Disease relevance of Disoprofol

• Only exposure to propofol, a lipid-based anesthetic agent, was significantly associated with the postoperative complications at all seven hospitals [1].
• Propofol provides at least as effective sedation as midazolam and results in a faster time to extubation, with an increased risk of hypotension and higher cost [2].
• Comparison of propofol and midazolam for sedation in critically ill patients [3].
• Propofol infusion for the treatment of status epilepticus [4].
• Monitoring with capnography allowed for rapid titration of propofol at the earliest signs of respiratory depression [5].

Psychiatry related information on Disoprofol

• Propofol and electroconvulsive therapy [6].
• Motor neuron disease after enflurane/propofol anaesthesia in patient with alcohol abuse [7].
• In conclusion, propofol may well prove to be the anaesthetic of choice for DCC in cardiac patients because of good amnesia, low incidence of side-effects and short recovery time (mean 5.3 min) [8].
• Use of propofol for alcohol withdrawal delirium: a case report [9].
• BACKGROUND: Midazolam and propofol often provoke retrograde amnesia after recovery from anesthesia in humans [10].

High impact information on Disoprofol

• Gastroenterologist-administered propofol versus meperidine and midazolam for advanced upper endoscopy: a prospective, randomized trial [5].
• Propofol leads to significantly improved recovery of baseline activity and food intake 24 hours after the procedure [5].
• Propofol infusion syndrome is a rare but frequently fatal complication in critically ill children given long-term propofol infusions [11].
• Propofol use in head-injury patients [12].
• Subhypnotic doses of propofol relieve pruritus associated with liver disease [13].

Chemical compound and disease context of Disoprofol

• In Sprague-Dawley rats maintained under propofol anaesthesia, proteomic or Western blot analysis revealed a progressive augmentation of HSP60 expression in the RVLM after intravenous administration of Escherichia coli lipopolysaccharide (30 mg kg(-1)) [14].
• OBJECTIVE: Chronic congestive heart failure (CHF) was induced in rabbits with doxorubicin in order to evaluate: (1) haemodynamic and regional blood flow responses to propofol anaesthesia; (2) modification of these cardiovascular responses with background intravenous infusions of enalaprilat or dopexamine [15].
• Sevoflurane or propofol was given until loss of consciousness [16].
• CONCLUSIONS: We defined the propofol concentration required for loss of consciousness and showed that it is reduced by increasing fentanyl concentration and by increasing age [17].
• Time course of ventilatory depression following induction doses of propofol and thiopental [18].

Biological context of Disoprofol

• Heart rate was lower in patients who received propofol [3].
• Insertion of transvenous leads and prepectoral subfascial ICD implantation were performed in electrophysiology laboratories under local anesthesia and conscious sedation with intravenous midazolam and propofol [19].
• UGT1A9 was identified as the isozyme catalyzing biotransformation of the two compounds in HT29 cells and propofol as an effective competitive inhibitor of this metabolism [20].
• Our finding on propofol pharmacokinetics may be the first example demonstrating the theoretic prediction of the well-stirred model [21].
• Favorable operating conditions and rapid recovery are claimed as the main advantages in using propofol, whereas disadvantages include a relatively high incidence of apnea, and blood pressure reductions [22].

Anatomical context of Disoprofol

• Two other structurally different intravenous anesthetics, i.e. propofol (10 microm) and etomidate (3 microm), prolonged the duration of the glycinergic mIPSC in the rat spinal dorsal horn neurons [23].
• In an in vitro study the effect of propofol on the metabolism of midazolam was studied with human liver microsomes and recombinant CYP3A4 [24].
• To test this hypothesis, the effect of propofol on oxidative injury of human erythrocytes was examined [25].
• Propofol pretreatment greatly attenuated the impairment in comparison with midazolam, which agrees with the concept of antioxidant activity in the presence of membranes [26].
• High signal in subarachnoid spaces on FLAIR MR images in an adult with propofol sedation [27].

Associations of Disoprofol with other chemical compounds

• GABARs responsive to these low EtOH concentrations require the GABAR delta-subunit, which is thought to be associated exclusively with alpha 4- and alpha 6-subunits in vivo, and the beta 3-subunit, which has recently been shown to be essential for the in vivo anesthetic actions of etomidate and propofol [28].
• Further, a greater preservation of red blood cell counts was seen after surgery with propofol compared with conventional sevoflurane anesthesia [25].
• Patients underwent premedication with midazolam before induction of anesthesia with propofol and fentanyl [29].
• These results are consistent with direct inhibition of oxytocin and vasopressin release from the neurohypophysis by isoflurane and propofol [30].
• METHODS: The EEG waveforms from 31 adults receiving infusions of alfentanil, propofol, or midazolam were analyzed [31].
• Time to recovery (4.1 ± 1.9 min vs. 11.5 ± 5.0 min, p < 0.001), and time to discharge (38.0 ± 9 min vs. 110 ± 42 min, p < 0.001) were significantly shorter with propofol than midazolam [32].

Gene context of Disoprofol

• All of the CYPs evaluated were capable of hydroxylating propofol; however, CYP2B6 and CYP2C9 were most active [33].
• A competitive inhibition of CYP2E1 by propofol was observed with low inhibition constants in the therapeutic range in both porcine (19 microM) and human (48 microM) liver microsomes [34].
• CONCLUSIONS: Cytochrome P-450 2B6, and to a lesser extent CYP2C9, contribute to the oxidative metabolism of propofol [33].
• Here we studied the effects of propofol on recombinant HCN1, HCN2, and HCN4 channels and found that the drug inhibits and slows activation of all three channels at clinically relevant concentrations [35].
• Valproic acid inhibited UGT1A9 catalyzed propofol glucuronidation in an uncompetitive manner and UGT2B7 catalyzed AZT glucuronidation competitively (K(i)=1.6+/-0.06mM) [36].

Analytical, diagnostic and therapeutic context of Disoprofol

• We suggest that propofol infusion at rates higher than 5 mg/kg per h should be discouraged for long-term sedation in the intensive-care unit [37].
• With incremental cost-effectiveness analysis, gastroenterologist-administered propofol cost an additional $403.00 per additional patient at 100% of baseline for both activity level and food intake when compared with standard sedation and analgesia [5].
• Propofol for conscious sedation [38]?
• 101 critically ill patients admitted to five intensive-care units were allocated randomly to receive a continuous intravenous infusion of either propofol or midazolam for sedation for up to 24 h [3].
• Propofol for endoscopy sedation [39].

References