Iontophoretically applied lidocaine reduces pain on propofol injection.
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We have compared iontophoretically and locally applied lidocaine for relief of pain on propofol injection. Pain was assessed on insertion of a 20-gauge i.v. cannula and at 10-s intervals for 30 s after injection of propofol. Pain scores on cannulation were significantly less in the iontophoresis group (median 1.1) than in the sham (control) group (median 2.8) (P < 0.005). Pain after injection of propofol was significantly reduced at 10 (P < 0.002), 20 (P < 0.001) and 30 s (P < 0.001). We conclude that iontophoretically applied lidocaine decreased the pain of cannulation and propofol injection. (+info)
Suppression of central nervous system sodium channels by propofol.
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BACKGROUND: Previous studies have provided evidence that clinical levels of propofol alter the functions of voltage-dependent sodium channels, thereby inhibiting synaptic release of glutamate. However, most of these experiments were conducted in the presence of sodium-channel activators, which alter channel inactivation. This study electrophysiologically characterized the interactions of propofol with unmodified sodium channels. METHODS: Sodium currents were measured using whole-cell patch-clamp recordings of rat brain IIa sodium channels expressed in a stably transfected Chinese hamster ovary cell line. Standard electrophysiologic protocols were used to record sodium currents in the presence or absence of externally applied propofol. RESULTS: Propofol, at concentrations achieved clinically in the brain, significantly altered sodium channel currents by two mechanisms: a voltage-independent block of peak currents and a concentration-dependent shift in steady-state inactivation to hyperpolarized potentials, leading to a voltage dependence of current suppression. The two effects combined to give an apparent concentration yielding a half-maximal inhibitory effect of 10 microM near the threshold potential of action potential firing (about -60 mV). Propofol inhibition was also use-dependent, causing a further block of sodium currents at these anesthetic concentrations. CONCLUSIONS: In these experiments with pharmacologically unaltered sodium channels, propofol inhibition of currents occurred at concentrations about eight-fold above clinical plasma levels and thus at brain concentrations reached during clinical anesthesia. Therefore, the results indicate a possible role for sodium-channel suppression in propofol anesthesia. (+info)
Repeated propofol anesthesia for a patient with a history of neuroleptic malignant syndrome.
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Neuroleptic malignant syndrome (NMS) is the most serious side effect produced by the administration of antipsychotic drugs. NMS shares many clinical similarities with malignant hyperthermia (MH), but the etiology of NMS and the relation between NMS and MH remain unknown. Anesthetic regimens for patients with NMS are not well established. We gave repeated anesthesia to a patient with a history of NMS undergoing electroconvulsive therapy for the treatment of depression. Propofol and vecuronium were used in twelve consecutive ECT sessions without complications. In this case report, we describe the safe and satisfactory repeated use of propofol in a patient with a history of NMS, and outline NMS and its questionable relation to MH. (+info)
Haemodynamic effects of propofol vs thiopental in infants: an echocardiographic study.
(44/1774)
Rapid i.v. induction of general anaesthesia is indicated in infants at risk of vomiting or regurgitation to reduce the risk of aspiration of gastric contents. Propofol is an alternative to thiopental in infants, and we have compared cardiovascular changes when propofol or thiopental was used for induction of anaesthesia in infants. Twenty infants, ASA I or II, aged 1-11 months, undergoing elective surgery were allocated randomly to receive either thiopental or propofol for i.v. induction. Cardiovascular and echocardiographic data were recorded in both groups before, during and for 5 min after induction of anaesthesia. Doses required to induce anaesthesia in each group were mean 10.3 (SD 0.9) mg kg-1 of thiopental and 6.1 (0.6) mg kg-1 of propofol. Thiopental did not alter significantly systolic or mean arterial pressure, afterload indices, rate-corrected velocity of circumferential fibre shortening or cardiac index, but decreased shortening fraction at 1 and 5 min after induction compared with awake values. Propofol did not alter heart rate, shortening fraction, rate-corrected velocity of circumferential fibre shortening or cardiac index at 1 and 5 min after i.v. induction compared with awake values. After induction, systolic and mean arterial pressures and afterload indices decreased more after induction with both agents, but did not become abnormal. Thus propofol decreased arterial pressure more than thiopental because of an effect on afterload. Cardiac output remained unchanged with both agents. (+info)
Patient-controlled sedation using propofol in elderly patients in day-case cataract surgery.
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Patient-controlled sedation (PCS) with propofol has been used successfully as an adjunct to local anaesthetic procedures. We studied a group of elderly patients (mean age 75.4 yr) undergoing cataract surgery and attempted to increase patient acceptability and comfort of local anaesthesia. Propofol was self-administered in a dose of 0.25 mg kg-1 for patients more than 60 yr of age, with a lockout period of 3 min. A total of 14 of 20 patients used PCS; eight of 20 used the PCS only once and another six had three tries or less. Despite this, 18 of 20 patients claimed they found the PCS useful. However, while it is possible to administer PCS successfully to elderly patients undergoing cataract surgery and produce a decrease in the level of anxiety, we found it unacceptable because of head movement in two patients. These patients received only two and three divided doses, to a maximum of 29 and 30 mg, respectively. There were no other adverse events. (+info)
Huntington's disease: review and anesthetic case management.
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Huntington's disease is a dominantly inherited progressive autosomal disease that affects the basal ganglia. Symptoms appear later in life and manifest as progressive mental deterioration and involuntary choreiform movements. Patients with Huntington's disease develop a progressive but variable dementia. Dysphagia, the most significant related motor symptom, hinders nutrition intake and places the patient at risk for aspiration. The combination of involuntary choreoathetoid movements, depression, and apathy leads to cachexia. Factors of considerable concern to the anesthesiologist who treats patients with Huntington's disease may include how to treat frail elderly people incapable of cooperation, how to treat patients suffering from malnourishment, and how to treat patients with an increased risk for aspiration or exaggerated responses to sodium thiopental and succinylcholine. The successful anesthetic management of a 65-yr-old woman with Huntington's disease who presented for full-mouth extractions is described. (+info)
Mechanisms underlying the inhibitory effect of propofol on the contraction of canine airway smooth muscle.
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BACKGROUND: Propofol has been shown to produce relaxation of preconstricted airway smooth muscle. Although the inhibition of calcium mobilization is supposed to be the major mechanism of action, the whole picture of the mechanisms is not completely clear. METHODS: Contractile response was performed using canine tracheal rings. The effects of propofol on carbachol-induced mobilization of intracellular Ca2+ and phosphoinositide hydrolysis were measured using cultured canine tracheal smooth muscle cells by monitoring fura-2 signal and assessing the accumulation of [3H]-inositol phosphates. To detect the effect of propofol on muscarinic receptor density and affinity, [3H]N-methyl-scopolamine was used as a radioligand for receptor binding assay. RESULTS: Pretreatment with propofol shifts the concentration-response curves of carbachol-induced smooth muscle contraction to the right in a concentration-dependent manner without changing the maximal response. Propofol not only decreased the release of Ca2+ from internal stores but also inhibited the calcium influx induced by carbachol. In addition, carbachol-induced inositol phosphate accumulation was attenuated by propofol; the inhibitory pattern was similar to the contractile response. Moreover, propofol did not alter the density of muscarinic receptors. The dissociation constant value was not altered by pretreatment with 100 microM propofol but was significantly increased by 300 microM (propofol, 952+/-229 pM; control, 588+/-98 pM; P<0.05). CONCLUSIONS: Propofol attenuates the muscarinic receptor-mediated airway muscle contraction. The mechanism underlying these effects was attenuation of inositol phosphate generation and inhibition of Ca2+ mobilization through the inhibition of the receptor-coupled signal-transduction pathway. (+info)
Ketamine preserves and propofol potentiates hypoxic pulmonary vasoconstriction compared with the conscious state in chronically instrumented dogs.
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BACKGROUND: The authors tested the hypothesis that ketamine and propofol anesthesia would alter the magnitude of hypoxic pulmonary vasoconstriction compared with the conscious state. In addition, they assessed the extent to which cyclooxygenase pathway inhibition and adenosine triphosphate-sensitive potassium channel inhibition modulate hypoxic pulmonary vasoconstriction in the conscious state, and whether these pathways are altered during propofol anesthesia. METHODS: Twenty conditioned, male mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow relationship. Pressure-flow plots were measured during normoxia and hypoxia (systemic arterial PO2 reduced to about 60 and about 50 mm Hg) on separate days in the conscious state, during ketamine anesthesia, and during propofol anesthesia. The effects of indomethacin and glibenclamide on the magnitude of hypoxic pulmonary vasoconstriction were also assessed in the conscious and propofol-anesthetized states. RESULTS: Neither ketamine nor propofol had an effect on the baseline pressure-flow relationship during normoxia compared with the conscious state. Hypoxia resulted in stimulus-dependent pulmonary vasoconstriction (P<0.01) in the conscious state. Compared with the conscious state, the magnitude of hypoxic pulmonary vasoconstriction was preserved during ketamine but was potentiated (P<0.01) during propofol anesthesia. Indomethacin enhanced (P<0.01) hypoxic pulmonary vasoconstriction in both the conscious and propofol-anesthetized states. In contrast, glibenclamide only enhanced (P<0.01) hypoxic pulmonary vasoconstriction in the conscious state and had no effect during propofol anesthesia. CONCLUSION: Hypoxic pulmonary vasoconstriction is preserved during ketamine anesthesia but is potentiated during propofol anesthesia. The potentiated response during propofol anesthesia appears to be caused by inhibition of adenosine triphosphate-sensitive potassium channel-mediated pulmonary vasodilation. (+info)