valve and aortic valve replacement surgery on cardiopulmonary bypass. Ann Card Anaesth. 2015 Apr-Jun;18(2):172–8. https://doiorg.publicaciones.saludcastillayleon.es/10.4103/0971-9784.154470.

  14. Panayiotou A, Griffin M, Georgiou N, Bond D, Tyllis T, Tziakouri-Shiakalli C, Fessas C, Nicolaides A. ApoB/ApoA1 ratio and subclinical atherosclerosis. Int Angiol. 2008;27(1):74–80.

    CAS  PubMed  Google Scholar 

  15. Walldius G, Jungner I, Aastveit AH, Holme I, Furberg CD, Sniderman AD. The apoB/apoA-I ratio is better than the cholesterol ratios to estimate the balance between plasma proatherogenic and antiatherogenic lipoproteins and to predict coronary risk. Clin Chem Lab Med. 2004;42(12):1355–63. https://doiorg.publicaciones.saludcastillayleon.es/10.1515/CCLM.2004.254.

    Article  CAS  PubMed  Google Scholar 

  16. Van S, Lam V, Patel K, Humphries A, Siddiqi J. Propofol-related infusion syndrome: a bibliometric analysis of the 100 most-cited articles. Cureus. 2023;15(10):e46497. https://doiorg.publicaciones.saludcastillayleon.es/10.7759/cureus.46497.

    Article  PubMed  PubMed Central  Google Scholar 

  17. Liu H, Hao M, Liu W, Chen H, Han C, Shao Y, Wang L. Medium- and long-chain triglyceride propofol activates PI3K/AKT pathway and inhibits non-alcoholic fatty liver disease by inhibiting lipid accumulation. J Bioenerg Biomembr. 2024;56(1):45–53. https://doiorg.publicaciones.saludcastillayleon.es/10.1007/s10863-023-09997-0.

    Article  CAS  PubMed  Google Scholar 

  18. Machata AM, Willschke H, Kabon B, Kettner SC, Marhofer P. Propofol-based sedation regimen for infants and children undergoing ambulatory magnetic resonance imaging. Br J Anaesth. 2008;101(2):239–43. https://doiorg.publicaciones.saludcastillayleon.es/10.1093/bja/aen153.

    Article  CAS  PubMed  Google Scholar 

  19. Trapani G, Altomare C, Liso G, Sanna E, Biggio G. Propofol in anesthesia. Mechanism of action, structure-activity relationships, and drug delivery. Curr Med Chem. 2000;7(2):249–71. https://doiorg.publicaciones.saludcastillayleon.es/10.2174/0929867003375335.

    Article  CAS  PubMed  Google Scholar 

  20. Gao X, Yang X, Shu H, Yu Y, Liu H, Yuan Y, Zou X, Yuan S, Shang Y. Fospropofol Disodium for Sedation of postoperative ICU patients: a dose-finding study. Am J Ther 2024 Jul-Aug 01;31(4):e435–9. https://doiorg.publicaciones.saludcastillayleon.es/10.1097/MJT.0000000000001650

  21. Gao X, Yang X, Tang Y, Fang X, Yuan Y, Qi H, Li R, Shu H, Zou X, Shang Y. Fospropofol disodium versus propofol for long-term sedation during invasive mechanical ventilation: a pilot randomized clinical trial. J Clin Anesth. 2024;95:111442. https://doiorg.publicaciones.saludcastillayleon.es/10.1016/j.jclinane.2024.111442.

    Article  CAS  PubMed  Google Scholar 

  22. Wang S, Li T, He H, Li Y. Dynamical changes of interaction across functional brain communities during propofol-induced sedation. Cereb Cortex. 2024;34(6):bhae263. https://doiorg.publicaciones.saludcastillayleon.es/10.1093/cercor/bhae263.

    Article  PubMed  Google Scholar 

  23. Ke JJ, Zhan J, Feng XB, Wu Y, Rao Y, Wang YL. A comparison of the effect of total intravenous anaesthesia with propofol and remifentanil and inhalational anaesthesia with isoflurane on the release of pro- and anti-inflammatory cytokines in patients undergoing open cholecystectomy. Anaesth Intensive Care. 2008;36(1):74–8. https://doiorg.publicaciones.saludcastillayleon.es/10.1177/0310057X0803600113.

    Article  CAS  PubMed  Google Scholar 

  24. Wu CM, Zhang WS, Liu J, Zhang WY, Ke BW. Efficacy and Safety of Fospropofol Disodium for Injection in General Anesthesia Induction for adult patients: a phase 3 trial. Front Pharmacol. 2021;12:687894. https://doiorg.publicaciones.saludcastillayleon.es/10.3389/fphar.2021.687894.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Liu LQ, Hong PX, Song XH, Zhou CC, Ling R, Kang Y, Qi QR, Yang J. Design, synthesis, and activity study of Water-Soluble, Rapid-Release Propofol Prodrugs. J Med Chem. 2020;63(14):7857–66. https://doiorg.publicaciones.saludcastillayleon.es/10.1021/acs.jmedchem.0c00698.

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

We would like to thank Dr. Biao Li, Dr. Wen-Kong Sun, and Dr. Xin Tang for their valuable contributions to the data collection, interpretation, and analysis of this research project.

Funding

This study was funded by the Guiding Science and Technology Plan Project of Guangyuan City (Grant Number: 22ZDYF0095). The funding body had no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.

Author information

Authors and Affiliations

Authors

Contributions

Chuan Yang: Conceptualization, Data curation, Formal Analysis, Funding acquisition, Writing– original draft. Tian-Bo Chai: Data curation, Formal Analysis, Software, Writing– original draft. Xing-Zhu Yao: Data curation, Formal Analysis, Visualization.Li Zhang: Data curation, Formal Analysis, Investigation.Wen-Ming Qin: Data curation, Formal Analysis. Hong Liang: Data curation, Formal Analysis, Software.Qiong-Zhen He: Data curation, Formal Analysis.Ze-Yu Zhao: Formal Analysis, Validation, Writing– review & editing.All authors read and approved the final draft.

Corresponding authors

Correspondence to Chuan Yang or Ze-Yu Zhao.

Ethics declarations

Ethics approval and consent to participate

This controlled trial was approved by the Ethics Committee of Guangyuan First People’s Hospital (Approval Number: GYYYKY20220102901) and registered in the Chinese Clinical Trial Register website (www.chictr.org.cn, ChiCTR2400088910). This study was conducted in accordance with the declaration of Helsinki. Written informed consent was obtained from all participants.

Consent for publication

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Yang, C., Chai, TB., Yao, XZ. et al. Impact of fospropofol disodium on lipid metabolism and inflammatory response in patients with hyperlipidemia: a randomized trial. BMC Anesthesiol 25, 99 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12871-025-02965-8

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