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Journal articles on the topic 'Propofol'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 September 2024

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1

Djordjevic, Biljana, Dragana Loncar-Stojiljkovic, Dragan Ivanovic, Gordana Ivanovic, and Milos Stojiljkovic. "Co-induction in outpatient anesthesia." Vojnosanitetski pregled 59, no. 6 (2002): 609–14. http://dx.doi.org/10.2298/vsp0206609d.

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Cilj. Koindukcija u anesteziji je veoma korisna: sinergisticki efekti dva indukciona leka mogu da smanje indukcionu dozu i pojavu nezeljenih efekata. Cilj rada bio je da se ispitaju i uporede dve tehnike anestezije za kratke ginekoloske intervencije u ambulantnim uslovima. Grupa od 80 zena zakazana za hirurski prekid trudnoce podeljena je metodom slucajnog uzorka na dve jednake grupe - kontrolnu i koindukcionu. Metode. Prva grupa dobila je: atropin 0,5 mg, iv., alfentanil 0,5 mg iv. i propofol kao frakcionisani iv. bolus do gasenja refleksa trepavica. Druga grupa je dobila: atropin 0,5 mg, alfentanil 0,5 mg, midazolam 3 mg i propofol na isti nacin kao i prva grupa. Anestezija je odrzavana dodatnim dozama. Registrovani su kardiovaskularni parametri, kvalitet anestezije, nezeljena dejstva i brzina oporavka. Rezultati. Kod osoba koje su dobijale midazolam indukciona doza propofola bila je znacajno niza, dok kardiovaskularni parametri nisu bili znacajno razliciti. Oporavak posle anestezije bio je nakon koindukcije malo duzi, sto nije imalo klinicki znacaj. U koindukcionoj grupi uoceno je smanjenje nezeljenih dejstava. Zakljucak. Rezultati studije pokazali su da u ambulantnoj anesteziji koindukcija kombinacijom midazolam-propofol u poredjenju sa propofolom ima sledece prednosti: smanjenje doze propofola, bolji kvalitet anestezije i smanjenje nezeljenih dejstava. Oporavak je bio brzi u grupi koja nije dobijala midazolam, sto nije imalo klinicki znacaj. Zakljucak je da koindukcija kombinacijom midazolam-propofol ima prednost kod intervencija u ambulantnim uslovima.

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2

Özaltun, Betül, and Zeliha Selamoğlu. "Affinity of Propofol to Human Serum Albumin and Cardiovascular Effects." Turkish Journal of Agriculture - Food Science and Technology 7, no. 4 (April 24, 2019): 684. http://dx.doi.org/10.24925/turjaf.v7i4.684-687.2486.

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Propofol is used in general anesthesia and sedation. İt is an lipofilic agent and metabolize to inactive form in liver then excreted in the urine. In body it is turnover changes by human serum albumin amount. >97% of propofol is bound to serum albumin. So that hypoalbunemia changes propofol effects. Free form of propopol can pass all membrans such as the blood-brain barrier and the cellular membrane of the cardiac endothelium. Propofol may cause significant myocardial depression, decrease blood pressure and cause life threatining arytmias. Changes in the ratio of free and bound forms of propofol and albumin depending on the dose and duration of administration, the effects of this ratio on cardiac profile are discussed in this study. According to the findings, it was determined that the albumin affinity of propofol decreased in all dose groups in time. Since free HSA and free propofol ratio will increase, this situation is thought to affect the cardiac profile negatively.

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3

Penning, Donald, Simona Cazacu, Raphael Nizar, Cunli Xiang, Hodaya Goldstein, Matan Krasner, Efrat Barbiro-Michaely, et al. "SYST-24 PROPOFOL EXERTS ANTI-TUMOR EFFECTS IN GLIOMA AND THE TUMOR MICROENVIRONMENT VIA NON-CODING RNAS AND SECRETED EXOSOMES." Neuro-Oncology Advances 5, Supplement_3 (August 1, 2023): iii32. http://dx.doi.org/10.1093/noajnl/vdad070.126.

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Abstract BACKGROUND Glioblastoma (GBM), is the most common primary brain tumor. GBM contains a small subpopulation of glioma stem cells (GSCs) that are implicated in tumor recurrence and treatment resistance and therefore represent important therapeutic targets. Recent clinical studies suggest propofol impacts subsequent tumor response to treatments and patient prognosis. The effects of propofol on patient derived GSCs alone and in combination with radiation and temozolomide, (TMZ) have not been reported. Objectives: The molecular mechanisms underlying propofol’s anti-tumor effects on GSCs and its effect on cellular communication with microglia was studied. Using GSC spheroids, differentiated glioma and tumor cells on a microfluid chip, effects of propofol alone and together with radiation and TMZ on the self-renewal and stemness of GSCs, their mesenchymal transit and the proliferation and apoptosis of differentiated glioma cells was analyzed. Using transwell plates, the effects of propofol on the cross-talk of GSCs with human microglia cells was examined. RESULTS Propofol exerted a dose-dependent inhibitory effect on the self-renewal, expression of mesenchymal markers and migration of GSCs and sensitized them to both temozolomide (TMZ) and radiation. At higher concentrations propofol induced a large degree of cell death as demonstrated using microfluid chip. Propofol increased the expression of the lncRNA BDNF-AS, which acts as a tumor suppressor in GBM and silencing of this lncRNA partially abrogated propofol’s anti-tumor effects. Propofol also inhibited the pro-tumorigenic GSC-microglia cross talk via extracellular vesicles (EVs) and delivery of BDNF-AS. CONCLUSIONS Propofol exerted anti-tumor effects on GSCs and differentiated glioma cells by inhibiting cell renewal, proliferation, and mesenchymal transition and by inducing cell death at higher concentration. Propofol also sensitized GSCs to radiation and TMZ. Propofol, which is widely used in GBM surgeries, should be further explored as a potential repurposed drug during resection and an effective adjunct to radiation and TMZ.

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4

Alphin, Robert S., Jeffrey R. Martens, and Donn M. Dennis. "Frequency-dependent Effects of Propofol on Atrioventricular Nodal Conduction in Guinea Pig Isolated Heart." Anesthesiology 83, no. 2 (August 1, 1995): 382–94. http://dx.doi.org/10.1097/00000542-199508000-00019.

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Background The use of propofol has been associated with episodes of bradycardias. The mechanism(s) underlying these phenomena are not well defined. Therefore we investigated (1) the chronotropic and dromotropic effects of propofol, (2) the frequency-dependent effects of propofol on the atrioventricular (AV) node, and (3) the physiologic mechanism(s) underlying propofol's effects on AV nodal conduction. Methods Guinea pig isolated, perfused hearts were instrumented for measurement of atrial rate and AV nodal conduction time in spontaneously beating hearts, or stimulus-to-His bundle (S-H) intervals in atrially paced hearts. In addition, the Wenckebach cycle length, effective refractory period and S-H interval prolongation to an abrupt increase in pacing rate were measured to further define propofol's dromotropic effects and frequency-dependent behavior. Results Propofol, in a concentration-dependent manner, (1) slowed atrial rate and AV nodal conduction time in spontaneously beating hearts, (2) prolonged the S-H interval in atrially paced hearts, and (3) prolonged Wenckebach cycle length and effective refractory period. The negative dromotropic effect of propofol was greater during atrial pacing than in spontaneously beating hearts. Furthermore, this effect was enhanced at faster pacing rates, indicating frequency-dependent behavior. Atropine significantly antagonized propofol-induced S-H interval prolongation. The results of competition binding studies also supported a M2-muscarinic receptor-mediated mechanism. Conclusions We conclude that in the isolated guinea pig heart, propofol slows atrial rate and depresses AV nodal conduction in a concentration-dependent manner. The negative dromotropic effect of propofol shows frequency dependence and is predominantly mediated by M2-muscarinic receptors. Given the marked rate dependence of propofol's AV nodal actions, this anesthetic agent may impart antidysrhythmic protection to those patients susceptible to supraventricular tachycardias.

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5

Nizar, Rephael, Simona Cazacu, Cunli Xiang, Matan Krasner, Efrat Barbiro-Michaely, Doron Gerber, Jonathan Schwartz, et al. "Propofol Inhibits Glioma Stem Cell Growth and Migration and Their Interaction with Microglia via BDNF-AS and Extracellular Vesicles." Cells 12, no. 15 (July 25, 2023): 1921. http://dx.doi.org/10.3390/cells12151921.

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Glioblastoma (GBM) is the most common and aggressive primary brain tumor. GBM contains a small subpopulation of glioma stem cells (GSCs) that are implicated in treatment resistance, tumor infiltration, and recurrence, and are thereby considered important therapeutic targets. Recent clinical studies have suggested that the choice of general anesthetic (GA), particularly propofol, during tumor resection, affects subsequent tumor response to treatments and patient prognosis. In this study, we investigated the molecular mechanisms underlying propofol’s anti-tumor effects on GSCs and their interaction with microglia cells. Propofol exerted a dose-dependent inhibitory effect on the self-renewal, expression of mesenchymal markers, and migration of GSCs and sensitized them to both temozolomide (TMZ) and radiation. At higher concentrations, propofol induced a large degree of cell death, as demonstrated using microfluid chip technology. Propofol increased the expression of the lncRNA BDNF-AS, which acts as a tumor suppressor in GBM, and silencing of this lncRNA partially abrogated propofol’s effects. Propofol also inhibited the pro-tumorigenic GSC-microglia crosstalk via extracellular vesicles (EVs) and delivery of BDNF-AS. In conclusion, propofol exerted anti-tumor effects on GSCs, sensitized these cells to radiation and TMZ, and inhibited their pro-tumorigenic interactions with microglia via transfer of BDNF-AS by EVs.

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6

Pollina, Cole, Luis Fernandez-Nava, and Cooper Phillips. "The effects of body habitus, age, and sex on adequate propofol dosing and infusion for general anesthesia." Southwest Respiratory and Critical Care Chronicles 11, no. 47 (April 25, 2023): 21–25. http://dx.doi.org/10.12746/swrccc.v11i47.1119.

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Propofol (Diprivan) is the most widely used intravenous (IV) anesthetic for the induction and maintenance of general anesthesia. Its rapid onset, fast recovery, and antiemetic properties make propofol a popular anesthetic drug over competing drugs, such as etomidate, ketamine, and halogenated gases. While there is general agreement about the physiological effects of propofol, inconsistent dosing metrics likely complicate its disputed effects on peri- and post-operative hemodynamics and cardiac function in the literature. This review provides the rationale for the recommended dosing metric of propofol and clarifies the bodily effects of dose-appropriate propofol use. This was achieved through a systematic review of propofol’s mechanism of action and observed physiological effects with respect to body habitus, age, and sex.Keywords:propofol, anesthesia, hemodynamics, induction

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7

Li, Weiguang, Yu Zhang, Yanru Liu, Feng Yue, Yiming Lu, Huanrong Qiu, Dawen Gao, et al. "In Vitro Kinetic Evaluation of the Free Radical Scavenging Ability of Propofol." Anesthesiology 116, no. 6 (June 1, 2012): 1258–66. http://dx.doi.org/10.1097/aln.0b013e3182567dcc.

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Background Propofol is a widely used, short-acting, and intravenously administered hypnotic agent with notable antioxidant and free radical scavenging activities. However, there are relatively few kinetic studies on the free radical scavenging ability of propofol. The goal of this study is to evaluate the kinetics of propofol scavenging 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical (ABTS(·+)). Methods The stock solution of ABTS(·+) was prepared by incubating 7 mM ABTS with 2.8 mM potassium persulfate in deionized water, and then diluted with 5 mM phosphate-buffered saline (pH 7.2) to get a working solution (36 μM ABTS(·+) and 18 μM ABTS). The reaction was monitored by measuring specific absorbance changes of ABTS and ABTS(·+) after adding 4 μM propofol (final concentration) to the working solution. The propofol-ABTS(·+) reaction products were analyzed by high-performance liquid chromatography and liquid chromatography mass spectrometry/mass spectrometry. Results Wave scanning and kinetic evaluation demonstrated that the ABTS(·+) scavenging process of propofol is relatively fast. The ABTS(·+) consumption rate by propofol is greater than the rate of ABTS formation. The degradation products of reaction between propofol and ABTS(·+) were mainly ABTS-propofol, a part of the ABTS molecule, and a combination of propofol with a part of the ABTS molecule. Conclusions Propofol scavenges ABTS(·+) with a fast and stable kinetic feature in vitro, which is useful and important for understanding propofol's antioxidant properties. The kinetic process of the free radical scavenging activity of propofol may also play a role in dynamic protection in the body.

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8

Kraut, Richard A. "Propofol." Oral and Maxillofacial Surgery Clinics of North America 4, no. 4 (November 1992): 825–30. http://dx.doi.org/10.1016/s1042-3699(20)30647-6.

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9

&NA;. "Propofol." Reactions Weekly &NA;, no. 1376 (November 2011): 24–25. http://dx.doi.org/10.2165/00128415-201113760-00078.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1376 (November 2011): 25. http://dx.doi.org/10.2165/00128415-201113760-00083.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1379 (November 2011): 31. http://dx.doi.org/10.2165/00128415-201113790-00118.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1385 (January 2012): 38. http://dx.doi.org/10.2165/00128415-201213850-00140.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1385 (January 2012): 38. http://dx.doi.org/10.2165/00128415-201213850-00141.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1389 (February 2012): 36. http://dx.doi.org/10.2165/00128415-201213890-00134.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1390 (February 2012): 35. http://dx.doi.org/10.2165/00128415-201213900-00136.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1396 (April 2012): 34. http://dx.doi.org/10.2165/00128415-201213960-00119.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1397 (April 2012): 27. http://dx.doi.org/10.2165/00128415-201213970-00098.

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18

Victory, R. A., N. Pace, and P. F. White. "PROPOFOL." Anesthesiology Clinics of North America 11, no. 4 (December 1993): 831–44. http://dx.doi.org/10.1016/s0889-8537(21)00739-2.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 690 (February 1998): 12. http://dx.doi.org/10.2165/00128415-199806900-00028.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 702 (May 1998): 10. http://dx.doi.org/10.2165/00128415-199807020-00032.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 704 (June 1998): 11–12. http://dx.doi.org/10.2165/00128415-199807040-00030.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 713 (August 1998): 10. http://dx.doi.org/10.2165/00128415-199807130-00030.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 740 (February 1999): 10. http://dx.doi.org/10.2165/00128415-199907400-00028.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 753 (May 1999): 11. http://dx.doi.org/10.2165/00128415-199907530-00039.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 768 (September 1999): 10. http://dx.doi.org/10.2165/00128415-199907680-00036.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1163 (August 2007): 22–23. http://dx.doi.org/10.2165/00128415-200711630-00068.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1120 (September 2006): 15. http://dx.doi.org/10.2165/00128415-200611200-00057.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1125 (October 2006): 14. http://dx.doi.org/10.2165/00128415-200611250-00042.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1130 (December 2006): 21. http://dx.doi.org/10.2165/00128415-200611300-00058.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1131 (December 2006): 29–30. http://dx.doi.org/10.2165/00128415-200611310-00095.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1135 (January 2007): 27–28. http://dx.doi.org/10.2165/00128415-200711350-00105.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1136 (January 2007): 22. http://dx.doi.org/10.2165/00128415-200711360-00069.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1141 (March 2007): 19. http://dx.doi.org/10.2165/00128415-200711410-00068.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1148 (April 2007): 29. http://dx.doi.org/10.2165/00128415-200711480-00092.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1160 (July 2007): 26. http://dx.doi.org/10.2165/00128415-200711600-00076.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1356 (June 2011): 31. http://dx.doi.org/10.2165/00128415-201113560-00107.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1358 (July 2011): 27. http://dx.doi.org/10.2165/00128415-201113580-00103.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1359 (July 2011): 31. http://dx.doi.org/10.2165/00128415-201113590-00119.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1361 (July 2011): 36. http://dx.doi.org/10.2165/00128415-201113610-00129.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1362 (July 2011): 27. http://dx.doi.org/10.2165/00128415-201113620-00098.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1365 (August 2011): 39. http://dx.doi.org/10.2165/00128415-201113650-00147.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1368 (September 2011): 34. http://dx.doi.org/10.2165/00128415-201113680-00124.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1369 (September 2011): 32–33. http://dx.doi.org/10.2165/00128415-201113690-00116.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1371 (October 2011): 32. http://dx.doi.org/10.2165/00128415-201113710-00119.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 1374 (October 2011): 31. http://dx.doi.org/10.2165/00128415-201113740-00111.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 534 (January 1995): 10. http://dx.doi.org/10.2165/00128415-199505340-00038.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 541 (March 1995): 10. http://dx.doi.org/10.2165/00128415-199505410-00039.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 542 (March 1995): 11. http://dx.doi.org/10.2165/00128415-199505420-00038.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 583 (January 1996): 12. http://dx.doi.org/10.2165/00128415-199605830-00030.

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&NA;. "Propofol." Reactions Weekly &NA;, no. 588 (February 1996): 10. http://dx.doi.org/10.2165/00128415-199605880-00033.

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