Contractility in humans after coronary artery surgery.
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BACKGROUND: Propofol's unique pharmacokinetic profile offers advantages for titration and rapid emergence in patients after coronary artery bypass graft (CABG) surgery, but concern for negative inotropic properties potentially limits its use in these patients. The current study analyzed the effect of various propofol plasma concentrations on left ventricular (LV) contractility by means of a single-beat contractile index based on LV maximal power (PWR(max)). METHODS: The study was conducted in 30 patients after CABG surgery. Immediately after admission to the intensive care unit (ICU), four different plasma concentrations of propofol 0.65, 1.30, 1.95, and 2.60 microg/ml were established. At each concentration level, the cardiac and vascular effects of propofol were studied by combining echocardiographic data with invasively derived aortic root pressure. Preload was characterized by LV end-diastolic dimensions. Afterload was indicated in terms of indexed systemic vascular resistance (SVRI), LV end-systolic meridional wall stress (LV-ESWS), and arterial elastance (Ea). Quantification of effects on contractility was achieved by preload-adjusted PWRmax. RESULTS: Myocardial contractility did not change during a fourfold increase in propofol plasma concentration. Preload-adjusted PWRmax amounted to 3.90+/-1.75 W x ml(-2) x 10(4), 3.98+/-1.69, 3.94+/-1.70, and 3.88+/-1.72, respectively (mean+/-SD). With respect to ventricular loading conditions, propofol caused a significant reduction in both pre- and afterload. CONCLUSIONS: The current results strongly suggest that propofol lacks direct cardiac depressant effects. Nevertheless, meaningful vascular actions of propofol could be demonstrated. Significant decreases in ventricular loading conditions accounted for a marked decrease in arterial blood pressure and supported the concept that propofol in clinically relevant concentration is a vasodilator. (+info)
Optimal propofol-alfentanil combinations for supplementing nitrous oxide for outpatient surgery.
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BACKGROUND: The combination of propofol and alfentanil with nitrous oxide provides balanced anesthesia with rapid recovery and minimal emetic side effects. The object of this study was to compare recovery parameters at varying proportions of propofol and alfentanil, and to determine the dosing rate and plasma concentration of propofol necessary to supplement nitrous oxide in the presence of varying concentrations of alfentanil METHODS: Forty-eight patients were anesthetized with nitrous oxide, targeted manual infusions of alfentanil (target plasma concentrations of 0, 50, 100, and 150 ng/ml), and propofol at rates that were varied up or down by 25% depending on the response (movement/no movement) of the preceding patient (at the same alfentanil target concentrations) to ulnar-nerve stimulation. The minimum concentrations of propofol and alfentanil required to prevent movement in 50% of patients (EC50) was determined by logistic regression. Speed of emergence and recovery of cognitive function, time to discharge, and incidence of side effects were compared for four different combinations of propofol and alfentanil with nitrous oxide. RESULTS: The EC50 for propofol alone with nitrous oxide was 6.1 microg/ml. AlfentaniL at concentrations of 41+/-17 (SD), 113+/-54, and 130+/-61 ng/mL reduced the EC50 of propofol to 3.3, 2.3, and 2.2 microg/ml, respectively, and decreased emergence time (eye opening) to 8.1, 4.9, and 3.4 min, compared with 24.3 min for propofol alone. Side effects did not differ between groups. CONCLUSIONS: The authors conclude that there is a synergistic effect between propofol and alfentanil, and that combining alfentanil with propofol is associated with faster early recovery. (+info)
The mechanism of inhibitory actions of propofol on rat supraoptic neurons.
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BACKGROUND: In the perioperative period, plasma osmotic pressure, systemic blood pressure, and blood volume often change dramatically. Arginine vasopressin is a key factor in the regulation of these parameters. This study was performed to evaluate the direct and the mechanism of the actions of propofol on arginine vasopressin release from magnocellular neurosecretory neurons in the rat supraoptic nucleus. METHODS: Somatodendritic arginine vasopressin release from supraoptic nucleus slice preparations was measured by radioimmunoassay. Ionic currents were measured using the whole-cell mode of the patch-clamp technique in supraoptic nucleus slice preparations or in single dissociated supraoptic nucleus neurons of the rat. RESULTS: Propofol at concentrations greater than 10(-5) M inhibited the arginine vasopressin release stimulated by potassium chloride (50 mM). This inhibition by propofol was not reversed by picrotoxin, a gamma-aminobutyric acid(A)(GABA(A)) receptor antagonist, whereas arginine vasopressin release induced by glutamate (10(-3) M) was also inhibited by propofol at a clinically relevant concentration (10(-6) M). The latter effect was reversed by picrotoxin. Propofol evoked Cl- currents at concentrations ranging 10(-6) to 10(-4) M. Propofol (10(-6) M) enhanced the GABA (10(-6) M)-induced current synergistically. Moreover, propofol (10(-6) M) prolonged the time constant of spontaneous GABA-mediated inhibitory postsynaptic currents. Furthermore, propofol (10(-5) M and 10(-4) M) reversibly inhibited voltage-gated Ca2+ currents, whereas it did not affect currents induced by glutamate (10(-3) M). CONCLUSIONS: Propofol inhibits somatodendritic arginine vasopressin release from the supraoptic nucleus, and the enhancement of GABAergic inhibitory synaptic inputs and the inhibition of voltage-gated Ca2+ entry are involved in the inhibition of arginine vasopressin release. (+info)
Recovery profile, costs, and patient satisfaction with propofol and sevoflurane for fast-track office-based anesthesia.
(36/1774)
BACKGROUND: Office-based surgery is becoming increasingly popular because of its cost-saving potential Both propofol and sevoflurane are commonly used in the ambulatory setting because of their favorable recovery profiles. This clinical investigation was designed to compare the clinical effects, recovery characteristics, and cost-effectiveness of propofol and sevoflurane when used alone or in combination for office-based anesthesia. METHODS: One hundred four outpatients undergoing superficial surgical procedures at an office-based surgical center were randomly assigned to one of three general anesthetic groups. In groups I and II, propofol 2 mg/kg was administered for induction followed by propofol 75-150 microg x kg(-1) x min(-1) (group I) or sevoflurane 1-2% (group II) with N2O 67% in oxygen for maintenance of anesthesia In group m, anesthesia was induced and maintained with sevoflurane in combination with N2O 67% in oxygen. Local anesthetics were injected at the incision site before skin incision and during the surgical procedure. The recovery profiles, costs of drugs, and resources used, as well as patient satisfaction, were compared among the three treatment groups. RESULTS: Although early recovery variables (e.g., eye opening, response to commands, and sitting up) were similar in all three groups, the times to standing up and to be "home ready" were significantly prolonged when sevoflurane-N2O was used for both induction and maintenance of anesthesia. The time to tolerating fluids, recovery room stay, and discharge times were significantly decreased when propofol was used for both induction and maintenance of anesthesia. Similarly, the incidence of postoperative nausea and vomiting and the need for rescue antiemetics were also significantly reduced after propofol anesthesia. Finally, the total costs and patient satisfaction were more favorable when propofol was used for induction and maintenance of office-based anesthesia CONCLUSION: Compared with sevoflurane-N2O, use of propofol-N2O for office-based anesthesia was associated with an improved recovery profile, greater patient satisfaction, and lower costs. There were significantly more patients who were dissatisfied with the sevoflurane anesthetic technique. (+info)
Effect-site modelling of propofol using auditory evoked potentials.
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Auditory evoked potentials (AEP) were used to monitor central nervous system effects during induction and recovery from anaesthesia produced by infusion of propofol 30 mg kg-1 h-1 in 22 healthy male patients. Non-parametric and parametric modelling techniques were used successfully to calculate the parameter keo which linked pharmacokinetic with pharmacodynamic aspects of drug action in only 15 of the study patients. In the non-parametric analysis, keo was found to have a mean value of 0.2 (range 0.1-0.36) min-1. Estimation of keo allowed calculation of the effect-site concentration (Ce50) associated with 50% of AEP effect for the population (2.08 micrograms ml-1; 95% confidence limits 1.7-2.45). There were no significant differences between keo values calculated by non-parametric and individual parametric modelling techniques. During recovery, 50% of patients demonstrated evidence of waking at an effect-site concentration of 2.28 micrograms ml-1. (+info)
Effects of propofol, propofol-nitrous oxide and midazolam on cortical somatosensory evoked potentials during sufentanil anaesthesia for major spinal surgery.
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Recording of cortical somatosensory evoked potentials (CSEP) enables monitoring of spinal cord function. We studied the effects of propofol, propofol-nitrous oxide or midazolam during sufentanil anaesthesia on CSEP monitoring during major spinal surgery. Thirty patients with normal preoperative CSEP were allocated randomly to one of the following anaesthesia regimens: propofol (2.5 mg kg-1 followed by 10-6 mg kg-1 h-1) with or without nitrous oxide, or midazolam (0.3 mg kg-1 followed by 0.15 mg kg-1 h-1) combined with sufentanil 0.5 microgram kg-1 h-1 in the propofol and midazolam groups, or 0.25 microgram kg-1 h-1 in the propofol-nitrous oxide group. CSEP were elicited by alternate right and left tibial posterior nerve stimulation and recorded before and after induction (15 min, 1, 2 and 3 h), and during skin closure. CSEP latencies were not significantly modified in the three groups. CSEP amplitude decreased significantly in the propofol-nitrous oxide group (from mean 2.0 (SEM 0.3) to 0.6 (0.1) microV; P < 0.05) but not in the propofol (from 1.8 (0.6) to 2.2 (0.3) microV) or midazolam (1.7 (0.5) to 1.6 (0.5) microV) groups. The time to the first postoperative voluntary motor response (recovery) delay was significantly greater in the midazolam group (115 (19) min) compared with the propofol and propofol-nitrous oxide groups (43 (8) and 41 (3) min, respectively). Consequently, the use of propofol without nitrous oxide can be recommended during spinal surgery when CSEP monitoring is required. (+info)
Propofol, bradycardia and the Bezold-Jarisch reflex in rabbits.
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Propofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuated these responses; for example, at the highest dose of 5-HT (8 micrograms kg-1), delta HR, delta MAP and duration of abolition of RSNA were reduced by 57% (P < 0.001), 53% (P < 0.05) and 79% (P < 0.05), respectively. In contrast, reductions in delta HR and delta MAP produced by propofol were statistically significant only at very high doses (8 mg kg-1). Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex. (+info)
Patient-maintained propofol sedation as premedication in day-case surgery: assessment of a target-controlled system.
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We have assessed the efficacy and safety of a system which allowed 20 patients undergoing day-case anaesthesia to operate a target-controlled infusion of propofol to provide anxiolytic premedication. A target-controlled infusion of propofol was started with a target blood concentration of 1 microgram ml-1, and the patient was allowed to increase the target by 0.2 microgram ml-1 by operating a control button. There was a lockout time of 2 min and a maximum target concentration of 3 micrograms ml-1. There were significant reductions in anxiety scores from presedation baseline values and those measured at 15 min after the start of sedation. Values remained low until induction of anaesthesia. Median blood target concentration of propofol varied from 1.0 to 1.2 micrograms ml-1 and mean propofol consumption was 50.3 (SD 17.6) micrograms kg-1 min-1. No patient became oversedated and all remained cardiovascularly stable. Two individuals required low-dose supplementary oxygen for mild arterial oxygen desaturation but there were no instances of airway obstruction. Patient satisfaction with the system was high. (+info)