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At least 19 recordsLinked to original sources
PubMed2001

Intravenous anesthetics.

Intravenous anesthetics continue to be a mainstay in the modern anesthesiologist's armamentarium. In this review the authors will discuss new advancements in the use of propofol, as well as a greater understanding as to its mechanism of action. Further, we will discuss the use of target controlled infusion systems, touch upon the possible benefits of the ultra-short acting opioids, and consider the role of alpha-2 agonists as an adjunct to anesthetic management.

Journal Article↗
PubMed1993

[Action mechanisms of intravenous anesthetics].

Intravenous anaesthetic agents depress the activity of the brain by acting on receptor-operated ion channels. Barbiturates enhance gamma-aminobutyric acid (GABA)-mediated inhibition, depress glutamate-mediated excitation, and hyperpolarize the membrane by increased potassium conductance. Benzodiazepines facilitate GABA-mediated inhibition by binding to a benzodiazepine recognition site on the GABA receptor complex, and affect potassium channels. Opioids bind to opioid receptors and hyperpolarize the membrane by enhanced potassium and calcium conductances. Ketamine depresses excitatory synaptic transmission by acting on glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype. Propofol acts at a recognition site on the GABA receptor, which differs from the binding sites of both barbiturates and benzodiazepines.

Analgesics, Opioid↗
PubMed1997

Inhibition of nitric oxide synthase decreases anesthetic requirements of intravenous anesthetics in Xenopus laevis.

BACKGROUND: Acute inhibition of nitric oxide synthase (NOS) has been demonstrated to reduce the anesthetic requirements of volatile anesthetics. Recent data suggest that not only volatile but also intravenous anesthetic agents interact with nitric oxide (NO) metabolism. The aim of this study was to examine the effect of NOS inhibition by nitroG-L-arginine-methyl-ester (L-NAME) on the anesthetic action of the intravenous anesthetics thiopental, propofol, and ketamine. METHODS: The anesthetic potencies of thiopental, propofol, and ketamine were determined in Xenopus laevis tadpoles in the absence and presence of L-NAME. Anesthesia was defined as loss of righting reflex for 5 s. A nonlinear logistic regression curve was fitted to the data and half-maximal effective concentrations (EC50) were calculated. A second set of experiments was performed with different concentrations of L-NAME in the presence of the previously determined the EC50 of the intravenous anesthetics. RESULTS: The EC50s of the anesthetics thiopental, propofol, and ketamine were determined to be 25.5 +/- 2.0 microM, 1.9 +/- 0.1 microM, and 59.7 +/- 0.7 microM, respectively. The addition of L-NAME shifted the concentration-response curves to the left in a concentration-dependent manner. In the presence of 1 mM L-NAME, the EC50 of thiopental was reduced by 43%, the EC50 of propofol by 26%, and the EC50 of ketamine by 63%. The addition of D-NAME did not change the EC50 values of the three anesthetics. In the presence of L-arginine, the effect of L-NAME on the EC50 of thiopental was reversed. When administered by itself in a concentration range from 0.1 microM to 10 mM, L-NAME did not alter the behavior of the tadpoles. CONCLUSIONS: The results of the present study show that acute inhibition of NOS by L-NAME results in reduced anesthetic requirements of the intravenous anesthetics thiopental, propofol, and ketamine. This interaction of acutely administered L-NAME and intravenous anesthetics indicates that the NO-cyclic guanosine 3',5'-monophosphate system is involved in mediating the anesthetic effect of these compounds.

Anesthetics, Intravenous↗
PubMed2000

[Perioperative management with short-acting intravenous anesthetics].

Total intravenous anaesthesia (TIVA) with short-acting drugs is a standard procedure for day case surgery and is increasingly used for neurosurgical, cardiac surgical and paediatric surgical operations. The combination of propofol with alfentanil or remifentanil is frequently applied due to its favourable pharmacological properties. Propofol is characterized by a large volume of distribution at steady state and a relatively long elimination half time (t1/2 beta). Because of a high metabolic clearance, the clinical effects of propofol decline rapidly even after prolonged intravenous drug infusion. In patients with increased age, obesity or liver or renal failure, decreased doses of propofol for induction of anaesthesia are recommended. The short-acting opioids alfentanil and remifentanil provide small volumes of distribution at steady state, a short blood-brain equilibration time and decreased t1/2 beta. Remifentanil has unique pharmacological properties due to an ester binding and its elimination via extrahepatic hydrolysis by non-specific blood and tissue esterases. The context sensitive half time of remifentanil is significantly shorter than that of other opioids. Its analgetic potency is equal to fentanyl and 20 to 30 times higher than alfentanil. The advantages of total intravenous anaesthesia include fewer haemodynamic side-effects, a decreased incidence of postoperative nausea and vomiting and less neurohumoral stress response to surgery. Adequate pain therapy is mandatory after total intravenous anaesthesia with short-acting drugs. Continuous infusion of remifentanil for postoperative analgesia or supplementation of regional anaesthesia requires careful monitoring of vital functions. The economic aspects of TIVA remain to be determined.

Adult↗
PubMed2006

Inhibition of glutamatergic activation of extracellular signal-regulated protein kinases in hippocampal neurons by the intravenous anesthetic propofol.

BACKGROUND: Intravenous anesthetics cause amnesia, but the underlying molecular mechanisms are poorly understood. Recent studies reveal a significant role of extracellular signal-regulated protein kinases (ERKs) in controlling synaptic plasticity and memory formation. As a major synapse-to-nucleus superhighway, ERK transmits N-methyl-D-aspartate (NMDA) receptor signals to inducible transcriptional events essential for NMDA receptor-dependent forms of synaptic plasticity and memory. This study investigated the role of the widely used intravenous anesthetic propofol in regulating NMDA receptor-dependent ERK phosphorylation. METHODS: The possible effect of propofol on NMDA receptor-mediated ERK phosphorylation was detected in cultured rat hippocampal neurons with Western blot analysis. RESULTS: The authors found that propofol at clinical relevant concentrations (1-10 microm) reduced NMDA receptor-mediated ERK phosphorylation. This reduction was independent of gamma-aminobutyric acid transmission. The inhibition of the NMDA receptor seems to contribute to the effect of propofol on NMDA-stimulated ERK phosphorylation, because propofol reduced constitutive NMDA receptor NR1 subunit phosphorylation and impaired NMDA receptor-mediated Ca influx. Furthermore, by inhibiting the ERK pathway, propofol blocked NMDA receptor-dependent activation of two key transcription factors, Elk-1 and cyclic adenosine monophosphate response element-binding protein (CREB), and, as a result, attenuated Elk-1/CREB-dependent reporter gene (c-Fos) expression. CONCLUSIONS: These results suggest that propofol possesses the ability to inhibit NMDA receptor activation of the ERK pathway and subsequent transcriptional activities in hippocampal neurons. These findings indicate a new avenue to explore a transcription-dependent mechanism that may underlie anesthetic interference with synaptic plasticity related to amnesic properties of intravenous anesthetics.

Anesthetics, Intravenous↗
PubMed2000

[Recovery of balanced anesthesia with various inhalation anesthetics in comparison to intravenous anesthetics: a retrospective analysis of 20,060 patients].

BACKGROUND: The aim of this investigation was to compare routine balanced anaesthesia with different inhalation agents to intravenous anaesthesia (IVA) using an Anaesthesia-Information-Management-System (AIMS) with regard to time of recovery from anaesthesia, the time of discharge from the postanaesthesia care unit (PACU) and postoperative nausea as well as postoperative therapy with analgesics. METHODS: In 1997 and 1998 all relevant data of each anaesthesia procedure have been recorded using the online documentation Software NarkoData. These data sets have been stored into a relational database during each anaesthesia procedure. For evaluation the information has been exported from the database to a statistics program via 'Structured Query Langvage' (SOL). Balanced anaesthesia has been performed using isoflurane, halothane, and sevoflurane, respectively, supplemented with or without nitrous Oxide (N2O). The intravenous based anaesthesia-groups included propofol-fentanyl or propofol-remifentanil. RESULTS: The fastest recovery was seen in patients of the isoflurane group (11.2 +/- 7.7 minutes), and the longest time for extubation was observed in patients wich halothane anaesthesia (12.8 +/- 9.3 minutes); the overall mean difference was 1.7 minutes. The earliest patient admitted to the PACU had received sevoflurane (7.0 +/- 6.3 minutes) and propofol-remifentanil (7.0 +/- 7.4 minutes) whereas patients of the halothane group (9.5 +/- 7.5 minutes) took more. The shortest stay in PACU was seen in patients of the sevoflurane and isoflurane groups (105.13 +/- 35.7 and 108.4 +/- 60.5 minutes), whereas propofol-remifentanil (126.2 +/- 89.1 minutes) and halothan (120.0 +/- 86.1 minutes) anaesthetised patients had the longest stay in PACU. No difference was noted in the incidence of postoperative nausea and vomiting nor in the amount of postoperatively given analgesics. CONCLUSION: Results achieved in routine correspond only in part to results from studies. In our investigation balanced anaesthesia with isoflurane and sevoflurane correspond with the shortest stay in PACU compared to balanced anaesthesia with halothane and IVAs with propofol-fentanyl or propofol-remifentanil. One reason for this could be the intraoperatively administered opioide piritramide in IVAs. Furthermore we conclude that an AIMS may provide additional information about overall costs-effectiveness. However this information depends largely on local factors, e.g. patient case mix, staffing, policy of discharge from the PACU etc.

Adolescent↗
PubMed2006

Second-hand exposure to aerosolized intravenous anesthetics propofol and fentanyl may cause sensitization and subsequent opiate addiction among anesthesiologists and surgeons.

We hypothesize that aerosolization of anesthetics administered intravenously to patients in the operating room may be an unintended source of exposure to physicians. This may lead to inadvertent sensitization, which is associated with an increased risk for developing addiction. This may contribute to the over-representation of certain specialties among physicians with addiction. We retrospectively reviewed the de-identified demographic information of all licensed physicians treated for substance abuse in the State of Florida since 1980, to determine if medical specialty was associated with addiction in this group of individuals. Then, to identify the potential for exposure, two mass spectrometry assays were developed to detect two intravenously administered drugs, fentanyl and propofol, in air. Since 1980, 7.6% of licensed Florida physicians underwent treatment for addiction. Addiction in anesthesiologists was higher than expected. Opiate abuse was greater in anesthesiologists and surgeons compared to other specialties. Aerosolized fentanyl was detected in the air of the cardiothoracic operating room, in patients' expiratory circuits, and in the headspace above sharps boxes, but not in adjoining hallways. Aerosolized propofol was detected in the expirations of a patient undergoing transurethral prostatectomy. While access and stress may place anesthesiologists and surgeons at greater risk for substance abuse, an additional risk factor may be unintended occupational exposure to addictive drugs. This report provides preliminary evidence of detection of aerosolized intravenous anesthetics using two newly developed analytical methods. We conclude that the potential exists for chronic exposure to low levels of airborne intravenously administered drugs. Further studies are under way to determine the significance of this exposure.

Aerosols↗
PubMed1990

An evaluation of three intravenous anesthetic regimens in New Zealand rabbits.

Intravenous anesthetics can be readily administered to rabbits through the marginal ear vein. In this study, three intravenous anesthetic protocols were evaluated in New Zealand White rabbits. The three anesthetic regimens were: (a) pentobarbital (40 mg/kg); (b) ketamine-xylazine (25-5 mg/kg); (c) midazolam-xylazine-alfentanil (1-1-0.1 mg/kg). The anesthetics were injected slowly over defined time intervals. Reactions to noxious stimuli were determined before and after administration of the anesthetics. Additionally, the effects of the anesthetic agents on the rabbit's cardiopulmonary system were evaluated. Rabbits anesthetized with midazolam-xylazine-alfentanil did not have a pedal withdrawal or ear pinch reflex throughout the testing period. The ketamine-xylazine combination produced a shorter duration of non-responsiveness to noxious stimuli. Rabbits anesthetized with pentobarbital had the greatest variability in response to noxious stimuli. Apnea occurred in at least one rabbit in each group. A side effect unique to the midazolam-xylazine-alfentanil group was the occurrence of opisthotonus or seizure activity during or shortly after the administration of alfentanil. Hypotension, hypercapnia and respiratory acidosis were characteristic of the cardiopulmonary effects of the anesthetics. When choosing an anesthetic regimen for rabbits, intravenous infusion should be considered as an option. Advantages include ease of administration, possibility of redosing as required, and minimal requirements for equipment. Disadvantages of intravenous anesthetic infusion in rabbits include potential for lethal overdose and metabolic alterations after administration.

Alfentanil↗
PubMed2002

The effects of intravenous anesthetics and lidocaine on proliferation of cultured type II pneumocytes and lung fibroblasts.

UNLABELLED: Type II pneumocytes synthesize surfactant and differentiate into type I pneumocytes to maintain the epithelium (1). Alveolar type II cell proliferation is required for reepithelization after acute lung injury (ALI) and is thought to minimize the subsequent fibrotic response (1). Keratinocyte growth factor (KGF) and hepatocyte growth factor (HGF) are among the most potent mitogen for type II epithelial cells, but not for fibroblasts in the lung (1). These growth factors attenuate several experimental ALI models by promoting epithelial repair (2,3). Thus, KGF and HGF may be a promising therapeutic approach to ALI. Critically ill patients with ALI often receive IV anesthetics or sedatives to facilitate mechanical ventilation. Furthermore, these patients sometimes undergo bronchoscopy under local anesthesia to obtain bronchoalveolar lavage fluid or to remove respiratory secretions. Several IV and local anesthetics inhibit proliferation of various cells including epithelium (4,5). If these anesthetics impede proliferation of type II pneumocytes, this suppressive effect may be a disadvantage for alveolar reepithelization in the course of recovery from ALI. In this study, we examined the effects of midazolam, propofol, ketamine, thiopental, and lidocaine on proliferation of type II alveolar epithelial cells using in vitro culture system. Because fibroblast proliferation is a key event in late phase of ALI, inhibition of this fibroproliferation is probably beneficial. Thus, we further determined whether these anesthetics could regulate proliferation of lung fibroblasts. In the current study, rolipram was used as a positive control. In our previous preliminary experiment, we found that rolipram, a phosphodiesterase inhibitor type IV, augments spontaneous or KGF-/HGF-promoted type II cell proliferation (6). IMPLICATIONS: Midazolam, ketamine, thiopental, propofol, or lidocaine did not inhibit proliferation of cultured rat type II pneumocytes. Our findings suggest that these anesthetics do not impede alveolar reepithelization after acute lung injury.

Anesthetics, Dissociative↗
PubMed2003

The effects of local and intravenous anesthetics on recombinant rat VR1 vanilloid receptors.

UNLABELLED: Capsaicin, acting at the vanilloid 1 receptor (VR1), may potentiate local anesthetic activity, and as a ligand-gated ion channel of the transient receptor potential family, may also be a target for IV general anesthetics. We have examined whether local (lidocaine, prilocaine, and procaine 0.1-10 mM; 10 mM represents 0.25%-0.27% wt/vol) or IV anesthetics (propofol 10 micro M, thiopental 100 micro M, and ketamine 100 micro M) interact with recombinant rat VR1 expressed in human embryonic kidney (HEK293) cells (VR1-HEK293). We have assessed receptor interaction functionally by monitoring intracellular Ca(2+) ([Ca(2+)](i)) in Fura2-loaded cells at 37 degrees C. The addition of capsaicin (60 nM) produced a time-dependent biphasic increase in [Ca(2+)](i) amounting to 50-100 nM above than basal, which was inhibited by capsazepine 10 micro M and was absent in wild type HEK293 cells. Lidocaine and prilocaine alone (e.g., at 10 mM) significantly increased [Ca(2+)](i) by 67 +/- 6 nM and 33 +/- 7 nM, respectively, and concentration-dependently inhibited the capsaicin response. The effects of procaine were obscured by anesthetic-induced quenching of Fura2. In wild type HEK293 cells, lidocaine (10 mM) alone produced a small increase in [Ca(2+)](i). All IV anesthetics failed to modify capsaicin-increased [Ca(2+)](i). In conclusion, the present data suggest that local but not IV general anesthetics interact with recombinant rat VR1 receptors with the former anesthetics having antagonistic activity. IMPLICATIONS: Vanilloid receptors (VR1) are activated by capsaicin, the pain-producing component of hot chili peppers. We suggest that local (but not IV general) anesthetics may have inhibitory actions on this receptor.

Anesthetics, Intravenous↗
PubMed2001

Changes in effective and lethal doses of intravenous anesthetics and lidocaine when used in combination in mice.

We studied the interactions between a local anesthetic agent, lidocaine, and two general anesthetic drugs, propofol and ketamine, in mice. We used two end points: hypnosis, reflected by loss of the righting reflex, and death. The ED50 for hypnosis and the LD50 were determined for each drug separately, and a dose-response curve was prepared for each drug, using combinations of propofol-lidocane and ketamine-lidocaine at three different dose ratios. Probit and isobolographic analyses revealed supra-additive (synergistic) interactions between lidocaine and each of the other anesthetic agents regarding both the effective dose and the lethal dose. No significant difference was found between propofol and ketamine regarding the supraadditive effect.

Anesthetics, Dissociative↗
PubMed2005

In vitro effects of intravenous anesthetics on the sphincter of Oddi strips of sheep.

BACKGROUND: Intravenous anesthetics are often used for conscious sedation in endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic sphincter of Oddi (SO) manometry. This study was designed to investigate the direct effects of some intravenous anesthetics on SO in sheep. METHODS: In sheep SO rings, changes in isometric tension in response to cumulative concentrations of intravenous anesthetics were determined, and values for Emax (mean maximal inhibition) and pD2 (i.e. the negative logarithm of the concentration for the half-maximal response, EC50) were compared. RESULTS: Meperidine (10(-7) to 3 x 10(-5) M), fentanyl (10(-7) to 3 x 10(-5) M), midazolam (10(-7) to 3 x 10(-5) M) and propofol (10(-7) to 3 x 10(-4) M) induced concentration-dependent relaxations on SO precontracted with carbachol (10(-6) M). Emax and pD2 values following meperidine, fentanyl and midazolam administration were significantly greater than after propofol (p < 0.05). There were no significant differences in Emax and pD2 values for meperidine, fentanyl and midazolam. CONCLUSION: These results suggest that meperidine, fentanyl and midazolam are equipotent relaxants in the sheep SO in vitro. The relaxatory effect of propofol was 10 times less potent compared to the above agents, and it can be beneficial during SO manometry in controlled clinical human studies.

Adjuvants, Anesthesia↗
PubMed2002

Intravenous anesthetic, propofol inhibits invasion of cancer cells.

Intravenous anesthetic, propofol (2,6-diisopropylphenol), is extensively used for general anesthesia without knowing the effects on cancer. We found here that clinically relevant concentrations of propofol (1-5 microg/ml) decreased the invasion ability of human cancer cells (HeLa, HT1080, HOS and RPMI-7951). In the HeLa cells treated with propofol, formation of actin stress fibers as well as focal adhesion were inhibited, and propofol had little effect on the invasion ability of the HeLa cells with active Rho A (Val(14)-Rho A). In addition, continuous infusion of propofol inhibited pulmonary metastasis of murine osteosarcoma (LM 8) cells in mice. These results suggest that propofol inhibits the invasion ability of cancer cells by modulating Rho A and this agent might be an ideal anesthetic for cancer surgery.

Actins↗
PubMed2005

Intravenous anesthetics in sepsis.

Overactive inflammatory responses that destroy rather than protect are the crucial issues in the development of a spectrum of septic disease states, such as adult respiratory distress syndrome, systemic inflammatory response syndrome, septic shock, and multiple organ failure. This review focuses on an area in which alternative actions of intravenous anesthetics show much promise for sepsis: their effects on the inflammatory response and on inflammatory cells in vitro and in vivo. The endotoxin-induced pro-inflammatory cytokine activity and its consequent nitric oxide generation, free radicals production and neutrophil activity are generally depressed by intravenous anesthetics. Different intravenous anesthetics, such as propofol, ketamine, benzodiazepine and barbiturates, which produce different levels of inhibition of inflammatory effects, are discussed in this article. In addition, such modulations of inflammatory responses may be of great relevance to the practice of intensive care, and intravenous anesthetics may play significant roles in this regard.

Anesthetics, Intravenous↗
PubMed2003

Effects of local and intravenous anesthetics on the activity of glutamate transporter type 2.

Glutamate transporters may be important targets for anesthetic action in the central nervous system. The authors investigated the effects of the intravenous anesthetics, thiopental and ketamine, and the local anesthetics, lidocaine and bupivacaine, on the activity of glutamate transporter type 2, EAAT2. EAAT2 was expressed in Xenopus oocytes by injection of its mRNA. By using two-electrode voltage clamping, membrane currents were recorded after the application of L-glutamate (30 microM) in the presence or absence of various concentrations of anesthetics. Lidocaine and bupivacaine did not change glutamate-induced inward currents at the tested concentrations (1-1000 microM). Thiopental and ketamine also did not affect the activity of EAAT2 at the tested concentrations (0.3-300 microM). Our results suggest that the two commonly used local anesthetics (lidocaine and bupivacaine) and intravenous anesthetics (thiopental and ketamine) do not affect the activity of EAAT2 expressed in oocytes. EAAT2 may not be a target for these anesthetics.

Anesthetics, Intravenous↗