bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the Lateral Modified Approach for Continuous Interscalene Block after Shoulder Surgery
Authors: Borgeat Alain , Dullenkopf Alexander , Ekatodramis Georgios , Nagy Ladislav 
Published: November 2003

Background
Continuous interscalene block is the technique of choice for postoperative pain relief treatment after shoulder surgery. The authors prospectively evaluated the modified lateral approach for the performance of the interscalene catheter block and monitored 700 patients for clinical efficacy and complications during the first 6 months after placement of the catheter.

Methods
A total of 700 adults scheduled to undergo elective shoulder surgery performed with an interscalene brachial plexus block through an interscalene catheter were included in this study. The interscalene brachial plexus block procedure was standardized for all patients. Difficulties in placement of the catheter, clinical efficacy of anesthesia and analgesia, patient satisfaction, and acute and chronic complications were recorded. Patients were observed daily for 5 days for any complications and were evaluated at 1, 3, and 6 months after surgery. Persistence of neurologic complication was investigated by electroneuromyography.

Results
A total of 700 adults completed the study. Easy placement of the catheter (one attempt) was achieved in 86% of the patients. Resistance to thread the catheter was encountered in 6%; no major complications were observed during injection of the initial bolus. The success rate for anesthesia was 97%. Postoperative analgesia was efficient in 99%. The concentration and the rate of infusion of ropivacaine had to be increased in 31 patients (6%). In five patients (0.7%), signs of local infection around the puncture point were noted; in one patient (0.1%), a collection of pus was surgically drained. Patient satisfaction was 9.6 on a scale of 0-10. Minor neurologic complications (paresthesias, dysesthesias, pain not related to surgery) were observed in 2.4%, 0.3%, and 0% at 1, 3, and 6 months, respectively. At 1 month, three sulcus ulnaris syndromes, one carpal tunnel syndrome, and one complex regional pain syndrome were diagnosed. Two patients (0.2%) had sensory-motor deficit, which necessitated 19 and 28 weeks to recover. Electromyography was suggestive of partial axonotmesis.

Conclusion
The lateral modified approach provides good conditions for placement of the interscalene catheter. Anesthesia and analgesia performed through the catheter are efficient. The rates of infection and neurologic complications are low, and patient satisfaction is high.
Epidural, Cerebrospinal Fluid, and Plasma Pharmacokinetics of Epidural Opioids (Part 1)
Authors: Bernards Christopher M. , Shen Danny D. , Sterling Emily S. , Adkins Jason E. , Risler Linda , Phillips Brian , Ummenhofer Wolfgang 
Published: November 2003

Background
The pharmacokinetics of epidurally administered drugs has been the subject of many studies, yet drug concentration in the epidural space has never been measured. This study was undertaken to characterize the epidural, cerebrospinal fluid, and plasma pharmacokinetics of epidurally administered opioids on the basis of measurement of drug concentration in each of these compartments after epidural administration.

Methods
Morphine plus alfentanil, fentanyl, or sufentanil were administered epidurally in anesthetized pigs. Microdialysis was used to sample the epidural space and the cerebrospinal fluid for measurement of opioid concentration over time. Plasma samples were obtained from the central venous plasma and the epidural venous plasma. These data were used to calculate relevant pharmacokinetic parameters, including mean residence time, elimination half-lives, areas under the concentration versus time curves, clearance, and volume of distribution for each opioid in each compartment.

Results
Some of the more important findings were that the cerebrospinal fluid and plasma pharmacokinetics of the opioids did not parallel their epidural pharmacokinetics and that their hydrophobic character governed multiple aspects of their lumbar epidural pharmacokinetics.

Conclusions
The findings indicate that the spinal pharmacokinetics of these drugs are complex and, in some ways, counterintuitive. Also, the bioavailability of opioids in the cerebrospinal fluid and epidural space is determined primarily by their hydrophobicity, with less hydrophobic drugs having greater bioavailability.
Effect of Increasing Depth of Propofol Anesthesia on Upper Airway Configuration in Children
Authors: Evans Russell G. , Crawford Mark W. , Noseworthy Michael D. , Yoo Shi-Joon 
Published: November 2003

Background
The upper airway tends to be obstructed during anesthesia in spontaneously breathing patients. The purpose of the current study was to determine the effect of increasing depth of propofol anesthesia on airway size and configuration in children.

Methods
Magnetic resonance images of the upper airway were obtained in 15 children, aged 2-6 yr. Cross-sectional area, anteroposterior dimension, and transverse dimension were measured at the level of the soft palate, dorsum of the tongue, and tip of the epiglottis. Images were obtained during infusion of propofol at a rate of 50-80 microg.kg-1.min-1 and after increasing the depth of anesthesia by administering a bolus dose of propofol and increasing the infusion rate to 240 microg.kg-1.min-1.

Results
Overall, the cross-sectional area of the entire pharyngeal airway decreased with increasing depth of anesthesia. The reduction in cross-sectional area was greatest at the level of the epiglottis (24.5 mm2, 95% confidence interval = 16.9-32.2 mm2; P < 0.0001), intermediate at the level of the tongue (19.3 mm2, 95% confidence interval = 9.2-29.3 mm2; P < 0.0001), and least at the level of the soft palate (12.6 mm2, 95% confidence interval = 2.7-22.6 mm2; P < 0.005) in expiration and resulted predominantly from a reduction in anteroposterior dimension. The airway cross-sectional area decreased further in inspiration at the level of the epiglottis. The narrowest portion of the airway resided at the level of the soft palate or epiglottis in the majority of children.

Conclusion
Increasing depth of propofol anesthesia in children is associated with upper airway narrowing that occurs throughout the entire upper airway and is most pronounced in the hypopharynx at the level of the epiglottis.
Mechanisms of Direct Inhibitory Action of Isoflurane on Vascular Smooth Muscle of Mesenteric Resistance Arteries
Authors: Akata Takashi , Kanna Tomoo , Yoshino Jun , Takahashi Shosuke 
Published: November 2003

Background
Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries.

Methods
Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the beta-escin membrane-permeabilized strips.

Results
Isoflurane (3-5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 microM) or KCl (40 mM). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl- channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the beta-escin-permeabilized strips.

Conclusions
In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl- channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.
Corticotropin-releasing Factor Mediates the Antinociceptive Action of Nitrous Oxide in Rats
Authors: Sawamura Shigehito , Obara Mizuki , Takeda Kenji , Maze Mervyn , Hanaoka Kazuo 
Published: November 2003

Background
Exposure to nitrous oxide activates brainstem noradrenergic nuclei and descending inhibitory pathways, which produce the acute antinociceptive action of nitrous oxide. Because corticotropin-releasing factor (CRF) can produce activation of noradrenergic neurons in the locus ceruleus, the authors sought to determine whether it might be responsible for the antinociceptive action of nitrous oxide.

Methods
Male Sprague-Dawley rats (250-300 g) were exposed for 60 min to room air or 25, 50 or 70% nitrous oxide in oxygen. Brain sections including the hypothalamus were immunostained for both c-Fos (a marker of neuronal activation) and CRF and the percentage of CRF-positive neurons expressing c-Fos was determined. The functional consequences of changes in CRF were investigated by assessing the effect of intracerebroventricular administration of a CRF antagonist (alpha-helical CRF9-41, 20 microg/10 microl) on both activation of locus ceruleus noradrenergic neurons and the antinociception (with the tail-flick latency test) produced by nitrous oxide.

Results
Inhalation of nitrous oxide induced a dose-dependent increase in c-Fos expression in CRF-positive neurons in the paraventricular nucleus of the hypothalamus. Intracerebroventricular administration of CRF antagonist inhibited nitrous oxide-induced c-Fos expression in the locus ceruleus and the antinociceptive effect of nitrous oxide.

Conclusions
Nitrous oxide activates the CRF system in the brain, which results in stimulation of noradrenergic neurons in the locus ceruleus and its consequent antinociceptive effect.
High-dose Remifentanil Does Not Impair Cerebrovascular Carbon Dioxide Reactivity in Healthy Male Volunteers
Authors: Klimscha Walter , Ullrich Roman , Nasel Christian , Dietrich Wolfgang , Illievich Udo M. , Wildling Eckart , Tschernko Edda , Weidekamm Claudia , Adler Leopold , Heikenwälder Georg , Horvath Gyongyi , Sladen Robert N. 
Published: November 2003

Background
Cerebrovascular carbon dioxide reactivity during high-dose remifentanil infusion was investigated in volunteers by measurement of regional cerebral blood flow (rCBF) and mean CBF velocity (CBFv).

Methods
Ten healthy male volunteers with a laryngeal mask for artificial ventilation received remifentanil at an infusion rate of 2 and 4 microg x kg-1 x min-1 under normocapnia, hypocapnia, and hypercapnia. Stable xenon-enhanced computed tomography and transcranial Doppler ultrasonography of the left middle cerebral artery were used to assess rCBF and mean CBFv, respectively. If required, blood pressure was maintained within baseline values with intravenous phenylephrine to avoid confounding effects of altered hemodynamics.

Results
Hemodynamic parameters were maintained constant over time. Remifentanil infusion at 2 and 4 microg x kg-1 x min-1 significantly decreased rCBF and mean CBFv. Both rCBF and mean CBFv increased as the arterial carbon dioxide tension increased from hypocapnia to hypercapnia, indicating that cerebrovascular reactivity remained intact. The average slopes of rCBF reactivity were 0.56 +/- 0.27 and 0.49 +/- 0.28 ml. 100 g-1 x min-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.9 +/- 0.8 and 1.6 +/- 0.5, respectively). The average slopes for mean CBFv reactivity were 1.61 +/- 0.95 and 1.54 +/- 0.83 cm x s-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.86 +/- 0.59 and 1.79 +/- 0.59, respectively). Preanesthesia and postanesthesia values of rCBF and mean CBFv did not differ.

Conclusion
High-dose remifentanil decreases rCBF and mean CBFv without impairing cerebrovascular carbon dioxide reactivity. This, together with its known short duration of action, makes remifentanil a useful agent in the intensive care unit when sedation that can be titrated rapidly is required.
The Neuroprotective Effect of Xenon Administration during Transient Middle Cerebral Artery Occlusion in Mice
Authors: Homi H. Mayumi , Yokoo Noriko , Ma Daqing , Warner David S. , Franks Nicholas P. , Maze Mervyn , Grocott Hilary P. 
Published: November 2003

Background
Xenon has been shown to be neuroprotective in several models of in vitro and in vivo neuronal injury. However, its putative neuroprotective properties have not been evaluated in focal cerebral ischemia. The purpose of this study was to determine if xenon offers neuroprotection in a mouse model of middle cerebral artery occlusion.

Methods
C57BL/6 mice underwent 60 min of middle cerebral artery occlusion. The animals (n = 21 per group) were randomized to receive either 70% xenon + 30% O2, 70% N2O + 30% O2, or 35% xenon + 35% N2O + 30% O2. After 24 h, functional neurologic outcome (on three independent scales: four-point, general, and focal deficit scales) and cerebral infarct size were evaluated.

Results
The 70% xenon + 30% O2 group showed improved functional outcome (median [interquartile range], four-point scale: 2 [2], 70% xenon + 30% O2 versus 3 [2], 70% N2O + 30% O2, P = 0.0061; general deficit scale: 9 [6], 70% xenon + 30% O2 versus 10 [4], 70% N2O + 30% O2, P = 0.0346). Total cerebral infarct volumes were reduced in the 70% xenon + 30% O2 group compared with the 70% N2O + 30% O2 group (45 +/- 17 mm3 versus 59 +/- 11 mm3, respectively; P = 0.0009).

Conclusions
In this model of transient focal cerebral ischemia, xenon administration improved both functional and histologic outcome.
Isoflurane Pretreatment Has Immediate and Delayed Protective Effects against Cytokine-induced Injury in Endothelial and Vascular Smooth Muscle Cells
Authors: de Klaver Manuela J. M. , Buckingham Mary-Gordon , Rich George F. 
Published: November 2003

Background
Volatile anesthetics have protective effects against cytokine-induced injury in endothelial and vascular smooth muscle cells. The authors hypothesized that isoflurane pretreatment may trigger immediate and delayed protection that is modulated by adenosine triphosphate-sensitive potassium channels.

Methods
Human and bovine endothelial cells and rat vascular smooth muscle cells were pretreated with isoflurane (1.5% for 30 min) and then exposed to cytokines (tumor necrosis factor-alpha, interferon-gamma, and interleukin-beta) for 72 h. Cytokine exposure was initiated immediately after isoflurane pretreatment or after a delay of 1-48 h. Cell survival and viability were evaluated by trypan blue exclusion and lactate dehydrogenase release. The role of mitochondrial and cell membrane adenosine triphosphate-sensitive potassium channels, or both, were evaluated with the antagonists 5-hydroxydecanoate, HMR-1098, or glybenclamide.

Results
Immediate isoflurane pretreatment was approximately 70% effective in increasing cell survival and prevented lactate dehydrogenase release in all cell lines. However, cellular protection was completely lost if the time between isoflurane and cytokine exposure was extended to 2-12 h, depending on the cell type. Delayed protection was equal to immediate protection when the interval was extended to 12-24 h, with protection being sustained at 48 h in human endothelial and rat vascular smooth muscle cells. The immediate and delayed protection was inhibited by glybenclamide and 5-hydroxydecanoate but not by HMR-1098, whereas diazoxide, a mitochondrial adenosine triphosphate-sensitive potassium channels agonist, mimicked the time course of isoflurane-induced immediate and delayed protection in all cell lines.

Conclusion
Isoflurane pretreatment has immediate and delayed protective effects against cytokine-induced injury in endothelial and vascular smooth muscle cells that seem to be modulated by mitochondrial adenosine triphosphate-sensitive potassium channels. The time course of immediate and delayed protection is similar but not identical for each cell type.
Immunoneutralization of c-Fos Using Intrathecal Antibody Electroporation Attenuates Chronic Constrictive Injury-induced Hyperalgesia and Regulates Preprodynorphin Expression in Rats
Authors: Lan Chen-Yu , Tan Ping-Heng , Cheng Jiin-Tsuey , Lu Hsiao-Feng , Lin Ming-Wei , Hsiao Po-Ni , Lin Chung-Ren 
Published: November 2003

Background
In vivo electroporation has been successfully used for the introduction of DNA, RNA, oligonucleotides, and proteins into cells for experimental and therapeutic purposes. The authors evaluated the efficacy of electroporation-mediated c-Fos antibody therapy for neuropathic pain in vitro and in vivo.

Methods
First, the authors studied the inhibitory effects of intrathecal c-Fos antibody electroporation on the activating protein (AP-1) promoter activity in cultured spinal neuronal cells transfected with p-AP-Luc plasmid and activated with 100 microm glutamate. The inhibitory effect of c-Fos antibody electroporation in the regulation of AP-1 promoter activity was assessed according to the relative luciferase activity. Second, rats with chronic constrictive injury underwent electroporation treatment for neuropathic pain using c-Fos antibody. Thermal nociceptive thresholds were measured before chronic constrictive injury and then on even-numbered days, up to and including day 14, to assess and compare the therapeutic effects of intrathecal electroporation. The time course was assessed by Western blot analysis and by immunohistochemical analysis. Pronociceptive gene expression was measured by assessing prodynorphin mRNA and dynorphin peptides on days 2 and 10 after intrathecal c-Fos electroporation.

Results
Cotransfection of c-Fos antibody significantly decreased glutamate-induced AP-1 activity. Intrathecal electrotransfer of c-Fos antibody attenuated spinal dynorphin levels, as manifested by significantly elevated pain thresholds in the chronic constrictive injury-affected limbs.

Conclusion
This study shows that transfer of antibody into rat spinal cords by intrathecal electroporation is a useful method to study the function of endogenous factors of spinal-related disorders.
Women Have the Same Desflurane Minimum Alveolar Concentration as Men
Authors: Wadhwa Anupama , Durrani Jaleel , Sengupta Papiya , Doufas Anthony G. , Sessler Daniel I. 
Published: November 2003

Background
Women generally report greater sensitivity to pain than do men, and healthy young women require 20% more anesthetic than healthy age-matched men to prevent movement in response to noxious electrical stimulation. In contrast, minimum alveolar concentration (MAC) for xenon is 26% less in elderly Japanese women than in elderly Japanese men. Whether anesthetic requirement is similar in men and women thus remains in dispute. The authors therefore tested the hypothesis that the desflurane concentration required to prevent movement in response to skin incision (MAC) differs between men and women.

Methods
Using the Dixon "up and down" method, the authors determined MAC for desflurane in 15 female and 15 male patients (18-40 yr old) undergoing surgery.

Results
MAC was 6.2 +/- 0.4% desflurane for women versus 6.0 +/- 0.3% for men (P = 0.31), a difference of only 3%. These data provide 90% power to detect a 9% difference between the groups.

Conclusions
The MAC of desflurane did not differ between young men and women undergoing surgery with a true surgical incision. Although pain sensitivity may differ in women versus men, MAC of desflurane does not.
Using Front-end Kinetics to Optimize Target-controlled Drug Infusions
Authors: Avram Michael J. , Krejcie Tom C. 
Published: November 2003

Background
The mode of drug administration, blood sampling schedule, and sampling site affect the pharmacokinetic model derived. The present study tested the hypothesis that three-compartment pharmacokinetic model parameters derived from arterial drug concentrations obtained after rapid intravenous administration can be used to design a target-controlled drug infusion (TCI) that deviates minimally from the target.

Methods
Arterial thiopental concentration data obtained from the moment of injection in a previous study of five dogs were used. Three three-compartment models were constructed, one based on early concentrations classically obtained at 1, 2, and 3 min; another using all concentrations obtained beginning with the thiopental recirculation peak; and the last with the initial distribution volume (VC) fixed to the sum of VC and the nondistributive volume of the recirculatory model from the earlier study. Using these models, TCIs were designed that would maintain 20 mug/ml thiopental concentrations in VC for 60 min if simulated with the models used in their design. Drug concentrations resulting from these TCIs were then simulated using recirculatory model kinetics, and prediction errors were evaluated.

Results
Models with VCs estimated from intermittent or frequent early blood concentrations overestimated not only VC but also the volume and clearance of the rapidly equilibrating tissues, and their TCIs significantly overshot the target. With VC fixed to recirculatory model parameters, drug distribution was described in a manner consistent with that of the recirculatory model, and the TCI deviated minimally from the target. A similar three-compartment model was derived from data obtained from a simulation of a 2-min infusion using recirculatory kinetic parameters.

Conclusions
Because three-compartment models based on drug concentration histories obtained after rapid intravenous administration do not characterize VC accurately, TCIs based on them produce concentrations exceeding the target. A model capable of producing TCIs deviating minimally from the target can be derived from data obtained during and after a brief drug infusion.