bluuebunny/crossref_metadata_2025_split huggingface dataset:
Placental Transfer and Neonatal Effects of Epidural Sufentanil and Fentanyl Administered with Bupivacaine during Labor
Authors: Loftus John R. , Hill Harlan , Cohen Sheila E. 
Published: November 2003

Background
This randomized double-blind investigation was designed to study the placental transfer and neonatal effects of epidural sufentanil and fentanyl infused with bupivacaine for labor analgesia.

Methods
Healthy parturient women (n = 36) received epidural bupivacaine alone (group B) or with fentanyl (group B-F) or sufentanil (group B-S). Group B received a 12-ml bolus of 0.25% bupivacaine followed by a 10 ml/h infusion of 0.125% bupivacaine. Groups B-F and B-S received a 12-ml bolus of 0.125% bupivacaine with 75 micrograms fentanyl or 15 micrograms sufentanil, respectively, followed by 10 ml/h of 0.125% bupivacaine with fentanyl 1.5 micrograms/ml or sufentanil 0.25 micrograms/ml. Maternal venous (MV) and umbilical arterial (UA) and umbilical venous (UV) bupivacaine and opioid plasma concentrations were determined. Neonatal assessment included Apgar scores, umbilical cord blood gas analyses, and neurobehavioral testing at delivery and at 2 and 24 h of life using the Neurologic and Adaptive Capacity Score (NACS).

Results
The mean total dose of fentanyl was 136.6 +/- 13.1 micrograms (SEM), and of sufentanil, 23.8 +/- 1.8 micrograms. Although administered in a ratio of 5.7:1, fentanyl and sufentanil MV plasma concentrations were in the ratio of 27:1. UV/MV ratios were 0.37 for fentanyl and 0.81 for sufentanil. Fentanyl was detected in most UA samples, whereas sufentanil was present in only one sample. Neonatal condition was good and generally similar in all groups, with the exception of a lower NACS at 24 h in group B-F.

Conclusions
Although the degree of placental transfer of sufentanil appeared greater than that of fentanyl, lower MV sufentanil concentrations resulted in less fetal exposure to sufentanil. The lower NACS at 24 h in group B-F may reflect the continued presence of fentanyl in the neonate.
Binding of Halothane to Serum Albumin Demonstrated Using Tryptophan Fluorescence
Authors: Johansson Jonas S. , Eckenhoff Roderic G. , Dutton P. Leslie 
Published: November 2003

Background
The site of action of general anesthesia remains controversial, but evidence in favor of specific protein target(s) is accumulating. Saturable binding of halothane to bovine serum albumin (BSA) has recently been reported using photoaffinity labeling and fluorine 19 nuclear magnetic resonance spectroscopy. We report a new approach to study anesthetic binding to soluble proteins, based on native tryptophan fluorescence.

Methods
Thymol-free halothane and fatty acid-free BSA were equilibrated in gas-tight Hamilton syringes and dispensed into stoppered quartz cuvettes at predetermined dilutions. Steady-state fluorescence spectroscopy was used to study their interaction.

Results
Halothane quenched the tryptophan fluorescence of BSA in a concentration-dependent, saturable manner with a dissociation constant = 1.8 +/- 0.2 mM and a Hill number = 1.0 +/- 0.1. The two optical isomers of halothane bound to BSA with equal affinity. The ability of halothane to quench BSA tryptophan fluorescence was markedly decreased at pH 3.0 (which causes full uncoiling of BSA), with loss of saturable binding. Diethyl ether displaced a portion of halothane from its binding sites. Circular dichroism spectroscopy revealed no significant effect of halothane or diethyl ether on the secondary structure of BSA.

Conclusions
The results suggest that halothane binds in hydrophobic domains containing tryptophan in BSA. This approach may prove useful for studying the interaction of volatile anesthetics and proteins and has the advantage that the location of halothane in the protein is identified.
Interaction of Halothane with Inhibitory G-proteins in the Human Myocardium
Authors: Schmidt Ulrich , Schwinger Robert H. G. , Bohm Michael 
Published: November 2003

Background
Halothane has been reported to possess a catecholamine-sensitizing effect in laboratory animals and in anesthetized patients and to enhance the positive inotropic effect of isoproterenol in human papillary muscle strips. The current study was designed to investigate further the underlying subcellular mechanisms on human myocardium, in particular the mechanism of action of halothane on G-proteins.

Methods
To investigate the effect of halothane on adenylyl cyclase activity, isoproterenol-, guanylylimidodiphosphate (Gpp(NH)p)-, and forskolin-activated enzyme activities were studied alone and in the presence of halothane in native and manganese-treated membranes. The mechanisms of halothane interaction with inhibitory G-proteins (G1) were studied in adenosine diphosphate-ribosylation studies with pertussis toxin and immunochemical techniques.

Results
Halothane (1%) augmented isoproterenol- and Gpp(NH)p-stimulated adenylyl cyclase activity but had no effect on forskolin-stimulated enzyme activity. Manganese ions inhibited the stimulating effect of isoproterenol and Gpp(NH)p on adenylyl cyclase activity, but the effect of forskolin remained unchanged in control and halothane-treated membranes. In the presence of pertussis toxin, the effect of isoproterenol and Gpp(NH)p on adenylyl cyclase activity was enhanced, but further stimulation by halothane was abolished. Halothane did not influence the attachment of Gi alpha to the membrane. No effect of halothane on adenosine diphosphate-ribosylation of Gi alpha by pertussis toxin was observed.

Conclusions
Halothane stimulates adenylyl cyclase activity by inhibiting the function of the inhibitory G-proteins by interfering with the effects of the alpha subunits or beta gamma subunits with the effector. Decreased membrane attachment of Gi alpha in the presence of halothane does not occur. The interaction of alpha and beta gamma subunits is not affected by halothane. Halothane does not impair the binding of pertussis toxin to the Gi alpha-protein.
Inhibitory Effect of Lidocaine on Cultured Porcine Aortic Endothelial Cell-dependent Antiaggregation of Platelets
Authors: Az-ma Toshiharu , Hardian MD , Yuge Osafumi 
Published: November 2003

Background
Vascular spasm is a well-known complication during vascular surgery. Topical lidocaine is frequently used to prevent this spasm. However, the effects of lidocaine on the endothelium-dependent antiaggregation are not clear.

Methods
The aggregation of platelet-rich plasma (PRP) obtained from healthy volunteers was measured by the turbidimetric technique at 37 degrees C. (1) Cultured porcine aortic endothelial cells were preincubated with lidocaine (3.7 microM to 37 mM), NG-methyl-L-arginine (300 microM), or indomethacin (10 microM) for 30 min. The preincubation medium was exchanged with a medium containing +/- 1 microM bradykinin for 1-min stimulation of endothelial cells. One hundred microliters of the supernatant was then added to PRP (750 micro1) just after stimulation of PRP with collagen (4 micrograms/ml). (2) Authentic nitric oxide (NO) or prostacyclin (PGI2) was applied to collagen-stimulated PRP with or without lidocaine (100 micrograms/ml).

Results
(1) The supernatant from endothelial cells without bradykinin stimulation showed "basal" antiaggregation (13.8 +/- 3.2%; n = 6). Bradykinin enhanced the antiaggregation (100 +/- 0%; n = 6). NG-methyl-L-arginine or indomethacin (antagonists of NO or PGI2) inhibited the bradykinin-evoked antiaggregation (10.3 +/- 2.1% and 13.6 +/- 3.7%, respectively; n = 6). Simultaneous preincubation of both agents completely blocked the effect (-4.2 +/- 2.8%; n = 6). Lidocaine failed to influence basal antiaggregation, but it inhibited bradykinin-stimulated antiaggregation in a concentration-dependent manner (concentration causing 50% inhibition = 108 +/- 41 microM; n = 6). (2) In contrast, lidocaine did not shift the 50% effective concentration of NO (control, 1.3 +/- 0.1 microM vs. lidocaine, 1.6 +/- 0.1 microM) or PGI2 (control, 405 +/- 54 nM vs. lidocaine, 257 +/- 41 nM) for antiaggregation.

Conclusions
Our results suggest that lidocaine has an inhibitory effect on antiaggregation derived from endothelial cells, caused by the inhibition of NO and PGI2 released from endothelial cells.
Halothane Selectively Inhibits Bradykinin-induced Synovial Plasma Extravasation
Authors: Pierce Pamela A. , King Bryan S. , Rampil Ira J. , Levine Jon D. 
Published: November 2003

Background
In vitro studies demonstrate that halothane, but not isoflurane, inhibits bradykinin-induced calcium currents and prostacyclin release in cultured endothelial cells. Because bradykinin is an important endogenous mediator of inflammation, we assessed the effects of halothane, isoflurane, and pentobarbital on plasma extravasation, a component of tissue inflammation induced by bradykinin, in rats.

Methods
We anesthetized 23 rats with halothane (0.8 or 1.3 minimum alveolar concentration [MAC]), isoflurane (1.3 MAC), or pentobarbital (total of 85 mg/kg intraperitoneally). Their tracheas were intubated and their lungs mechanically ventilated. After intravenous administration of Evans blue dye, we perfused normal saline followed by bradykinin or platelet-activating factor, another inflammatory mediator, intraarticularly via needles placed in the knee joint. We collected perfusate and estimated extravasation by measuring dye in the perfusate using spectrophotometry.

Results
Bradykinin increased plasma extravasation eight- to ninefold above baseline in both pentobarbital- and isoflurane-anesthetized rats. In contrast, bradykinin-induced plasma extravasation at 0.8 MAC and 1.3 MAC of halothane was approximately 40% (P < 0.01) and 15% (P < 0.001), respectively, of that in pentobarbital- and isoflurane-anesthetized rats. Baseline plasma extravasation was lower in rats anesthetized with either concentration of halothane compared with pentobarbital or isoflurane (all P < 0.001). Platelet-activating factor-induced plasma extravasation was similar for all anesthetics.

Conclusion
Halothane, but not isoflurane or pentobarbital, inhibits both baseline and bradykinin-induced peripheral plasma extravasation, demonstrating that volatile anesthetics differentially modulate this important component of inflammation.
Relation between Functional Deficit and Intraneural Local Anesthetic during Peripheral Nerve Block
Authors: Popitz-Bergez F. A. , Leeson S. , Strichartz G. R. , Thalhammer J. G. 
Published: November 2003

Background
During peripheral nerve block, local anesthetic (LA) penetrates within and along the nerve to produce the observed functional deficits. Although much is known about the kinetics and steady-state relation for LA inhibition of impulse activity in vitro in isolated nerve, little is known about the relation between functional loss and intraneural LA content in vivo. This study was undertaken to investigate the relation of functional change to intraneural LA.

Methods
A sciatic nerve block was performed in rats with 0.1 ml 1% lidocaine radiolabeled with 14C. The total intraneural uptake of LA was determined at different times after injection, and the distribution of lidocaine along the nerve was assayed at different stages of functional block. Drug content was also compared with equilibrium lidocaine uptake in the isolated rat sciatic nerve.

Results
Total intraneural lidocaine in vivo increased to near steady-state in about 3 min, stabilizing at approximately 14.3 nmol/mg wet tissue for about 12 min before decreasing to zero at 70 min after injection. Although intraneural lidocaine was 1.6% of the injected dose during full block, only 0.3% was left when deep pain sensation returned and 0.065% was still detected when functions fully recovered. Despite these large differences in total lidocaine content, the longitudinal distribution remained constant. Intraneural lidocaine concentrations obtained at full block and partial recovery could be achieved in vitro by equilibration in 0.7-0.9 and 0.2-0.3 mM lidocaine, respectively.

Conclusions
During peripheral nerve block only a small amount of injected LA penetrates into the nerve. The intraneural content of LA correlates with the depth of functional block.
Isoflurane's Enhancement of Chloride Flux through Rat Brain γ-Aminobutyric Acid Type A Receptors Is Stereoselective
Authors: Quinlan Joseph J. , Firestone Susan , Firestone Leonard L. 
Published: November 2003

Background
Recent evidence is consistent with the view that volatile anesthetics interact directly with excitable membrane-bound channel proteins. If these agents interact directly with chiral centers in the neuronal cell membrane, then their effects should be stereoselective. Using rat brain membranes enriched in gamma-aminobutyric acid type A (GABAA) receptors, we investigated the hypothesis that the permeability response of this well-characterized central nervous system channel protein to stereoisomers of isoflurane is stereoselective.

Methods
Rat brain synaptic microvesicles were prepared by differential centrifugation. Agonist-stimulated 36Cl- flux through membrane-bound GABAA receptors was assayed in the presence of (+)- and (-)-isoflurane and compared with control conditions.

Results
Both isomers increased the potency and efficacy of GABA; however, (+)-isoflurane was significantly more potent and efficacious than the (-)-isomer. For example, the (+)-isomer (140 microM) reduced the median effective concentration of GABA from 12.7 +/- 1.0 to 5.4 +/- 0.5 microM, whereas the (-)-isomer reduced it to 9.6 +/- 1.0 microM (P < 0.001). The (+)-isomer also was 1.6 times as potent as the (-)-isomer in augmenting 5 microM GABA-gated flux (79 +/- 11 vs. 130 +/- 17 microM, respectively; P = 0.01). In addition, the (+)-isomer produced significantly greater maximal enhancement of flux (9.4 +/- 0.4 vs. 7.0 +/- 0.3 nmol.mg-1.3 s-1; P < 0.001).

Conclusions
Isoflurane's effects on GABA-gated chloride flux were stereoselective. This result supports direct interaction with a stereoselective site, possibly the GABAA channel protein itself, rather than a nonspecific perturbation of the surrounding membrane lipid. In addition, these findings, from a functional assay using mammalian brain, agree with recent observations in invertebrate ion channels and mammalian neuronal cell cultures.
Heat Flow and Distribution during Epidural Anesthesia
Authors: Matsukawa Takashi , Sessler Daniel I. , Christensen Richard , Ozaki Makoto , Schroeder Marc 
Published: November 2003

Abstract

Background
Core hypothermia after induction of epidural anesthesia results from both an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors thus evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution.
Role of the Vagus Nerve in the Antidysrhythmic Effect of Dexmedetomidine on Halothane/Epinephrine Dysrhythmias in Dogs
Authors: Kamibayashi Takahiko , Hayashi Yukio , Mammoto Tadanori , Yamatodani Atsushi , Sumikawa Koji , Yoshiya Ikuto 
Published: November 2003

Abstract

Background
Dexmedetomidine, an alpha2-adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha2adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhibit digitalis-induced dysrhythmias, dexmedetomidine may exert the antidysrhythmic property through vagal stimulation. To address this hypothesis, the effect of dexmedetomidine in vagotomized dogs was examined and compared with that in intact dogs. In addition, the effect of vagotomy on the antidysrhythmic action of doxazosin, an alpha1antagonist, was studied.
Where Are the Costs in Perioperative Care?: Analysis of Hospital Costs and Charges for Inpatient Surgical Care
Authors: Macario Alex , Vitez Terry S. , Dunn Brian , McDonald Tom 
Published: November 2003

Abstract

Background
Many health-care institutions are emphasizing cost reduction programs as a primary tool for managing profitability. The goal of this study was to elucidate the proportion of anesthesia costs relative to perioperative costs as determined by charges and actual costs.
Shivering Threshold during Spinal Anesthesia Is Reduced in Elderly Patients
Authors: Vassilieff Nicolas , Rosencher Nadia , Sessler Daniel I. , Conseiller Christian 
Published: November 2003

Abstract

Background
Both accidental and perioperative hypothermia are common in the elderly. The elderly are at risk because their responses to hypothermia may be delayed or less efficient than in those of younger subjects. For example, the vasoconstriction threshold during isoflurane anesthesia is [nearly equal] 1 degree Celsius less in elderly than younger patients. However, the extent to which other cold defenses are impaired in the elderly remains unclear, especially in those older than 80 yr. Operations suitable for spinal anesthesia provided an opportunity to quantify shivering thresholds in patients of varying ages. Accordingly, the hypothesis that the shivering threshold is reduced as a function of age during spinal anesthesia was tested.
Effects of Storage Time on Quantitative and Qualitative Platelet Function after Transfusion
Authors: Rosenfeld Brian A. , Herfel Barbara , Faraday Nauder , Fuller Alice , Braine Hayden 
Published: November 2003

Abstract

Background
Platelet transfusions are being used increasingly in patients with thrombocytopenia to improve hemostatic function before surgery and invasive procedures. However, there are limited data on the immediate quantitative and qualitative platelet response after transfusion. Some authors have suggested that transfused platelets require time in vivo to regain maximal function, which is dependent on the duration of platelet storage. Therefore, the timing of surgery and invasive procedures with optimal platelet function may not be occurring.
Visual Display Format Affects the Ability of Anesthesiologists to Detect Acute Physiologic Changes: A Laboratory Study Employing a Clinical Display Simulator
Authors: Gurushanthaiah Keerti , Weinger Matthew B. , Englund Carl E. 
Published: November 2003

Abstract

Background
Anesthesiologists use data presented on visual displays to monitor patients' physiologic status. Although studies in nonmedical fields have suggested differential effects on performance among display formats, few studies have examined the effect of display format on anesthesiologist monitoring performance.
Linearity of Pharmacokinetics and Model Estimation of Sufentanil
Authors: Gepts Elisabeth , Shafer Steven L. , Camu Frederic , Stanski Donald R. , Woestenborghs Robert , Van Peer Achiel , Heykants Jos J.P. 
Published: November 2003

Abstract

Background
The pharmacokinetic profiles of sufentanil available in the literature are conflicting because of methodologic differences. Length of sampling and assay sensitivity are key factors involved in accurately estimating the volumes of distribution, clearances, and elimination phase. The unit disposition function of increasing doses of sufentanil were investigated and the influence of dose administered on the linearity of pharmacokinetics was assessed.
Inhalation Toxicity Study of a Haloalkene Degradant of Sevoflurane, Compound A (PIFE), in Sprague-Dawley Rats
Authors: Keller K. A. , Callan C. , Prokocimer P. , Delgado-Herrera L. , Friedman M. B. , Hoffman G. M. , Wooding W. L. , Cusick P. K. , Krasula R. W. 
Published: November 2003

Abstract

Background
Under certain circumstances in the clinical setting, contact of the anesthetic sevoflurane with a CO2absorbant (e.g., soda lime, Baralyme) leads to the formation of a degradant designated as pentafluoroisopropenyl fluoromethyl ether (PIFE; Compound A). Previous studies have shown that the kidney is the primary target organ for toxicity in the rat. This study was designed to determine the impact of PIFE on rat renal histology correlated with functional changes. The findings are discussed in terms of probable mechanism of action and relevance to humans.
Propofol Reduces Neuronal Transmission Damage and Attenuates the Changes in Calcium, Potassium, and Sodium during Hyperthermic Anoxia in the Rat Hippocampal Slice
Authors: Amorim Pedro , Chambers Geoffrey , Cottrell James , Kass Ira S. 
Published: November 2003

Abstract

Background
Propofol reduces cerebral blood flow, cerebral metabolic rate for oxygen, and intracranial pressure and is being increasingly used in neuroanesthesia. In vivo studies have yielded conflicting results on its ability to protect against ischemic brain damage. In the current study, an in vitro model was used to examine the mechanism of propofol's action on anoxic neuronal transmission damage.
Calcium Administration Augments Pancreatic Injury and Ectopic Trypsinogen Activation after Temporary Systemic Hypotension in Rats
Authors: Mithofer Kai , Warshaw Andrew L. , Frick Thomas W. , Lewandrowski Kent B. , Koski Greg , Rattner David W. , Fernandez-del Castillo Carlos 
Published: November 2003

Abstract

Background
Calcium infusion and hypotension have been described as the most important risk factors for pancreatic injury after cardiopulmonary bypass.
Inhibitory Effects of Thiopental, Ketamine, and Propofol on Voltage-dependent Calcium sup 2+ Channels in Porcine Tracheal Smooth Muscle Cells
Authors: Yamakage Michiaki , Hirshman Carol A. , Croxton Thomas L. 
Published: November 2003

Abstract

Background
Intravenously administered anesthetics directly inhibit airway smooth muscle contraction. Because many anesthetic agents affect membrane ion channel function and sustained contraction of airway smooth muscle requires the influx of Calcium2+ through voltage-dependent Calcium2+ channels, it was hypothesized that intravenous anesthetics inhibit airway smooth muscle voltage-dependent Calcium2+ channels.
Cerebral Vasoconstriction by Indomethacin in Intracranial Hypertension: An Experimental Investigation in Pigs
Authors: Nilsson F. , Bjorkman S. , Rosen I. , Messeter K. , Nordstrom C.-H. 
Published: November 2003

Abstract

Background
Uncontrolled increase in intracranial pressure is the most significant cause of mortality in patients with severe traumatic brain lesions, and the efficacy of common nonsurgical treatments has been questioned. Pharmacologically induced cerebral vasoconstriction aiming at a decrease of cerebral blood volume and brain edema has recently been suggested as an alternative. Limited clinical experience with indomethacin as a cerebral vasoconstrictor has been reported but dose- or concentration-effect relationships were not investigated. In particular, there is a lack of data showing whether a therapeutic window exists in which risk of cerebral ischemia is minimized.
Quaternary Ammonium Derivative of Lidocaine as a Long-acting Local Anesthetic
Authors: Wang G. K. , Quan C. , Vladimirov M. , Mok W. M. , Thalhammer J. G. 
Published: November 2003

Abstract

Background
Use of long-acting local anesthetics that elicit complete neural blockade for more than 3 h often is desirable in pain management. Unfortunately, clinically available local anesthetics are in general not suitable for prolonged analgesia. This report describes the organic synthesis and functional testing of a lidocaine derivative that appears to fulfill the criteria of long-acting local anesthetics.