bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Randomized Controlled Trial Comparing the Cuffed Oropharyngeal Airway and the Laryngeal Mask Airway in Spontaneously Breathing Anesthetized Adults
Authors: Greenberg Robert S. , Brimacombe Joseph MB , Berry Alison , Gouze Victoria , Piantadosi Steven , Dake Elizabeth M. 
Published: November 2003

Background
The cuffed oropharyngeal airway (COPA), a modified Guedel airway, was compared with the laryngeal mask airway (LMA) during spontaneous breathing anesthesia. Specifically examined were ease of use, physiologic tolerance, and the frequency of problems.

Methods
Adult patients consented to random (2:1) assignment to either COPA (n = 302) or LMA (n = 151) for airway management during anesthesia with propofol, nitrous oxide, and oxygen.

Results
Ease of insertion was similar, but the first-time successful insertion rate was higher with the LMA (COPA, 81% compared with LMA, 89%; P = 0.05). More brief manipulations (head tilt, chin lift, jaw thrust) were reported in the COPA group (average total number of manipulations: COPA, 1.1 +/- 1.6 compared with LMA, 0.1 +/- 0.2; P < 0.001). Continuous airway support was used more frequently in the COPA group (COPA, 30% compared with LMA, 0%; P < 0.0005). The incidences of aspiration, regurgitation, laryngospasm, wheezing, succinylcholine administration, oxygen saturation (SpO2) < 92%, failed use, and minor intraoperative problems were similar. When the airways were removed, blood was detected on the COPA less frequently than on the LMA (COPA, 5.8% compared with LMA, 15.3%; P = 0.001). The incidence of early and late sore throat was greater with the LMA (early: COPA, 4.7% compared with LMA, 21.9% [P = 0.001]; late: COPA, 8.4% compared with LMA, 16.1%; P = 0.01). The LMA did better than the COPA when anesthetists analyzed the technical aspects of the two devices.

Conclusions
Although the COPA and LMA are equivalent devices in terms of physiologic alterations and overall clinical problems associated with their use, the LMA was associated with a higher first-time insertion rate and fewer manipulations, suggesting that it is easier to use. The COPA was associated with less blood on the device and fewer sore throats, suggesting it may cause less pharyngeal trauma. Ultimately, both devices were similar in establishing a safe and effective airway for spontaneously breathing anesthetized adults.
The Pharmacokinetics and Steady State Pharmacodynamics of Mivacurium in Children
Authors: Markakis Dorothea A. , Lau Marie , Brown Ronald , Luks Andrew M. , Sharma Manohar L. , Fisher Dennis M. 
Published: November 2003

Background
The authors previously showed that children require larger infusion rates of mivacurium than adults to maintain target twitch depression. Here, they determined whether there are differences between children and adults in mivacurium's pharmacokinetic and pharmacodynamic properties.

Methods
Twenty-seven patients aged 1-58 yr were anesthetized with nitrous oxide and isoflurane. Cholinesterase activity and adductor pollicis twitch tension in response to train-of-four stimuli were measured. Mivacurium was infused, targeting 90% twitch depression. When twitch was stably depressed 85%-95% for 10 min with no change in infusion rate for 15 min, plasma was sampled to determine concentrations of mivacurium's stereoisomers. Clearance of the trans-trans (Cl(trans-trans)) and cis-trans (Cl(cis-trans)) isomers was determined as the mivacurium infusion rate (adjusted for isomer composition) divided by the concentration of that isomer. Using the Hill equation, assuming equipotency of the trans-trans and cis-trans isomers, and ignoring the contribution of the nonpotent cis-cis isomer, the authors estimated the steady state plasma concentration yielding 90% twitch depression, C90. The effect of age on cholinesterase activity, the infusion rate depressing twitch tension by 90% (IR90), C90, Cl(trans-trans), and Cl(cis-trans) was determined using linear regression.

Results
Cholinesterase activity, IR90, and C90 did not vary with age. Both Cl(trans-trans) (r2 = 0.19, P = 0.01) and Cl(cis-trans) (r2 = 0.19, P = 0.02) decreased with age.

Conclusion
Clearance of mivacurium's potent isomers is larger in younger patients, consistent with the larger mivacurium infusion requirement in children than in adults reported previously.
Effects of Neuromuscular Blocking Agents on Excitatory Transmission and γ-Aminobutyric Acid-A-mediated Inhibition in the Rat Hippocampal Slice
Authors: Chiodini Florence C. , Tassonyi Edomer , Fuchs-Buder Thomas , Fathi Marc , Bertrand Daniel , Muller Dominique 
Published: November 2003

Background
Although neuromuscular blocking agents do not cross the blood-brain barrier, they may penetrate the central nervous system under particular circumstances and eventually cause neurotoxic consequences.

Methods
The effects of neuromuscular blocking agents on excitatory and inhibitory transmission in area CA1 of rat hippocampal slices were investigated using extracellular and intracellular recording techniques.

Results
Application of atracurium in the perfusion medium resulted in a dose-dependent enhancement of excitatory synaptic responses averaging 48.7 +/- 4.3% at a concentration of 10 nM. This effect was correlated with an increase in the size of the presynaptic fiber volley. Laudanosine, but not pancuronium bromide or vecuronium bromide, produced similar changes. In addition, atracurium and laudanosine blocked inhibitory transmission and reduced intracellularly recorded gamma-aminobutyric acidA receptor-mediated potentials. These effects were observed only at concentrations >1 microM and were not reproduced by pancuronium bromide and vecuronium bromide.

Conclusions
Atracurium and its metabolite, laudanosine, contrary to pancuronium bromide and vecuronium bromide, produce two distinct effects on hippocampal slices. They enhance excitatory transmission and neuronal excitability and they block inhibitory gamma-aminobutyric acidA-mediated synaptic responses.
Induction of Cyclooxygenase-2 in Alveolar Macrophages after Acid Aspiration
Authors: Ohara Maria , Sawa Teiji , Kurahashi Kiyoyasu , Wiener-Kronish Jeanine P. , Doshi Vatsal , Kudoh Ichidai , Gropper Michael A. 
Published: November 2003

Background
Gastric acid aspiration can result in acute lung injury. In this study, the authors determined whether alveolar macrophages express cyclooxygenase-2 as a source of inflammatory mediators after acid aspiration.

Methods
Seventy-five microliters of hydrochloric acid solution, pH 1.15, was instilled into one lung in mice. After exposure, alveolar macrophages were harvested, and competitive polymerase chain reaction and enzyme-linked immunosorbent assay were performed to measure expression of cyclooxygenase-1 and -2, interleukin-1beta and -6, tumor necrosis factor-alpha, and inducible nitric oxide synthase (iNOS). The authors used immunocytochemistry to demonstrate expression of cyclooxygenase-2 in alveolar macrophages. Selective cyclooxygenase-2 blockade using N-2(-cyclohexyloxy-4-nitrophenyl) methane-sulphonamide was done to characterize prostaglandin-cytokine interaction.

Results
Acid aspiration induced upregulation of cyclooxygenase-2 and interleukin-6. Tumor necrosis factor-alpha and iNOS were not upregulated. Interleukin-1beta was upregulated even with saline instillation but could not be detected in the supernatant of the cell culture. Alveolar macrophages harvested from mice instilled with acid showed a trend toward more production of prostaglandin E2 and produced higher concentrations of interleukin-6 compared with alveolar macrophages from mice instilled with saline. Selective cyclooxygenase-2 blockade significantly decreased release of interleukin-6 from alveolar macrophages harvested from mice instilled with acid.

Conclusions
Acid aspiration induces strong expression of cyclooxygenase-2 and production of interleukin-6 in alveolar macrophages. Selective cyclooxygenase-2 blockade reduced production of interleukin-6 by acid-stimulated alveolar macrophages. These studies suggest that the induction of cyclooxygenase-2 plays an important role in the systemic inflammatory response induced by acid aspiration.
Effect of Differential Delivery of Isoflurane to Head and Torso on Lumbar Dorsal Horn Activity
Authors: Antognini Joseph F. , Carstens Earl , Tabo Etsuo , Buzin Viktor 
Published: November 2003

Background
The spinal cord appears to be the site where anesthetic agents prevent movement in response to noxious stimuli. When isoflurane is differentially delivered to the head and torso (with low torso concentrations), cranial anesthetic requirements increase compared with systemic administration. The aim of the current study was to test the hypothesis that isoflurane action in the brain has descending influences on spinal cord dorsal horn neurons. A secondary aim was to determine the association, if any, of high cranial concentrations of isoflurane (>6%) with dorsal horn activity.

Methods
Ten goats were anesthetized with isoflurane and the carotid arteries and jugular veins isolated and cannulated for cerebral bypass. A laminectomy was performed for recording from single lumbar dorsal horn neurons with hind limb mechanical receptive fields (one cell per goat). A standard noxious mechanical stimulus was applied to the dew claw or hoof bulb during a control period with end-tidal isoflurane at 1.3% and during bypass with the following head/torso isoflurane concentrations: 1.3%/1.3%, 3.2%/1.3%, 9.4%/1.3%, 1.3%/0.2%, 3.0%/0.2% and 8.8%/0.3%.

Results
When torso isoflurane concentration was 1.3%, increasing cranial isoflurane concentration to 3% or 9% had no significant effect on the activity of dorsal horn units. When torso isoflurane was 0.2-0.3%, spontaneous activity increased; however, at these torso concentrations, evoked responses were significantly decreased (-60%) only when cranial isoflurane concentration was increased to 9%.

Conclusions
Isoflurane action in the brain had an inhibitory effect on dorsal horn activity with the combination of supraclinical cranial and low torso concentrations.
Pretreatment or Resuscitation with a Lipid Infusion Shifts the Dose-Response to Bupivacaine-induced Asystole in Rats
Authors: Weinberg Guy L. , VadeBoncouer Timothy , Ramaraju Gopal A. , Garcia-Amaro Marcelo F. , Cwik Michael J. 
Published: November 2003

Background
The authors sought to confirm a chance observation that intravenous lipid treatment increases the dose of bupivacaine required to produce asystole in rats. The authors also measured the partitioning of bupivacaine between the lipid and aqueous phases of a plasma-lipid emulsion mixture.

Methods
Anesthetized Sprague-Dawley rats were used in pretreatment (protocol 1) and resuscitation (protocol 2) experiments. In protocol 1, animals were pretreated with saline or 10%, 20%, or 30% Intralipid (n = 6 for all groups), then received 0.75% bupivacaine hydrochloride at a rate of 10 ml x kg x min(-1) to asystole. In protocol 2, mortality was compared over a range of bolus doses of bupivacaine after resuscitation with either saline or 30% Intralipid (n = 6 for all groups). The lipid:aqueous partitioning of bupivacaine in a mixture of plasma and Intralipid was measured using radiolabeled bupivacaine.

Results
Median doses of bupivacaine (in milligrams per kilogram) producing asystole in protocol 1 were for 17.7 for saline, 27.6 for 10% Intralipid, 49.7 for 20% Intralipid, and 82.0 for 30% Intralipid (P < 0.001 for differences between all groups). Differences in mean +/- SE concentrations of bupivacaine in plasma (in micrograms per milliliter) were significant (P < 0.05) for the difference between saline (93.3 +/- 7.6) and 30% Intralipid (212 +/- 45). In protocol 2, lipid infusion increased the dose of bupivacaine required to cause death in 50% of animals by 48%, from 12.5 to 18.5 mg/kg. The mean lipid:aqueous ratio of concentrations of bupivacaine in a plasma-Intralipid mixture was 11.9 +/- 1.77 (n = 3).

Conclusions
Lipid infusion shifts the dose-response to bupivacaine-induced asystole in rats. Partitioning of bupivacaine into the newly created lipid phase may partially explain this effect. These results suggest a potential application for lipid infusion in treating cardiotoxicity resulting from bupivacaine.
Effects of Halothane on the Sarcoplasmic Reticulum Ca2+Stores and Contractile Proteins in Rabbit Pulmonary Arteries
Authors: Su Judy Y. , Tang Luo-Jia 
Published: November 2003

Background
The authors' purpose of this study was to elucidate the mechanisms of direct effects of halothane on the contractile proteins and Ca2+ release from the sarcoplasmic reticulum Ca2+ stores using isolated skinned strips (sarcolemma permealized with saponin) from rabbit pulmonary arteries.

Methods
The sarcoplasmic reticular Ca2+ stores were examined by immersing the skinned strips sequentially in solutions to load Ca2+ into and release Ca2+ from the sarcoplasmic reticulum using caffeine, inositol 1,4,5-trisphosphate, or halothane. The contractile proteins were assessed by activating the strips with Ca2+ followed by administration of halothane (with or without protein kinase C inhibitors). Tension, fura-2 fluorescence activated by Ca2+ release, and phosphorylation of myosin light chains were measured.

Results
Halothane (0.07-3.00%) increased Ca2+, tension, and phosphorylation of myosin light chains in a dose-dependent manner. Halothane decreased accumulation of Ca2+ in the sarcoplasmic reticulum and enhanced the caffeine-induced tension transients. In strips pretreated with caffeine or inositol 1,4,5-trisphosphate, halothane-induced tension transients were reduced but Ca2+ was not. In strips activated by 1 microM Ca2+, halothane (0.5-3.0%) decreased 20-45% of the activated force at 15 min. Halothane (3%) transiently increased the force (20%) associated with increases in Ca2+ and phosphorylation of myosin light chains. The increased force was abolished and the subsequent relaxation was enhanced by the protein kinase C inhibitor bisindolylmaleimide but not by indolocarbazole Gö-6976.

Conclusions
In skinned pulmonary arterial strips, halothane, at clinical concentrations, inhibits uptake of Ca2+ by and induces release of Ca2+ from intracellular stores possibly shared by caffeine and inositol 1,4,5-trisphosphate, which are regulated by phosphorylation of myosin light chains. The time-dependent inhibition of the contractile proteins by halothane may be mediated by Ca2+-independent protein kinase C.
Profound Increase in Epinephrine Concentration in Plasma and Cardiovascular Stimulation after [micro sign]-Opioid Receptor Blockade in Opioid-addicted Patients during Barbiturate-induced Anesthesia for Acute Detoxification
Authors: Kienbaum Peter , Thurauf Norbert , Michel Martin C. , Scherbaum Norbert , Gastpar Markus , Peters Jurgen 
Published: November 2003

Background
Acute displacement of opioids from their receptors by administration of large doses of opioid antagonists during general anesthesia is a new approach for detoxification of patients addicted to opioids. The authors tested the hypothesis that mu-opioid receptor blockade by naloxone induces cardiovascular stimulation mediated by the sympathoadrenal system.

Methods
Heart rate, cardiac index, and intravascular pressures were measured in 10 patients addicted to opioids (drug history; mean +/- SD, 71 +/- 51 months) during a program of methadone substitution (96 +/- 57 mg/day). Cardiovascular variables and concentrations of catecholamine in plasma were measured in the awake state, during methohexital-induced anesthesia (dose, 74 +/- 44 microg x kg(-1) x min(-1)) before administration of naloxone, and repeatedly during the first 3 h of mu-opioid receptor blockade. Naloxone was administered initially in an intravenous dose of 0.4 mg, followed by incremental bolus doses (0.8, 1.6, 3.2, and 6.4 mg) at 15-min intervals until a total dose of 12.4 mg had been administered within 60 min; administration was then continued by infusion (0.8 mg/h).

Results
Concentration of epinephrine in plasma increased 30-fold (15 +/- 9 to 458 +/- 304 pg/ml), whereas concentration of norepinephrine in plasma only increased to a minor extent (76 +/- 44 to 226 +/- 58 pg/ml, P < 0.05). Cardiac index increased by 74% (2.7 +/- 0.41 to 4.7 +/- 1.7 min(-1) x m(-2)), because of increases in heart rate (89 +/- 16 to 108 +/- 17 beats/min) and stroke volume (+44%), reaching maximum 45 min after the initial injection of naloxone. In parallel, systemic vascular resistance index decreased (-40%). Systolic arterial pressure significantly increased (113 +/- 16 to 138 +/- 16 mmHg), whereas diastolic arterial pressure did not change.

Conclusions
Despite barbiturate-induced anesthesia, acute mu-opioid receptor blockade in patients addicted to opioids induces profound epinephrine release and cardiovascular stimulation. These data suggest that long-term opioid receptor stimulation changes sympathoadrenal and cardiovascular function, which is acutely unmasked by mu-opioid receptor blockade. Because of the attendant cardiovascular stimulation, acute detoxification using naloxone should be performed by trained anesthesiologists or intensivists.
Comparison of the Effect of Etomidate and Desflurane on Brain Tissue Gases and pH during Prolonged Middle Cerebral Artery Occlusion
Authors: Hoffman William E. , Charbel Fady T. , Edelman Guy , Misra Mukesh , Ausman James I. 
Published: November 2003

Background
The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min.

Methods
After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg.

Results
During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15).

Conclusion
These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.
The Glottic Aperture Seal Airway
Authors: Benumof Jonathan L. 
Published: November 2003

Background
None of the presently used airway devices are ideal regarding ease of insertion, alignment with the laryngeal inlet, and provision of a high-pressure seal from the environment. The purpose of this study was to determine, in awake volunteers, the performance of a new ventilatory device, the glottic aperture seal airway, regarding ease of insertion, alignment with the laryngeal inlet, and forced exhalation seal pressure (PFES).

Methods
The glottic aperture seal airway consists of a curved tubular component that ends in the middle of an elliptical foam cushion glottic component. The posterior surface of the foam has a curved flexible plastic backing, which imparts a 60 degree angle between the proximal half and the distal half of the foam cushion. When the glottic aperture seal airway is properly in situ in a supine patient, the proximal half of the foam cushion is opposite the laryngeal inlet. The posterior surface of the plastic backing has a balloon attached to it. Inflation of the balloon presses the ventilation hole and foam cushion up against the laryngeal inlet, thereby creating a seal from the environment. Using the laryngeal mask airway as a control device, the glottic aperture seal airway was tested for time and ease of insertion, fiberoptic alignment with the laryngeal inlet, and PFES in 18 lightly sedated and locally anesthetized volunteers.

Results
The glottic aperture seal and laryngeal mask airways were inserted with equal ease and speed. The fiberoptic alignment with the larynx was excellent for both the glottic aperture seal and laryngeal mask airways. In all volunteers, the mean +/- SD PFES values at 0-, 10-, 20-, 30-, and 40-ml balloon inflation volumes of the glottic aperture seal airway were 23.4 +/- 11.8, 29.6 +/- 12.4, 42.7 +/- 12.5, 56.9 +/- 5.6, and 60 +/- 0 cm H2O, respectively; the PFES at > or = 20 ml balloon inflation volume of the glottic aperture seal airway was significantly greater than with the laryngeal mask airway (19.4 +/- 6.7 cm H2O, P < 0.01). A PFES of > or =60 cm H2O was achieved with the glottic aperture seal airway in all volunteers (n = 2 at 10 ml, n = 3 at 20 ml, n = 9 at 30 ml, and n = 4 at 40 ml). The glottic aperture seal airway did not cause any trauma.

Conclusion
In awake volunteers, the glottic aperture seal and laryngeal mask airways were equally easy to insert and position. The glottic aperture seal airway was capable of achieving a higher PFES than the laryngeal mask airway.
Nitric Oxide Synthase Inhibitors Alter Ventilation in Isoflurane Anesthetized Rats
Authors: Patel Gaurav M. , Horstman Damian J. , Adams Milton J. , Rich George F. 
Published: November 2003

Background
Nitric oxide (NO) is present in medullary structures and can modulate respiratory rhythm. The authors determined if spontaneous ventilation at rest and in response to increased carbon dioxide is altered by selective neuronal NO synthase (NOS; 7-nitro-indazole, 7-NI) or nonselective (neuronal plus endothelial) NOS (NG-L-arginine methyl ester [L-NAME] and NG-monomethyl L-arginine [L-NMMA]) inhibitors in rats anesthetized with isoflurane.

Methods
Fifty-four rats received either L-NAME or L-NMMA (1, 10, and 30 mg/kg) or 7-NI (20, 80, and 400 mg/kg) and were compared with time controls (isoflurane = 1.4%), with isoflurane concentrations (1.6%, 1.8%, and 2%) increased consistent with the increased anesthetic depth caused by NOS inhibitors, or with L-arginine (300 mg/kg). Tidal volume (VT), respiratory frequency (f), minute ventilation (VE), and ventilatory responses to increasing carbon dioxide were determined.

Results
L-NAME and L-NMMA decreased resting VT and VE, whereas 7-NI had no effect. Increasing concentrations of isoflurane decreased resting f, VT, and VE. L-NAME and L-NMMA decreased VT and VE, whereas 7-NI had no effect at 8%, 9%, and 10% end-tidal carbon dioxide (ETCO2). Increasing concentrations of isoflurane decreased f, VT, and VE at 8%, 9%, and 10% ETCO2. The slope of VE versus ETCO2 was decreased by isoflurane but was unaffected by L-NAME, L-NMMA, or 7-NI. L-arginine alone had no effect on ventilation.

Conclusions
Nonselective NOS inhibitors decreased VT and VE at rest and at increased carbon dioxide levels but did not alter the slope of the carbon dioxide response. Selective neuronal NOS inhibition had no effect, suggesting that endothelial NOS may be the isoform responsible for altering ventilation. Finally, the cause of the decreased ventilation is not a result of the enhanced anesthetic depth caused by NOS inhibitors.