bluuebunny/crossref_metadata_2025_split huggingface dataset:
Susceptibility to Upper Airway Obstruction during Partial Neuromuscular Block
Authors: D'Honneur Gilles , Lofaso Frederic , Drummond Gordon B. , Rimaniol Jean-Marc , Aubineau Jean V. , Harf Alain , Duvaldestin Philippe 
Published: November 2003

Background
Airway obstruction after anesthesia may be caused or exaggerated by residual neuromuscular block, with loss of muscle support for collapsible upper airway structures.

Methods
Six male volunteers were studied before treatment, during stable partial neuromuscular block with vecuronium at a mean train-of-four (TOF) ratio of 50% (95% CI, 36-61%), and after reversal by neostigmine. Catheter-mounted transducers were placed in the pharynx and esophagus to estimate, respectively, the upper airway resistance, and the work of breathing (calculated as the time integral of the inspiratory pressure developed by the respiratory muscles, esophageal pressure time product) during quiet breathing, during breathing 5% carbon dioxide, and while breathing with an inspiratory resistor. Breathing with pressure at the airway opening held at pressures from -5 to 40 cm H2O were also tested to assess airway collapsibility.

Results
Although breathing through a resistor increased upper airway resistance from 1.2 (0.67, 1.72) cm H2O x l(-1) x s to 2.5 (1.32, 3.38) cm H2O x l(-1) x s, and carbon dioxide stimulation reduced resistance to 0.8 (0.46, 1.33) cm H2O x l(-1) x s, no effect of partial neuromuscular block (mean TOF ratio, 52%) on upper airway properties could be shown.

Conclusions
Neuromuscular block with a TOF ratio of 50% can be present yet clinically difficult to detect in patients recovering from anesthesia. This degree of block has no effect on airway patency in volunteers, even during challenge. Airway obstruction during recovery from anesthesia thus is more likely to be caused by residual effects of general anesthetic agents or centrally acting analgesics, either alone or perhaps in concert with residual neuromuscular block.
In Vivo Effects of Dexmedetomidine on Laser-Doppler Flow and Pial Arteriolar Diameter
Authors: Ganjoo Pragati , Farber Neil E. , Hudetz Antal , Smith Jeremy J. , Samso Enric , Kampine John P. , Schmeling William T. 
Published: November 2003

Background
The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter.

Methods
Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min).

Results
Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored.

Conclusions
These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.
Inhibitory Effects of Propofol on Intracellular Signaling by Endothelin-1 in Aortic Smooth Muscle Cells
Authors: Tanabe Kumiko , Kozawa Osamu , Kaida Takehiro , Matsuno Hiroyuki , Niwa Masayuki , Ohta Shuichiro , Dohi Shuji , Uematsu Toshihiko 
Published: November 2003

Background
Blood pressure decreases when propofol is administered. However, the exact mechanism underlying the vascular effects of propofol has not yet been elucidated. Endothelin produced by vascular endothelial cells is a potent vasoactive peptide that elicits prolonged contraction of vascular smooth muscle cells. The effects of propofol on endothelin-1-induced intracellular signaling in an aortic smooth muscle cell line, A10 cells, were examined.

Methods
Cultured A10 cells were pretreated with propofol for 20 min and then stimulated with endothelin-1. The effect of propofol on the endothelin-1-induced Ca2+ influx into A10 cells was evaluated by measuring intracellular 45Ca2+. The effects of propofol on the endothelin-1-induced activation of phosphatidylinositol-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D were evaluated by measuring the formation of inositol phosphates and choline, respectively. The effect of propofol on endothelin-1 binding to its receptor was determined by an [125I] endothelin-1-binding assay.

Results
Propofol inhibited the endothelin-1-induced Ca2+ influx, but this was significant only at supuraclinical concentrations. The endothelin-1-stimulated formation of inositol phosphates was significantly suppressed by propofol. However, propofol had no effect on the formation of inositol phosphates induced by NaF, an activator of heterotrimeric guanosine triphosphate (GTP)-binding proteins. Propofol inhibited the endothelin-1-induced formation of choline. Propofol had no effect on the binding of endothelin-1 to its receptor.

Conclusions
These results suggest that propofol inhibits endothelin-1-induced intracellular signaling in vascular smooth muscle cells. The inhibitory effect of propofol might be exerted at a point between the endothelin-1 receptor and its GTP-binding protein. However, because all significant effects are observed at high concentrations, clinical relevance is unclear.
Fructose-1,6-Bisphosphate Preserves Adenosine Triphosphate but Not Intracellular pH during Hypoxia in Respiring Neonatal Rat Brain Slices
Authors: Espanol Maryceline T. , Litt Lawrence , Hasegawa Koh , Chang Lee-Hong , Macdonald Jeffrey M. , Gregory George , James Thomas L. , Chan Pak H. 
Published: November 2003

Background
Fructose-1,6-bisphosphate (FBP) sometimes provides substantial cerebral protection during hypoxia or ischemia. 31P/1H nuclear magnetic resonance spectroscopy of cerebrocortical slices was used to study the effects of FBP on hypoxia-induced metabolic changes. In addition, 13C-labeled glucose was administered and 13C nuclear magnetic resonance spectroscopy was used to search for FBP-induced modulations in glycolysis and the pentose-phosphate pathway.

Methods
In each experiment, 80 slices (350 microm) obtained from ten 7-day-old Sprague-Dawley rat litter mates were placed together in a 20-mm nuclear magnetic resonance tube, perfused, and subjected to 30 min of hypoxia (PO2 < 3 mmHg). Nine experiments were performed, with n = 3 in each of three groups: (1) no treatment with FBP; (2) 60 min of prehypoxia treatment with FBP (2 mM); and (3) 60 min of posthypoxia treatment with FBP (2 mM). 31P/1H Interleaved nuclear magnetic resonance spectra at 4.7 T provided average adenosine triphosphate, intracellular pH, and lactate. Cresyl violet stains of random slices taken at predetermined time points were studied histologically. Some experiments had [2-13C]glucose in the perfusate. Slices from these studies were frozen for perchloric acid extraction of intracellular metabolites and studied with high-resolution 13C nuclear magnetic resonance spectroscopy at 11.75 T.

Results
With no pretreatment with FBP, hypoxia caused an approximately 50% loss of adenosine triphosphate, an approximately 700% increase in lactate, and a decrease in intracellular pH to approximately 6.4. Pretreatment with FBP resulted in no detectable loss of adenosine triphosphate, no increase in lactate, and minimal morphologic changes but did not alter decreases in intracellular pH. 13C Nuclear magnetic resonance spectra of extracted metabolites showed that pretreatment caused accumulation of [1-13C]fructose-6-phosphate, an early pentose-phosphate pathway metabolite. Posthypoxic treatment with FBP had no effects compared with no treatment.

Conclusions
During severe hypoxia, pretreatment with FBP completely preserves adenosine triphosphate and almost completely preserves cell morphology but does not alter hypoxia-induced decreases in intracellular pH. Pretreatment also substantially augments the flux of glucose into the pentose-phosphate pathway.
Bayesian Modeling of Muscle Biopsy Contracture Testing for Malignant Hyperthermia Susceptibility
Authors: Loke Julian C. P. , MacLennan David H. 
Published: November 2003

Background
Phenotyping malignant hyperthermia (MH) by contracture testing has a low but quantifiable degree of inaccuracy, measured by its sensitivity and specificity. Quantifying the limitations inherent in diagnostic testing for MH can help resolve issues in clinical practice, such as the interpretation of a negative test and the apparent lack of complete genetic linkage to RYR1.

Methods
Bayesian models, mathematical descriptions of the outcome of diagnostic testing, were constructed. The inputs to the model include patient factors, summarized in a single number called pretest probability (PTP), and sensitivity and specificity that specify the accuracy of the entire test process. The outputs of the model include positive predictive value (PPV) and negative predictive value (NPV), which are numeric expressions of diagnostic certainty of positive and negative test results. A special case was constructed for equivocal results.

Results
The PPV, NPV, and efficiency of contracture testing for MH are functions of PTP, sensitivity, and specificity. The NPV is high for all clinical PTP, whereas PPV is clinically useful for moderate to high PTP.

Conclusions
Diagnostic contracture testing for MH is clinically useful because of high NPV and can exclude MH with near certainty. For MH probands, the clinical grading scale for MH may guide PTP estimation, whereas for relatives of probands, PTP is a function of kinship to a known MH-susceptible relative. A sequential testing strategy optimizes diagnostic information by maximizing PTP within a pedigree. Incomplete testing of parents of an MH susceptible child can pose a significant risk of false-negative results for the untested parent. Even with optimal pedigree testing strategies, the PPV drift effect results in a considerable source of phenotypic uncertainty for genetic linkage studies.
Transient Neurologic Symptoms after Spinal Anesthesia with Mepivacaine and Lidocaine
Authors: Liguori Gregory A. , Zayas Victor M. , Chisholm Mary F. 
Published: November 2003

Background
Spinal anesthesia with lidocaine is ideal for ambulatory surgery because of its short duration of action. However, transient neurologic symptoms (TNS) occur in 0-40% of patients. The incidence of TNS with mepivacaine, which has a similar duration of action, is unknown.

Methods
Sixty ambulatory patients undergoing knee arthroscopy received spinal anesthesia in a randomized, double-blinded manner, with either 45 mg 1.5% mepivacaine or 60 mg 2% lidocaine. An L3-L4 midline approach was used with a 27-gauge Whitacre needle and a 20-gauge introducer. The local anesthetic was injected over approximately 30 s with the aperture of the Whitacre needle in a cephalad direction. Two to 4 days after operation, each patient was questioned about the development of TNS. In addition, the two groups were compared for time to regression of sensory and motor blockade and time to discharge milestones.

Results
Three patients receiving lidocaine were lost to follow-up. None of the 30 patients in the mepivacaine group developed TNS, whereas 6 of 27 (22%) in the lidocaine group did (P = 0.008). Time to regression to the L5 sensory level and to complete resolution of motor block were similar in both groups. The times to discharge milestones were also comparable.

Conclusions
The incidence of TNS is greater with 2% lidocaine than with 1.5% mepivacaine for patients having unilateral knee arthroscopy under spinal anesthesia. Mepivacaine seems to be a promising alternative to lidocaine for outpatient surgical procedures because of its similar duration of action. Further studies are warranted to determine the optimal dose of intrathecal mepivacaine for ambulatory surgery and the incidence of TNS with other doses and concentrations of intrathecal mepivacaine.
Transient Neurologic Symptoms after Spinal Anesthesia
Authors: Hampl Karl F. , Heinzmann-Wiedmer Sidonie , Luginbuehl Igor , Harms Christoph , Seeberger Manfred , Schneider Markus C. , Drasner Kenneth 
Published: November 2003

Background
Recent evidence suggests that transient neurologic symptoms (TNSs) frequently follow lidocaine spinal anesthesia but are infrequent with bupivacaine. However, identification of a short-acting local anesthetic to substitute for lidocaine for brief surgical procedures remains an important goal. Prilocaine is an amide local anesthetic with a duration of action similar to that of lidocaine. Accordingly, the present, prospective double-blind study compares prilocaine with lidocaine and bupivacaine with respect to duration of action and relative risk of TNSs.

Methods
Ninety patients classified as American Society of Anesthesiologists physical status I or II who were scheduled for short gynecologic procedures under spinal anesthesia were randomly allocated to receive 2.5 ml 2% lidocaine in 7.5% glucose, 2% prilocaine in 7.5% glucose, or 0.5% bupivacaine in 7.5% glucose. All solutions were provided in blinded vials by the hospital pharmacy. Details of spinal puncture, extension and regression of spinal block, and the times to reach discharge criteria were noted. In the evening of postoperative day 1, patients were evaluated for TNSs by a physician unaware of the drug administered and the details of the anesthetic procedure.

Results
Nine of 30 patients receiving lidocaine experienced TNSs, 1 of 30 patients receiving prilocaine (P = 0.03) had them, and none of 30 patients receiving bupivacaine had TNSs. Times to ambulate and to void were similar after lidocaine and prilocaine (150 vs. 165 min and 238 vs. 253 min, respectively) but prolonged after bupivacaine (200 and 299 min, respectively; P < 0.05).

Conclusions
Prilocaine may be preferable to lidocaine for short surgical procedures because it has a similar duration of action but a lower incidence of TNSs.
Electroencephalographic Derivatives as a Tool for Predicting the Depth of Sedation and Anesthesia Induced by Sevoflurane
Authors: Katoh Takasumi , Suzuki Akira , Ikeda Kazuyuki 
Published: November 2003

Background
The electroencephalogram (EEG) has been evaluated as a tool for measuring depth of anesthesia, but the use of the EEG monitoring is still controversial. The current study was designed to evaluate the accuracy of three EEG parameters and anesthetic concentration for predicting depth of sedation and anesthesia during sevoflurane anesthesia

Methods
One low and one high equilibrated concentration ranging from 0.2-1.8% were assigned randomly and administered consecutively to 69 patients. The bispectral index (BIS; version 3.2), 95% spectral edge frequency (SEF), and median power frequency (MPF) were obtained from a bipolar frontomastoid (Fp1-A1, Fp2-A2) montage using an EEG monitor. Sedation was assessed using the responsiveness portion of the observer's assessment of alertness-sedation scale. In the second phase of the study, the 47 patients who were scheduled to have skin incisions were observed for purposeful movement in response to skin incision at sevoflurane concentrations between 1.6% and 2.4%. The relation among BIS, 95% SEF, MPF, sevoflurane concentration, sedation score, and movement or no movement after skin incision, was determined. Prediction probability values for EEG parameters and sevoflurane concentration to predict depth of sedation and anesthesia were also calculated.

Results
The BIS and sevoflurane concentration correlated closely with the sedation score. Both 95% SEF and MPF changed significantly but biphasically with increasing sedation. The prediction probability values for BIS and sevoflurane concentration were 0.966 and 0.945, respectively, indicating a high predictive performance for depth of sedation. No EEG parameters predicted movement after skin incision better than chance alone.

Conclusions
Parameters derived from EEG, such as BIS, and 95% SEF are reliable guides to the depth of sedation, but not to the adequacy of anesthesia level for preventing movement during sevoflurane anesthesia.
Hypoxia Causes Apnea during Epidural Anesthesia in Rabbits
Authors: Hogan Quinn H. , Amuzu John , Clifford Philip S. , Bosnjak Zeljko J. , Kampine John P. 
Published: November 2003

Background
Although pulmonary function is minimally changed by neuraxial blockade in most cases, ventilatory arrest may ensue in rare cases. The authors examined the mechanism of apnea in a rabbit model of sudden ventilatory arrest during the combination of epidural anesthesia and hypoxia.

Methods
Rabbits were studied during alpha-chloralose sedation and spontaneous ventilation through a tracheostomy tube. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Respiratory rate and tidal volume were measured by pneumotachograph. Responses were recorded during administration of oxygen at inspired oxygen concentrations of 11% for 2.5 min and 0% for 40 s, before and after either thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or intramuscular lidocaine (15 mg/kg). In a third group of animals, epinephrine was given intravenously during epidural blockade to return mean arterial pressure to baseline values before hypoxia. In a fourth group of animals, which did not get lidocaine, sympathetic blockade and hypotension were produced with intravenously administered trimethaphan rather than epidural blockade.

Results
Thoracolumbar epidural anesthesia decreased mean arterial pressure from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during hypoxia occurred in 90% of these animals (nine of ten) but in only 11% of animals (one of nine) after intramuscularly administered lidocaine (P < 0.01). Treatment of epidural hypotension with epinephrine prevented apnea (zero of nine animals). Apnea during hypoxia occurred in 50% (three of six) of animals given trimethaphan. Apnea in all groups was sudden in onset, with no preceding decreases in respiratory rate or tidal volume.

Conclusions
Epidural anesthesia results in a narrowed margin of safety for oxygen delivery to the brain and predisposes subjects to ventilatory arrest during hypoxia. This results from the combined effects of decreased blood oxygen content, which is due to decreased inspired oxygen concentration superimposed on circulatory depression due to neural blockade.
Ketamine Inhibits Monoamine Transporters Expressed in Human Embryonic Kidney 293 Cells
Authors: Nishimura Mitsuhiro , Sato Kohji , Okada Tomoya , Yoshiya Ikuto , Schloss Patrick , Shimada Shoichi , Tohyama Masaya 
Published: November 2003

Background
Ketamine has been characterized as having psychotomimetic and sympathomimetic effects. These symptoms have raised the possibility that ketamine affects monoaminergic neurotransmission. To elucidate the relation between ketamine and monoamine transporters, the authors constructed three cell lines that stably express the norepinephrine, dopamine, and serotonin transporters and investigated the effects of ketamine on these transporters.

Methods
Human embryonic kidney cells were transfected using the Chen-Okayama method with the human norepinephrine, rat dopamine, and rat serotonin transporter cDNA subcloned into the eukaryotic expression vector. Using cells stably expressing these transporters, the authors investigated the effects of ketamine on the uptake of these compounds and compared them with those of pentobarbital.

Results
Inhibition analysis showed that ketamine significantly inhibited the uptake of all three monoamine transporters in a dose-dependent manner. The Ki (inhibition constant) values of ketamine on the norepinephrine, dopamine, and serotonin transporters were 66.8 microM, 62.9 microM, and 162 microM, respectively. Pentobarbital, a typical general anesthetic agent with no psychotic symptoms, did not affect the uptake of monoamines, however. Further, neither the glycine transporter 1 nor the glutamate/aspartate transporter was affected by ketamine, indicating that ketamine preferentially inhibits monoamine transporters.

Conclusions
Ketamine inhibited monoamine transporters expressed in human embryonic kidney cells in a dose-dependent manner. This result suggests that the ketamine-induced inhibition of monoamine transporters might contribute to its psychotomimetic and sympathomimetic effects through potentiating monoaminergic neurotransmission.