bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhalation Anesthetics Inhibit the Release of Endothelium-derived Hyperpolarizing Factor in the Rabbit Carotid Artery
Authors: Lischke Volker , Busse Rudi , Hecker Markus 
Published: November 2003

Background
Inhalation anesthetics may interfere with the synthesis or action of endothelium-derived vasoactive factors. We investigated the effects of desflurane, enflurane, halothane, isoflurane, and sevoflurane on the release of nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) in the isolated endothelium-intact carotid artery of the rabbit.

Methods
Isolated segments of the carotid artery were suspended in Krebs-Henseleit solution (37 degrees C) and preconstricted with phenylephrine (1 microM). Relaxations caused by acetylcholine (ACh) (0.03-10 microM) or sodium nitroprusside (0.01-10 microM) were compared in the presence or absence of the nitric oxide synthase inhibitor NG-nitro-L-arginine (0.1 mM) in segments exposed to desflurane (8%), enflurane (2-4%), halothane (2-3.5%), isoflurane (2-4%), or sevoflurane (2%) as well as in NG-nitro-L- arginine-treated segments exposed to enflurane (2%) in combination with the KCa(+)-channel blocker tetrabutylammonium (0.3 mM) or the cytochrome P450 inhibitor clotrimazole (3 microM).

Results
Desflurane, enflurane, and sevoflurane selectively inhibited the ACh-induced release of EDHF. Halothane and isoflurane also weakly affected the nitric oxide-mediated relaxant response to ACh. The inhibitory effect of these two anesthetics on EDHF release was concentration-dependent. Relaxations induced by sodium nitroprusside were not inhibited by any of the anesthetics tested. Three structurally unrelated cytochrome P450 inhibitors clotrimazole (0.1 mM), metyrapone (1 mM), and SKF525a (proadifen, 0.1 mM) abolished the EDHF-mediated relaxation elicited by ACh. The pharmacologic profile of the inhibitory effect of enflurane on the release of EDHF closely resembled that of clotrimazole but not that of tetrabutylammonium. Moreover, all anesthetics inhibited the cytochrome P450-catalyzed O-dealkylation of 7-ethoxycoumarin by rabbit liver microsomes in a concentration-dependent manner.

Conclusions
Inhalation anesthetics significantly attenuate the EDHF-mediated relaxant response to ACh in the rabbit carotid artery. This effect appears to be attributable to inhibition of the cytochrome P450-dependent synthesis of EDHF by the endothelium.
Volatile Anesthetics Depress Calcium sup 2+ Transients and Glutamate Release in Isolated Cerebral Synaptosomes
Authors: Miao Ning , Frazer Martha J. , Lynch Carl III 
Published: November 2003

Background
The current study was performed to determine whether volatile anesthetics may include as part of their action in the central nervous system the depression of presynaptic transmitter release by alteration in intrasynaptic [Ca2+] ([Ca2+]i).

Methods
Guinea pig cerebrocortical synaptosomes were studied at 37 degrees C suspended in control buffer solution containing 1.3 mM external [Ca2+] ([Ca2+]e). Spectrofluorometric assays were used to monitor [Ca2+]i with the Ca(2+)-sensitive fluorophore Fura-2 and to monitor glutamate release with an enzyme-coupled assay that produced the fluorescent product nicotinamide adenine dinucleotide phosphate. To activate the increase in [Ca2+]i and glutamate release, synaptosomes were depolarized by abruptly increasing external [K+] from 5 to 35 mM. Responses were determined in solutions equilibrated with approximately 1 or 2 minimum alveolar concentration (MAC) isoflurane, enflurane, or halothane and also in solutions with decreased [Ca2+]e (0.025, 0.05, 0.1, 0.2, 0.4, and 0.6 mM).

Results
Although they had no action on basal behavior, the anesthetics depressed the K(+)-depolarization-induced increase in both [Ca2+]i and glutamate release in a dose-dependent fashion. The [Ca2+]i transient was inhibited by 13-21% per MAC, and glutamate release was depressed 14-28% per MAC. The depression of both [Ca2+]i and glutamate release caused by 2.5% isoflurane, 3.4% enflurane, and 1.5% halothane could be reproduced by a reduction in [Ca2+]e to 0.2-0.4 mM.

Conclusions
In this setting, isoflurane, enflurane, and halothane decrease [Ca2+]i in a manner consistent with inhibition of Ca2+ entry, possibly by specific voltage-gated neuronal Ca2+ channels. This decrease in [Ca2+]i is sufficient to account for all or most of the associated decrease in glutamate release.
Preoperative Dipyridamole Thallium Imaging and Ambulatory Electrocardiographic Monitoring as a Predictor of Perioperative Cardiac Events and Long-term Outcome
Authors: Fleisher Lee A. , Rosenbaum Stanley H. , Nelson Ann H. , Jain Diwaker , Th Wackers Frans J. , Zaret Barry L. 
Published: November 2003

Abstract

Background
Dipyridamole thallium imaging (DTI) and ambulatory electrocardiography (AEGC) have been advocated as means to stratify risk before vascular surgery. The purpose of this study was to compare the predictive value of both tests in noncardiac surgery patients for perioperative cardiac morbidity and long-term mortality.
Pharmacokinetics of Computer-controlled Alfentanil Administration in Children Undergoing Cardiac Surgery
Authors: Fiset Pierre , Mathers Lawrence , Engstrom Ray , Fitzgerald David , Brand Stephen C. , Hsu Faye , Shafer Steven L. 
Published: November 2003

Abstract

Background
Cardiopulmonary bypass (CPB) induces changes in the pharmacokinetics of drugs. The purpose of this study was to model the pharmacokinetics of alfentanil in children undergoing cardiac surgery to provide accurate dosage titration intraoperatively as well as in the postoperative period.
Effect of Antiemetic Therapy on Recovery and Hospital Discharge Time
Authors: Davis Peter J. , McGowan Jr. Francis X. , Landsman Ira , Maloney Karen , Hoffmann Paul 
Published: November 2003

Abstract

Background
Postoperative nausea and vomiting continue to be a significant problem for pediatric ambulatory surgery patients. Although ondansetron has been demonstrated to be effective in the prophylactic treatment of postoperative nausea and vomiting (surrogate end point) no one has demonstrated a benefit of antiemetic therapy on patient recovery, postanesthesia care unit length of stay, and hospital length of stay (nonsurrogate end points). In a double-blind manner, the effects of ondansetron, droperidol, and placebo on the incidence of emesis, postanesthesia care unit stay, and hospital discharge time were evaluated in children undergoing dental surgery.
Measured Context-sensitive Half-times of Remifentanil and Alfentanil
Authors: Kapila Atul , Glass Peter S. A. , Jacobs James R. , Muir Keith T. , Hermann David J. , Shiraishi Masa , Howell Scott , Smith Richard L. 
Published: November 2003

Abstract

Background
The context-sensitive half-time, rather than the terminal elimination half-life, has been proposed as a more clinically relevant measure of decreasing drug concentration after a constant infusion of a given duration. The context-sensitive half-time is derived from computer modelling using known pharmacokinetic parameters. The modelled context-sensitive half-time for a 3-h infusion of alfentanil is 50–55 min and is 3 min for remifentanil. The terminal elimination half-life is 111 min for alfentanil and 12–30 min for remifentanil. It has not been tested whether the modelled context-sensitive half-time reflects the true time for a 50% decrease in drug concentration or drug effect.
Faster Recovery after Anesthesia in Infants after Intravenous Induction with Methohexital Instead of Thiopental
Authors: Beskow Annika , Werner Olof , Westrin Per 
Published: November 2003

Abstract

Background
To determine possible delays in recovery after intravenous anesthesia induction with thiopental, the drug was compared with methohexital in infants 1–12 months of age who were scheduled for hernia repair or circumcision.
Arteriovenous Differences in Plasma Concentrations of Catechols in Rats with Neuropathic Pain
Authors: Raja Srinivasa N. , Choi Yoon , Asano Yoshio , Holmes Courtney , Goldstein David S. 
Published: November 2003

Abstract

Background
Alterations in cutaneous temperature, sweating, and cutaneous blood flow in patients with pain states, such as reflex sympathetic dystrophy and causalgia, have been interpreted as evidence for exaggerated sympathetic outflow. It was determined whether pain behavior in a rat model of sympathetically maintained pain is associated with alterations in regional sympathoneural function.
Effects of Midazolam on Intracellular Calcium sup 2+ and Tension in Airway Smooth Muscles
Authors: Yoshimura Hayashi , Kai Tetsuya , Nishimura Junji , Kobayashi Sei , Takahashi Shosuke , Kanaide Hideo 
Published: November 2003

Abstract

Background
It has been demonstrated that a group of minor tranquilizers, benzodiazepines, are able to relax airway smooth muscles. To determine the underlying mechanisms of this phenomenon, the effects of midazolam on the intracellular Calcium2+ concentration ([Calcium2+]i) and tension in airway smooth muscles were investigated.
Intrathecal Amitriptyline
Authors: Eisenach James C. , Gebhart G. F. 
Published: November 2003

Abstract

Background
Systemically administered opioids induce analgesia in part by spinal noradrenergic, serotonergic, and cholinergic mechanisms. The current study tested whether antinociception from systemically administered opioids could therefore be enhanced by intrathecal injection of a monoamine reuptake inhibitor to potentiate the action of spinally released norepinephrine and serotonin (amitriptyline) and intrathecal injection of a cholinesterase inhibitor to potentiate the action of spinally released acetylcholine (neostigmine).
Intrathecal Amitriptyline Acts as an N-Methyl-D-Aspartate Receptor Antagonist in the Presence of Inflammatory Hyperalgesia in Rats
Authors: Eisenach James C. , Gebhart G. F. 
Published: November 2003

Abstract

Background
Amitriptyline and other tricyclic antidepressants exhibit high affinity binding to N-methyl-D-aspartate (NMDA) receptors in vitro and inhibit NMDA receptor activation-induced neuroplasticity in hippocampal slices. Because spinal NMDA receptor activation is believed to be central to generation and maintenance of hyperalgesic pain, the purpose of this study was to test whether intrathecal amitriptyline reduced inflammation-induced hyperalgesia in the rat.
One-day Hypothermic Preservation of Isolated Hearts with Halothane Improves Cardiac Function Better than Low Calcium
Authors: Stowe David F. , Habazettl Helmut , Graf Bernhard M. , Kampine John P. , Bosnjak Zeljko J. 
Published: November 2003

Abstract

Background
Halothane exerts a potent negative inotropic effect on the heart and mimics many of the cardiac effects of lowered extracellular CaCl2. Reduced slow inward Calcium2+ current and sarcoplasmic reticular effects on intracellular Calcium2+ are likely involved. The authors reported previously that halothane protects against hypoxic and ischemia reperfusion injury in isolated hearts. The aim of this isolated heart study was to compare protective effects of halothane and low CaCl sub 2 (0.5 mM) administered during 1 day of hypothermic perfusion on return of normothermic perfusion.
Epinephrine Is Metabolized by the Spinal Meninges of Monkeys and Pigs
Authors: Kern C. , Mautz D. S. , Bernards C. M. 
Published: November 2003

Abstract

Background
Epinephrine commonly is added to epidural opioids and local anesthetics, however, little is known about the fate of epidurally administered epinephrine. Studies have identified the epinephrine metabolizing enzyme, catechol-O-methyl transferase (COMT), in the cranial meninges of several species. The purpose of this study was to determine whether the spinal meninges also contain COMT and are capable of metabolizing epinephrine. If so, then the spinal meninges may have an important impact in limiting the bioavailability of epinephrine in both the spinal cord and epidural space.
Cardiovascular Stimulation Induced by Rapid Increases in Desflurane Concentration in Humans Results from Activation of Tracheopulmonary and Systemic Receptors
Authors: Weiskopf Richard B. , Eger II Edmond I. , Daniel Malcolm , Noorani Mariam 
Published: November 2003

Abstract

Background
It was hypothesized that stimulation of rapidly adapting airway receptors produces the transient (2–4 min) circulatory responses to rapid increases in desflurane concentrations greater than 6%. Accordingly, it was reasoned that increasing the concentration of desflurane in one lung, without altering the concentration of desflurane in systemic blood, should cause cardiovascular stimulation, whereas once the airway receptors had adapted to the stimulation, an initial increase in the systemic concentration of desflurane should have little effect.
Desflurane Slightly Increases the Sweating Threshold but Produces Marked, Nonlinear Decreases in the Vasoconstriction and Shivering Thresholds
Authors: Annadata Radhika , Sessler Daniel I. , Tayefeh Farzin , Kurz Andrea , Dechert Martha 
Published: November 2003

Abstract

Background
Shivering is rare during general anesthesia. This observation suggests that anesthetics profoundly impair shivering. However, the effects of surgical doses of volatile anesthetics on control of shivering have yet to be evaluated. Furthermore, the effects of desflurane on sweating and thermoregulatory vasoconstriction remain unknown. Accordingly, the authors determined the concentration-dependent effects of desflurane on sweating, vasoconstriction, and shivering.
Effect of Propofol on Spinal Dorsal Horn Neurons: Comparison with Lack of Ketamine Effects
Authors: Uchida Hiroshi , Kishikawa Kazuhiro , Collins J. G. 
Published: November 2003

Abstract

Background
Pentobarbital reduces low-threshold receptive field (RF) size and enhances responses of some spinal dorsal horn neurons to noxious stimulation in cats. To better understand the effects of general anesthetics on spinal sensory processing, this study was designed to determine if intravenous propofol and ketamine have similar effects.
Formal Instruction in Difficult Airway Management: A Survey of Anesthesiology Residency Programs
Authors: Koppel James N. , Reed Allan P. 
Published: November 2003

Abstract

Background
Up to 30% of all deaths attributable to anesthesia are related to difficulties with airway management. The purpose of this study was to determine whether anesthesiology residents are receiving specialized instruction in the various techniques and mechanical devices currently recommended for airway management in patients with anticipated or unanticipated difficult airways.
Differences in Respiratory Reflex Responses from the Larynx, Trachea, and Bronchi in Anesthetized Female Subjects
Authors: Nishino Takashi , Kochi Tetsuo , Ishii Masayuki 
Published: November 2003

Background
Animal studies show that airway receptors responsible for eliciting respiratory protective reflexes are not uniformly distributed in the airways. Based on this information, it is possible that the protective reflex responses to airway irritation in humans may vary, depending on the site of stimulation. The purpose of this study is to examine whether the protective reflex responses evoked from the larynx are different from those evoked from the lower airways and to see how change in depth of anesthesia modifies the protective reflex responses evoked from individual sites.

Methods
The airway mucosa of the larynx, tracheal carina, and bronchi were stimulated by injection of distilled water (0.5 ml) at two different depths of sevoflurane anesthesia (1.2 and 1.8 MAC) in 11 female subjects breathing spontaneously through the laryngeal mask airway. The respiratory responses were monitored by measuring ventilatory flow and airway pressure.

Results
At 1.2 MAC of sevoflurane anesthesia, both laryngeal and tracheal stimulation caused protective responses, such as forceful expiratory efforts, apnea, and spasmodic panting, whereas bronchial stimulation caused little or no such responses. There was no significant difference in the incidence of different types of reflex responses between the larynx and the trachea. At 1.8 MAC of sevoflurane, the nature of the elicited responses was very similar to that observed at 1.2 MAC of sevoflurane, showing little dose-dependence of anesthetic effect.

Conclusions
The respiratory reflex responses evoked by injection of water vary, depending on the site of stimulation. The incidence of various reflex responses was not affected by the changing depth of anesthesia. The sensitivity to airway irritation seems to be greater at the larynx and trachea than at the more peripheral airways.
Propofol Fails to Attenuate the Cardiovascular Response to Rapid Increases in Desflurane Concentration
Authors: Daniel Malcolm , Eger Edmond I , Weiskopf Richard B. , Noorani Mariam 
Published: November 2003

Background
A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses.

Methods
To test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg.kg-1 propofol, anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg.kg-1 propofol was administered either 2 or 5 min before increasing end-tidal desflurane concentration from 4% to 8%.

Results
Without propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63 +/- 3 beats/min to 108 +/- 5 beats/min, mean +/- SEM; P < 0.01), mean arterial pressure (from 73 +/- 1 mmHg to 118 +/- 6 mmHg; P < 0.01), and epinephrine concentration (from 14 +/- 1 pg.ml-1 to 279 +/- 51 pg.ml-1; P < 0.05). There was no significant change in norepinephrine concentration (from 198 +/- 37 pg.ml-1 to 277 +/- 46 pg.ml-1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158 +/- 35 pg.ml-1, propofol given 2 min before, and 146 + 41 pg.ml-1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses.

Conclusions
Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.
Pharmacokinetic Origin of Carbamazepine-induced Resistance to Vecuronium Neuromuscular Blockade in Anesthetized Patients
Authors: Alloul Karine , Whalley David G. , Shutway Fanny , Ebrahim Zeyd , Varin France 
Published: November 2003

Background
Patients receiving chronic carbamazepine therapy have shortened recovery times from a neuromuscular block induced by vecuronium. The current study investigates the pharmacokinetic or pharmacodynamic mechanisms responsible for this observation.

Methods
Pharmacokinetics and pharmacodynamics of 0.1 mg/kg intravenous bolus vecuronium in ten epileptic patients receiving chronic carbamazepine therapy were compared to that of ten control subjects. All patients were scheduled for neurosurgery while anesthetized with isoflurane and sufentanil. Arterial blood samples were collected for 6 h. Plasma vecuronium concentrations were measured by high-performance liquid chromatography coupled to electrochemical detection. The adductor pollicis force of contraction was recorded after supramaximal ulnar nerve stimulation. Plasma vecuronium concentrations were fitted to a two-compartment pharmacokinetic model, and the effect compartment equilibration rate constant was derived with a nonparametric link model. The effect compartment concentrations were fitted to a sigmoid Emax model. Results were compared using Student's t-test for independent samples.

Results
In the carbamazepine group, the mean recovery times to T(1) 25% were shorter (28.1 +/- 3.4 vs. 47.3 +/- 5.1 min in control subjects; P=0.007), and the T(1) 25% to T(1) 75% recovery index was decreased (7.6 +/- 1.2 vs. 21.9 +/- 6.8 min in control subjects; P=0.025). No changes in onset times were observed. Clearance was 9.0 +/- 1.2 ml x kg-1 x min-1 versus 3.8 +/- 0.3 in the control group (P=0.003), whereas no changes in volumes of distribution at steady-state were observed. Therefore, the mean residence time was halved (17.8 +/- 2.5 vs. 31.9 +/- 2.5 min in control subjects; P=0.001). No differences in the effect compartment equilibration rate constant, vecuronium effect compartment concentration present at a 50% block (EC50), or slope of the sigmoid between the two groups were found.

Conclusions
The twofold increase in clearance provides evidence of a pharmacokinetic origin to the carbamazepine-vecuronium interaction; however, the possibility of a concurrent pharmacodynamic alteration cannot be assessed. Greater knowledge of protein drug binding needs to be acquired to give a meaningful interpretation to the similar EC50 values observed in the two groups.
Role of Magnesium Sulfate in Postoperative Analgesia
Authors: Tramer Martin R. , Schneider Jurg , Marti Rene-Andreas , Rifat Kaplan 
Published: November 2003

Background
N-methyl-D-aspartate antagonists may play a role in the prevention of pain. An assessment was made of the effect of the physiologic N-methyl-D-aspartate antagonist magnesium on analgesic requirements, pain, comfort, and quality of sleep in the postoperative period.

Methods
In a randomized, double-blind study, 42 patients undergoing elective abdominal hysterectomy with general anesthesia received 20% magnesium sulfate or saline (control) 15 ml intravenously before start of surgery and 2.5 ml/h for the next 20 h. Postoperative morphine requirement was assessed for 48 h using patient-controlled analgesia. Maximum expiratory flow (peak flow), pain at rest and during peak flow, and discomfort were evaluated up to the 48th postoperative hour, and 1 week and 1 month after surgery. Insomnia was evaluated after the first and second postoperative nights.

Results
Compared to control subjects, magnesium-treated patients consumed less morphine during the first 48h (P<0.03), which was most pronounced during the first 6 h (P<0.004), and experienced less discomfort during the first and second postoperative days (P<0.05-0.005). The magnesium-treated group revealed no change in postoperative sleeping patterns when compared to preoperative patterns. Control patients showed an increase in insomnia during the first and second postoperative nights (P<0.002 and P<0.005, respectively) compared to preoperative values.

Conclusions
This is the first clinical study showing that the perioperative application of magnesium sulfate is associated with smaller analgesic requirement, less discomfort, and a better quality of sleep in the postoperative period but not with adverse effects. Magnesium could be of interest as an adjuvant to postoperative analgesia.