bluuebunny/crossref_metadata_2025_split huggingface dataset:
Behavioral Interactions in the Perioperative Environment
Authors: Caldwell-Andrews Alison A. , Blount Ronald L. , Mayes Linda C. , Kain Zeev N. 
Published: November 2005

Background
The authors suggest that research in the area of parental presence during induction of anesthesia should shift to emphasize what parents actually do during induction, rather than focusing simply on their presence. As a first step, the authors aimed to develop a behavioral coding system that would measure child and adult interactions in the perioperative environment.

Methods
The authors enrolled 45 parents and children (aged 2-12 yr) undergoing elective surgery and general anesthesia. A multidisciplinary team examined videotapes and transcriptions of interactions between children, parents, and medical personnel in the holding room and operating room. The team used an existing scale, the Child-Adult Medical Procedure Interaction Scale, as the prototype for the development of a new perioperative behavioral coding system. The research team conducted extensive revisions to the original scale and added multiple codes to the original scale, including nonverbal codes. Interrater reliability was assessed using weighted kappa statistics. Construct validity was also examined.

Results
The final Perioperative Child-Adult Medical Procedure Interaction Scale contains 40 codes in four domains. Analyses showed excellent reliability overall for verbal and nonverbal codes. Kappa values averaged 0.87 for verbal codes characterizing adult vocalizations, 0.92 for verbal codes characterizing child vocalizations, and 0.88 for nonverbal codes. Construct validity was demonstrated by finding the hypothesized associations between certain scale codes and children's anxiety (P = 0.0001).

Conclusion
Showing excellent reliability, the Perioperative Child-Adult Medical Procedure Interaction Scale is an appropriate tool for assessing child-adult behavioral interaction during the perioperative period. When sequential analyses are conducted and target behaviors are identified, empirically based parent preparation programs can be developed.
Optimal Puncture Site of the Right Internal Jugular Vein after Laryngeal Mask Airway Placement
Authors: Takeyama Kazuhide , Kobayashi Hiroyuki , Suzuki Toshiyasu 
Published: November 2005

Background
Puncturing of the internal jugular vein (IJV) after placement of a laryngeal mask airway (LMA) is difficult. Overlapping of the right internal jugular vein (IJV) and common carotid artery (CCA) after placement of an LMA-Classic (Laryngeal Mask Company, Henley-on-Thames, United Kingdom) was investigated using an ultrasound scanner. A study was conducted to determine the optimal puncture site in the case of puncturing the right IJV after LMA-Classic placement.

Methods
The subjects in this study consisted of 114 patients (60 men and 54 women) scheduled to undergo LMA-Classic placement (size 4 for men and size 3 for women). Overlapping between the IJV and CCA was investigated at three points (high, middle, and low points) on the right side of the neck after LMA-Classic placement. A test puncture was also made at the right low (supraclavicular) point after LMA-Classic placement.

Results
(1) The degree of overlapping of the right IJV and CCA after LMA-Classic placement was clearly greater than before LMA placement. (2) With the exception of some measurements, there were many cases in which the right IJV and CCA were completely overlapping after LMA-Classic placement. Furthermore, the CCA was not observed in the vicinity of the right IJV at the right low point. (3) There were no complications (including pneumothorax and accidental arterial puncture) during supraclavicular IJV puncture after LMA-Classic placement.

Conclusion
After placement of the LMA-Classic, overlapping of the IJV and CCA increased at the high and middle puncture points of the IJV; however, at the lower puncture point, the position of the vessels remained unaffected. Therefore, during IJV puncture at high or middle points, ultrasound guidance is advisable to avoid CCA puncture.
Respiratory Reflex Responses of the Larynx Differ between Sevoflurane and Propofol in Pediatric Patients
Authors: Oberer Christine , von Ungern-Sternberg Britta S. , Frei Franz J. , Erb Thomas O. 
Published: November 2005

Background
The effects of anesthetics on airway protective reflexes have not been extensively characterized in children. The aim of this study was to compare the laryngeal reflex responses in children anesthetized with either sevoflurane or propofol under two levels of hypnosis using the Bispectral Index score (BIS). The authors hypothesized that the incidence of apnea with laryngospasm evoked by laryngeal stimulation would not differ between sevoflurane and propofol when used in equipotent doses and that laryngeal responsiveness would be diminished with increased levels of hypnosis.

Methods
Seventy children, aged 2-6 yr, scheduled to undergo elective surgery were randomly allocated to undergo propofol or sevoflurane anesthesia while breathing spontaneously through a laryngeal mask airway. Anesthesia was titrated to achieve the assigned level of hypnosis (BIS 40 +/- 5 or BIS 60 +/- 5) in random order. Laryngeal and respiratory responses were elicited by spraying distilled water on the laryngeal mucosa, and a blinded reviewer assessed evoked responses.

Results
Apnea with laryngospasm occurred more often during anesthesia with sevoflurane compared with propofol independent of the level of hypnosis: episodes lasting longer than 5 s, 34% versus 19% at BIS 40 and 34% versus 16% at BIS 60; episodes lasting longer than 10 s, 26% versus 10% at BIS 40 and 26% versus 6% at BIS 60 (group differences P < 0.04 and P < 0.01, respectively). In contrast, cough and expiration reflex occurred significantly more frequently in children anesthetized with propofol.

Conclusion
Laryngeal and respiratory reflex responses in children aged 2-6 yr were different between sevoflurane and propofol independent of the levels of hypnosis examined in this study.
Intercellular Adhesion Molecule-1 Inhibition Attenuates Neurologic and Hepatic Damage after Resuscitation in Mice
Authors: Larmann Jan , Schmidt Christoph , Gammelin Harald , Van Aken Hugo K. , Frenzel Tim , Lanckohr Christian , Lox Marleen , Boese Nadine , Jurk Kerstin , Theilmeier Gregor 
Published: November 2005

Background
Cardiac arrest and cardiopulmonary resuscitation may result in multiorgan damage after global hypoxia due to neutrophil recruitment. Patients display all signs of a systemic inflammatory response syndrome. Reducing neutrophil recruitment may thus preserve organ function.

Methods
Mice were subjected to cardiac arrest and resuscitation. CD18/CD11b expression on circulating neutrophils was assessed by flow cytometry. Intercellular adhesion molecule-1 expression was analyzed by Western blot and immunofluorescence. Neutrophil recruitment was quantified by immunohistochemistry. Neurologic function was assessed by a balance test. For liver and kidney function, plasma alanine aminotransferase activity and creatinine concentrations were determined. To reduce neutrophil recruitment, mice received 100 microg anti-intercellular adhesion molecule-1 antibody intraperitoneally.

Results
Resuscitation led to severe hypoxia, acidosis, and hypercarbia. Adhesion molecule expression and neutrophil recruitment were increased in the liver, kidney, and brain. Neurologic performance was impaired 24 h after cardiac arrest. Creatinine and alanine aminotransferase concentrations were significantly increased. Immunoneutralization of intercellular adhesion molecule-1 attenuated neutrophil influx in the liver along with alanine aminotransferase activity, whereas creatinine concentrations and neutrophil influx in the kidney remained unchanged. Neurologic function was improved in the treatment group.

Conclusions
Global hypoxia induces activation of the endothelium in the brain, liver, and kidney. The resulting damage to the brain and liver are due to infiltration of neutrophils, whereas kidney damage is not, because reduction of neutrophil recruitment after cardiopulmonary resuscitation improves recovery of neurologic and hepatic but not renal function. Inhibition of intercellular adhesion molecule-1 after global hypoxia may be beneficial in patients experiencing cardiac arrest and resuscitation.
Memory Enhancing Effect of Low-dose Sevoflurane Does Not Occur in Basolateral Amygdala–lesioned Rats
Authors: Alkire Michael T. , Nathan Sheila V. , McReynolds Jayme R. 
Published: November 2005

Background
Certain anesthetics might enhance aversive memory at doses around 0.1 minimum alveolar concentration. This issue was investigated in a rat model of learning and memory. In addition, evidence for basolateral amygdala (BLA) involvement in mediating memory enhancement was sought.

Methods
First, the memory-enhancing potential of various anesthetics was determined. Rats underwent single-trial inhibitory avoidance training (0.3 mA shock/1 s) during exposure to air, 0.11% sevoflurane, 0.10% halothane, 0.77% desflurane, or 0.12% isoflurane. Memory was assessed at 24 h. Second, the BLA contribution to sevoflurane memory enhancement was determined. Rats received bilateral excitotoxic N-methyl-D-aspartate (12.5 mg in 0.2 microl per BLA) lesions of the BLA 1 week before training. Memory of lesioned and control rats was compared 24 h after training in air or sevoflurane.

Results
Sevoflurane exposure during training significantly enhanced 24-h retention performance for both nonoperated and sham-operated rats (P < 0.005 for both vs. their respective controls). Halothane, but not desflurane or isoflurane, also enhanced retention performance (P < 0.05). However, halothane-induced hyperalgesia during learning clouds interpreting enhanced retention performance solely as a memory consolidation effect. BLA lesions significantly reduced and equalized retention performance for both sevoflurane- and air-exposed animals. Lesions blocked memory enhancement without also causing a generalized inability to learn, because additional training revealed essentially normal task acquisition and 24-h memory.

Conclusions
Sevoflurane enhances aversive memory formation in the rat. The BLA likely contributes to this effect. The risk of aversive memory formation may be enhanced during exposure to low-dose sevoflurane.
Effects of Nitrous Oxide on the Rat Heart In Vivo
Authors: Weber Nina C. , Toma Octavian , Awan Saqib , Fräßdorf Jan , Preckel Benedikt , Schlack Wolfgang 
Published: November 2005

Background
For nitrous oxide, a preconditioning effect on the heart has yet not been investigated. This is important because nitrous oxide is commonly used in combination with volatile anesthetics, which are known to precondition the heart. The authors aimed to clarify (1) whether nitrous oxide preconditions the heart, (2) how it affects protein kinase C (PKC) and tyrosine kinases (such as Src) as central mediators of preconditioning, and (3) whether isoflurane-induced preconditioning is influenced by nitrous oxide.

Methods
For infarct size measurements, anesthetized rats were subjected to 25 min of coronary artery occlusion followed by 120 min of reperfusion. Rats received nitrous oxide (60%), isoflurane (1.4%) or isoflurane-nitrous oxide (1.4%/60%) during three 5-min periods before index ischemia (each group, n = 7). Control animals remained untreated for 45 min. Additional hearts (control, 60% nitrous oxide alone%, and isoflurane-nitrous oxide [0.6%/60%, in equianesthetic doses]) were excised for Western blot of PKC-epsilon and Src kinase (each group, n = 4).

Results
Nitrous oxide had no effect on infarct size (59.1 +/- 15.2% of the area at risk vs. 51.1 +/- 10.9% in controls). Isoflurane (1.4%) and isoflurane-nitrous oxide (1.4%/60%) reduced infarct size to 30.9 +/- 10.6 and 28.7 +/- 11.8% (both P < 0.01). Nitrous oxide (60%) had no effect on phosphorylation (2.3 +/- 1.8 vs. 2.5 +/- 1.7 in controls, average light intensity, arbitrary units) and translocation (7.0 +/- 4.3 vs. 7.4 +/- 5.2 in controls) of PKC-epsilon. Src kinase phosphorylation was not influenced by nitrous oxide (4.6 +/- 3.9 vs. 5.0 +/- 3.8; 3.2 +/- 2.2 vs. 3.5 +/- 3.0). Isoflurane-nitrous oxide (0.6%/60%, in equianesthetic doses) induced PKC-epsilon phosphorylation (5.4 +/- 1.9 vs. 2.8 +/- 1.5; P < 0.001) and translocation to membrane regions (13.8 +/- 13.0 vs. 6.7 +/- 2.0 in controls; P < 0.05).

Conclusions
Nitrous oxide is the first inhalational anesthetic without preconditioning effect on the heart. However, isoflurane-induced preconditioning and PKC-epsilon activation are not influenced by nitrous oxide.
Influence of Sevoflurane on the Metabolism and Renal Effects of Compound A in Rats
Authors: Kharasch Evan D. , Schroeder Jesara L. , Sheffels Pam , Liggitt H Denny 
Published: November 2005

Background
The sevoflurane degradation product compound A is nephrotoxic in rats. In contrast, patient exposure to compound A during sevoflurane anesthesia has no clinically significant renal effects. The mechanism for this difference is incompletely understood. One possibility is that the metabolism and toxicity of compound A in humans is prevented by sevoflurane. However, the effect of sevoflurane on compound A metabolism and nephrotoxicity is unknown. Thus, the purpose of this investigation was to determine the effect of sevoflurane on the metabolism and renal toxicity of compound A in rats.

Methods
Male rats received 0.25 mmol/kg intraperitoneal compound A, alone and during sevoflurane anesthesia (3%, 1.3 minimum alveolar concentration, for 3 h). Compound A metabolites in urine were quantified, and renal function was evaluated by serum creatinine and urea nitrogen, urine volume, osmolality, protein excretion, and renal tubular histology.

Results
Sevoflurane coadministration with compound A inhibited compound A defluorination while increasing relative metabolism through pathways of sulfoxidation and beta-lyase-catalyzed metabolism, which mediate toxicity. Sevoflurane coadministration with compound A increased some (serum creatinine and urea nitrogen, and necrosis) but not other (urine volume, osmolality, and protein excretion) indices of renal toxicity.

Conclusions
Sevoflurane does not suppress compound A nephrotoxicity in rats in vivo. These results do not suggest that lack of nephrotoxicity in surgical patients exposed to compound A during sevoflurane anesthesia results from an inhibitory effect of sevoflurane on compound A metabolism and toxicity. Rather, these results are consistent with differences between rats and humans in compound A exposure and inherent susceptibility to compound A nephrotoxicity.
Influence of Hemorrhagic Shock and Subsequent Fluid Resuscitation on the Electroencephalographic Effect of Isoflurane in a Swine Model
Authors: Kurita Tadayoshi , Morita Koji , Fukuda Kazushige , Uraoka Masahiro , Takata Kotaro , Sanjo Yoshimitsu , Sato Shigehito 
Published: November 2005

Background
The authors have previously reported that hemorrhage does not alter the electroencephalographic effect of isoflurane under conditions of compensated hemorrhagic shock. Here, they have investigated the influence of decompensated hemorrhagic shock and subsequent fluid resuscitation on the electroencephalographic effect of isoflurane.

Methods
Twelve swine were anesthetized through inhalation of 2% isoflurane. The inhalational concentration was then decreased to 0.5% and maintained for 25 min, before being returned to 2% and maintained for 25 min (control period). Hemorrhagic shock was then induced by removing 28 ml/kg blood over 30 min. After a 30-min stabilization period, the inhalational concentration was varied as in the control period. Finally, fluid infusion was performed over 30 min using a volume of hydroxyethyl starch equivalent to the blood withdrawn. After a 30-min stabilization period, the inhalational concentration was again varied as in the control period. End-tidal isoflurane concentrations and spectral edge frequency were recorded throughout the study. The pharmacodynamics were characterized using a sigmoidal inhibitory maximal effect model for spectral edge frequency versus effect site concentration.

Results
Decompensated hemorrhagic shock slightly but significantly shifted the concentration-effect relation to the left, demonstrating a 1.12-fold decrease in the effect site concentration required to achieve 50% of the maximal effect in the spectral edge frequency. Fluid resuscitation reversed the onset of isoflurane, which was delayed by hemorrhage, but did not reverse the increase in end-organ sensitivity.

Conclusions
Although decompensated hemorrhagic shock altered the electroencephalographic effect of isoflurane regardless of fluid resuscitation, the change seemed to be minimal, in contrast to several intravenous anesthetics.
Rapacuronium Augments Acetylcholine-induced Bronchoconstriction via Positive Allosteric Interactions at the M3 Muscarinic Receptor
Authors: Jooste Edmund H. , Sharma Amit , Zhang Yi , Emala Charles W. 
Published: November 2005

Background
Neuromuscular blocking agents' detrimental airway effects may occur as a result of interactions with muscarinic receptors, allergic reactions, or histamine release. Rapacuronium, a nondepolarizing muscle relaxant, was withdrawn from clinical use because of its association with fatal bronchospasm. Despite its withdrawal from clinical use, it is imperative that the mechanism by which bronchospasm occurred is understood so that new muscle relaxants introduced to clinical practice do not share these same detrimental airway effects.

Methods
Airway smooth muscle force was measured in guinea pig tracheal rings in organ baths exposed to muscle relaxants with or without subthreshold concentrations of acetylcholine. Antagonism of muscarinic, histamine, neurokinin, leukotriene receptors, or blockade of L-type calcium channels or depletion of nonadrenergic, noncholinergic neurotransmitters was performed. Muscle relaxants' potentiation of acetylcholine-stimulated inositol phosphate synthesis and allosteric interactions on the kinetics of atropine-induced [3H]N-methylscopolamine dissociation were measured in cells expressing recombinant human M3 muscarinic receptors.

Results
Rapacuronium, within clinically achieved concentrations, contracted tracheal rings in the presence but not in the absence of subthreshold concentrations of acetylcholine. This effect was prevented or reversed only by atropine. The allosteric action of rapacuronium was demonstrated by the slowing of atropine-induced dissociation of [3H]N-methylscopolamine, and positive cooperativity was demonstrated by potentiation of acetylcholine-induced inositol phosphate synthesis.

Conclusion
Many muscle relaxants have allosteric properties at muscarinic receptors; however, positive cooperativity at the M3 muscarinic receptor within clinically relevant concentrations is unique to rapacuronium. These findings establish novel parameters that should be considered in the evaluation of airway safety of any newly synthesized neuromuscular blocking agents considered for clinical practice.
Surfactants Reduce Platelet–Bubble and Platelet–Platelet Binding Induced by In Vitro Air Embolism
Authors: Eckmann David M. , Armstead Stephen C. , Mardini Feras 
Published: November 2005

Background
The effect of gas bubbles on platelet behavior is poorly characterized. The authors assessed platelet-bubble and platelet-platelet binding in platelet-rich plasma in the presence and absence of bubbles and three surface-active compounds.

Methods
Platelet-rich plasma was prepared from blood drawn from 16 volunteers. Experimental groups were surfactant alone, sparging (microbubble embolization) alone, sparging with surfactant, and neither sparging nor surfactant. The surfactants were Pluronic F-127 (Molecular Probes, Eugene, OR), Perftoran (OJSC SPC Perftoran, Moscow, Russia), and Dow Corning Antifoam 1510US (Dow Corning, Midland, MI). Videomicroscopy images of specimens drawn through rectangular glass microcapillaries on an inverted microscope and Coulter counter measurements were used to assess platelet-bubble and platelet-platelet binding, respectively, in calcium-free and recalcified samples. Histamine-induced and adenosine diphosphate-induced platelet-platelet binding were measured in unsparged samples. Differences between groups were considered significant for P < 0.05 using analysis of variance and the Bonferroni correction.

Results
Sixty to 100 platelets adhered to bubbles in sparged, surfactant-free samples. With sparging and surfactant, few platelets adhered to bubbles. Numbers of platelet singlets and multimers not adherent to bubbles were different (P < 0.05) compared both with unsparged samples and sparged samples without surfactant. No significant platelet-platelet binding occurred in uncalcified, sparged samples, although 20-30 platelets adhered to bubbles. Without sparging, histamine and adenosine diphosphate provoked platelet-platelet binding with and without surfactants present.

Conclusions
Sparging causes platelets to bind to air bubbles and each other. Surfactants added before sparging attenuate platelet-bubble and platelet-platelet binding. Surfactants may have a clinical role in attenuating gas embolism-induced platelet-bubble and platelet-platelet binding.
Comparison of Morphine, Ketorolac, and Their Combination for Postoperative Pain
Authors: Cepeda Maria Soledad , Carr Daniel B. , Miranda Nelcy , Diaz Adriana , Silva Claudia , Morales Olga 
Published: November 2005

Background
Meta-analyses report similar numbers needed to treat for nonsteroidal antiinflammatory drugs (NSAIDs) and opioids. Differences in baseline pain intensity among the studies from which these numbers needed to treat were derived may have confounded the results. NSAIDs have an opioid-sparing effect, but the importance of this effect is unclear. Therefore, the authors sought to compare the proportions of subjects who obtain pain relief with ketorolac versus morphine after surgery and to determine whether the opioid-sparing effect of an NSAID reduces the magnitude of opioid side effects.

Methods
The study was a double-blind, randomized controlled trial. The authors randomly assigned 1,003 adult patients to receive 30 mg ketorolac or 0.1 mg/kg morphine intravenously. They calculated the proportion of subjects who achieved at least 50% reduction in pain intensity 30 min after analgesic administration. Further, so long as pain intensity 30 min after analgesic administration was 5 or more out of 10, patients received 2.5 mg morphine every 10 min until pain intensity was 4 or less out of 10. The authors assessed the presence of opioid-related side effects.

Results
Five hundred patients received morphine and 503 received ketorolac. Fifty percent of patients in the morphine group achieved pain relief, compared with 31% in the ketorolac group (difference, 19%; 95% confidence interval, 13-25%). The ketorolac-morphine group required less morphine (difference, 6.5 mg; 95% confidence interval, -5.8 to -7.2) and had a lower incidence of side effects (difference, 11%; 95% confidence interval, 5-16%) than the morphine group.

Conclusions
Opioids are more efficacious analgesics than NSAIDs, although historic data for these two drugs yield similar numbers needed to treat. Adding NSAIDs to the opioid treatment reduces morphine requirements and opioid-related side effects in the early postoperative period.