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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine the direct actions of propofol, and whether propofol exerts any action on basal endothelium-derived relaxing factor release and vasodilator effect of acetylcholine on phenylephrine-induced contractile responses in isolated rat aortic rings. This compound is known to produce a fall in blood pressure in man and animals, and it has been suggested that the hypotension may result from a direct vasodilator action on the veins and arterioles. In this study, propofol did not induce any contractile response in aortic rings at various concentrations (10(-8)-10(-4) M). Propofol did not significantly alter phenylephrine-induced contractions at lower concentrations (10(-8)-10(-6) M) but at higher concentrations (10(-5)-10(-4) M) the depression caused by propofol was significant in both endothelium-intact and -denuded rings. Pretreatment of the endothelium-intact rings with propofol (10(-6) and 10(-5) M) produced a reduction in the relaxant effect of acetylcholine. The results obtained in this study demonstrate that clinically relevant concentrations of propofol (10(-6) M or less) have no direct vasodilator effects and that it reduces endothelium-dependent relaxation to acetylcholine.
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PMID:Effects of propofol on vascular smooth muscle function in isolated rat aorta. 805 85

The hemodynamic effects of propofol-fentanyl and isoflurane-fentanyl anesthesia during the prebypass period were compared in 42 patients undergoing coronary artery bypass grafting (CABG) and 22 patients undergoing valve replacement (VR) for stenotic lesions. Anesthesia was induced with fentanyl, 25 micrograms/kg, and pancuronium, 0.1 mg/kg, and was maintained with a propofol infusion commenced at 4 mg/kg/h (range 1 to 10 mg/kg/h) or with isoflurane commenced at 1% (range 0 to 2%). Additional fentanyl, 7.5 micrograms/kg, was given before sternotomy. Hemodynamic measurements were made before induction of anesthesia and at various times in the prebypass period. In the VR group, there were no significant differences between the two anesthetics in any hemodynamic variables during the study. Significant decreases (P < 0.05) in mean arterial pressure (MAP 14%), left ventricular stroke work index (LVSWI 29%), and stroke volume index (SVI 24%) occurred after 15 minutes of propofol anesthesia in the CABG group. With isoflurane MAP was well maintained with reductions in LVSWI and SVI of 22% and 20%, respectively. Isoflurane was, however, associated with a significant increase in heart rate (HR) in the CABG group (P < 0.05), whereas no significant change in HR occurred in CABG or VR patients receiving propofol. With both techniques there were no significant changes in right-sided or left-sided filling pressures or in systemic vascular resistance index in the CABG or VR groups, except for a decrease in pulmonary artery occlusion pressure in the propofol VR group and isoflurane CABG group at the time of aortic cannulation. Propofol produced similar hemodynamic changes in the CABG and VR groups. Both anesthetic techniques caused myocardial depression and effectively controlled the autonomic responses to sternotomy in both groups. The study suggests that propofol-fentanyl anesthesia is an acceptable technique for CABG surgery and for VR in patients with stenotic valvular heart disease.
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PMID:Propofol-fentanyl anesthesia: a comparison with isoflurane-fentanyl anesthesia in coronary artery bypass grafting and valve replacement surgery. 806 Dec 62

The effects of the anesthetic agents propofol and methohexital on seizure duration, clinical outcome, recovery, and memory in electroconvulsive therapy (ECT) were studied in a double-blind trial. The study comprised 53 patients, 47 patients with major depression and six patients with other diagnoses according to DSM-III. Several recent clinical studies with a crossover design have shown a reduced seizure duration for anesthesia with propofol in comparison with both methohexital and thiopental. Propofol significantly reduced the seizure duration in this study without reducing the therapeutic outcome as measured by the Montgomery-Asberg Depression Rating Scale. Propofol did not significantly alter the length of the course of ECT; however, a slightly prolonged course for women cannot be completely ruled out. There were no significant differences between the two agents in effects on recovery times after anesthesia and on anterograde memory. In general, it seems that propofol is as effective as methohexital as an induction agent for ECT.
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PMID:A comparison of propofol and methohexital as anesthetic agents for ECT: effects on seizure duration, therapeutic outcome, and memory. 817 18

This prospective study was designed to evaluate the sedative effect of two different anaesthetic drugs in patients undergoing ophthalmic surgery. Propofol is an intravenous hypnotic agent with a short half-life of about 30 min. A constant high oxygen saturation in continuous pulse oximetry was achieved in previous studies using propofol for sedation. Furthermore, an IOP-lowering effect was proved. Propofol was compared to diazepam, a well-established sedative, which has been used for many years for sedation of patients in local anaesthesia. METHOD. One hundred patients of comparable anaesthesiologic risk (ASA classes 2-4) undergoing identical surgical procedures received either propofol (n = 50), or diazepam (n = 50). Propofol was infused at a rate of 0.8-3.0 mg/kg/h, while diazepam was given as a slow intravenous bolus of 5 mg before surgery. All patients were monitored by continuous pulse oximetry. RESULTS. Oxygen saturation of patients receiving propofol was never less than 96%. In contrast, oxygen saturation of patients sedated by diazepam dropped to 85%, especially for the first 5 min following administration, before improving to 95% during the next 10 min. None of the patients who received propofol showed signs of motor unrest, a great handicap in ophthalmic surgery, while four patients who received diazepam were restless enough to hamper the procedure. None of the patients who received propofol developed respiratory depression. In contrast, marked respiratory depression, motor agitation, and postoperative fatigue slowing mobilization were common in patients who received diazepam.
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PMID:[Propofol versus diazepam. Sedation in ophthalmologic surgery under local anesthesia]. 827 89

We investigated the possibility that the effects of propofol on sarcoplasmic reticulum (SR) function may contribute to the myocardial depression induced by this anesthetic. With guinea pig isolated papillary muscles, the effects of propofol on transient alterations in contractility (termed "potentiated-state" contractions), after abrupt changes in stimulation frequency and brief periods of rest, were compared with those of enflurane and the inhibitor of SR function, ryanodine. These potentiated-state contractions are mediated by calcium derived largely from the SR. Propofol, enflurane, and ryanodine were applied at concentrations that produced approximately 50%-60% inhibition of "steady-state" contraction. Ryanodine abolished and enflurane attenuated the potentiated-state contractions, whereas propofol had no apparent effect. Although impairment of SR function may contribute to the depression of contractility induced by enflurane, propofol has no major effect on SR function.
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PMID:Differential effects of propofol and enflurane on contractions dependent on calcium derived from the sarcoplasmic reticulum of guinea pig isolated papillary muscles. 831 47

We compared the inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and rat. Propofol applied in clinical 10% intralipid emulsion showed concentration-dependent negative inotropic effects, accompanied by decreased action potential duration, in the guinea pig. Intralipid alone had no effect. Although thiamylal showed a concentration-dependent depression similar to propofol in the guinea pig, depolarization of resting membrane potential was seen at 0.1 and 0.3 mM, and a slight prolongation of action potential duration at 90% repolarization at 0.1 mM, and then a decrease of action potential duration at 0.3 mM. In rat papillary muscles, propofol did not produce any depression of contractile force, whereas thiamylal produced a concentration-dependent negative inotropic effect. The important findings observed in the action potential in rat papillary muscles were the modest shortening of action potential duration after propofol application, and the significant decrease of resting membrane potential and the significant prolongation of action potential duration caused by thiamylal. Both propofol and thiamylal depressed slow action potentials and contractile force in guinea pig papillary muscles depolarized by 25 mM K+ solution. In conclusion, the negative inotropic effects of propofol and thiamylal might be caused by inhibition of trans-sarcolemmal Ca2+ influx accompanied by shortening of action potential duration in guinea pig papillary muscles. The action potential of thiamylal might be affected by the suppression of K+ current in guinea pig and rat papillary muscles that was never observed in the propofol-treated tissue.
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PMID:Inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and the rat. 836 56

Propofol is an intravenous anaesthetic which is chemically unrelated to other iv anaesthetics. Most anaesthetists are now becoming familiar with propofol's pharmacokinetic and pharmacodynamic properties. It has proved to be a reliable drug that can be used safely for induction and maintenance of anaesthesia for most surgical procedures and unlike other anaesthetic agents, it can especially be extended into the postoperative setting or intensive care unit for sedation. Propofol's greatest attributes are its pharmacokinetic properties which result in a rapid, clear emergence and lack of cumulative effects even after prolonged administration. Compared with other iv anaesthetics, the induction dose of propofol has a relatively higher incidence of respiratory depression, short-lived apnoea and blood pressure reduction that may occasionally be marked. Possible mechanisms for the hypotension may relate to (1) its action on peripheral vasculature (vasodilatation), (2) decreased myocardial contractility, (3) resetting of the baroreflex activity and (4) inhibition of the sympathetic nervous system outflow. In vitro studies indicate that propofol depresses the immunological reaction to bacterial challenge as well as the chemotactic activity. Clinical studies, in cardiac surgery, have demonstrated that propofol, in association with an opioid, is a logical anaesthetic choice. Propofol is about to receive approval for continuous iv sedation. Comparative studies of propofol and midazolam have clearly demonstrated the superiority of propofol in terms of rapid recovery and precise control of the level of sedation.
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PMID:Propofol in patients with cardiac disease. 840 58

This study was done using Wistar rats to determine if the actions of propofol (22 +/- 1, 40 +/- 2, 64 +/- 3 and 103 +/- 3 mg.kg-1 x hr-1) decreased blood pressure and heart rate through depression of brain stem vasomotor centres. All rats were given atropine to block vagal influences on the heart. Propofol decreased renal nerve activity as well as blood pressure and heart rate in a dose-dependent manner. Infusion of the lowest dose of propofol (22 +/- 1 mg.kg-1 x hr-1) had no effect on blood pressure, heart rate and renal nerve activity. Infusion of propofol at 40 +/- 2 mg.kg-1 x hr-1 decreased renal activity by 22 +/- 4% (mean +/- SEM) and at 64 +/- 3 mg.kg-1 x hr-1 it decreased renal nerve activity by 36 +/- 6%. Finally, infusion of the largest dose of propofol (102 +/- 3 mg.kg-1 x hr-1) decreased nerve activity by 50 +/- 5%. The haemodynamic changes observed in our experiments during the infusion propofol paralleled the changes in sympathetic firing, suggesting that hypotension was caused by central actions of propofol to depress sympathetic firing. In experiments with bolus injections of propofol, the renal nerve activity returned to normal before arterial pressure and heart rate recovered. Because decreases in blood pressure and heart rate were longer-lasting than changes in renal nerve activity, a part of the vasodepression and bradycardia caused by propofol likely resulted from direct actions on blood vessels and the heart. Sympathetic and cardiovascular responses to blocking neurons in the ventrolateral medulla with microinjection of glycine were depressed by propofol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Action of propofol on central sympathetic mechanisms controlling blood pressure. 840 60

The mechanism(s) of action of anesthetics on cell membrane ionic currents are not known. To investigate this further the effects of clinically relevant concentrations of ketamine, methohexital, and propofol on the delayed rectifier (IK) and the inward rectifier (IK1) currents of single dispersed guinea pig ventricular myocytes were studied. These voltage-gated currents are major components of cardiac cell electrophysiologic function regulating resting potential and repolarization. Each of the three anesthetics had a distinct spectrum of activity. Ketamine (10(-4) M) decreased IK1 (P < 0.05) but had no effect on IK. Methohexital (10(-4) M) had no significant effect on either current. Propofol (2.8 x 10(-5) M) resulted in significant depression of IK (P < 0.001) but had no effect on IK1. These results suggest that these intravenous anesthetics may have more specific effects on sarcolemma than volatile anesthetics, whose effects may be more generalized membrane effects.
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PMID:Distinctive effects of three intravenous anesthetics on the inward rectifier (IK1) and the delayed rectifier (IK) potassium currents in myocardium: implications for the mechanism of action. 841 22

1. The effects of propofol (2,6 di-isopropylphenol) on responses to the selective glutamate receptor agonists, N-methyl-D-aspartate (NMDA) and kainate, were investigated in cultured hippocampal neurones of the mouse. Whole cell and single channel currents were recorded by patch-clamp techniques. Drugs were applied with a multi-barrel perfusion system. 2. Propofol produced a reversible, dose-dependent inhibition of whole cell currents activated by NMDA. The concentration of propofol which induced 50% of the maximal inhibition (IC50) was approximately 160 microM. The maximal inhibition was incomplete leaving a residual current of about 33% of the control response. This inhibitory action of propofol was neither voltage- nor use-dependent. 3. Analysis of the dose-response relation for whole cell NMDA-activated currents indicated that propofol caused no significant change in the apparent affinity of the receptor for NMDA. 4. Outside-out patch recordings of single channel currents evoked by NMDA (10 microM) revealed that propofol (100 microM) reversibly decreased the probability of channel opening but did not influence the average duration of channel opening or single channel conductance. 5. Whole-cell currents evoked by kainate (50 microM) were insensitive to propofol (1 microM-1 mM). 6. These results indicate that propofol inhibits the NMDA subtype of glutamate receptor, possibly through an allosteric modulation of channel gating rather than by blocking the open channel. Depression of NMDA-mediated excitatory neurotransmission may contribute to the anaesthetic, amnesic and anti-convulsant properties of propofol.
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PMID:Inhibition by propofol (2,6 di-isopropylphenol) of the N-methyl-D-aspartate subtype of glutamate receptor in cultured hippocampal neurones. 852 57


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