bluuebunny/crossref_metadata_2025_split huggingface dataset:
Carbon Monoxide Production from Desflurane, Enflurane, Halothane, Isoflurane, and Sevoflurane with Dry Soda Lime
Authors: Wissing Heimo , Kuhn Iris , Warnken Uwe , Dudziak Rafael 
Published: November 2003

Background
Previous studies in which volatile anesthetics were exposed to small amounts of dry soda lime, generally controlled at or close to ambient temperatures, have demonstrated a large carbon monoxide (CO) production from desflurane and enflurane, less from isoflurane, and none from halothane and sevoflurane. However, there is a report of increased CO hemoglobin in children who had been induced with sevoflurane that had passed through dry soda lime. Because this clinical report appears to be inconsistent with existing laboratory work, the authors investigated CO production from volatile anesthetics more realistically simulating conditions in clinical absorbers.

Methods
Each agent, 2.5 or 5% in 2 l/min oxygen, were passed for 2 h through a Dräger absorber canister (bottom to top) filled with dried soda lime (Drägersorb 800). CO concentrations were continuously measured at the absorber outlet. CO production was calculated. Experiments were performed in ambient air (19-20 degrees C). The absorbent temperature was not controlled.

Results
Carbon monoxide production peaked initially and was highest with desflurane (507 +/- 70, 656 +/- 59 ml CO), followed by enflurane (460 +/- 41, 475 +/- 99 ml CO), isoflurane (176 +/- 2.8, 227 +/- 21 ml CO), sevoflurane (34 +/- 1, 104 +/- 4 ml CO), and halothane (22 +/- 3, 20 +/- 1 ml CO) (mean +/- SD at 2.5 and 5%, respectively).

Conclusions
The absorbent temperature increased with all anesthetics but was highest for sevoflurane. The reported magnitude of CO formation from desflurane, enflurane, and isoflurane was confirmed. In contrast, a smaller but significant CO formation from sevoflurane was found, which may account for the CO hemoglobin concentrations reported in infants. With all agents, CO formation appears to be self-limited.
Halothane Inhibits Contraction and Action Potential Duration to a Greater Extent in Subendocardial than Subepicardial Myocytes from the Rat Left Ventricle
Authors: Rithalia Amber , Gibson Clare N. , Hopkins Philip M. , Harrison Simon M. 
Published: November 2003

Background
Halothane inhibits the 4-aminopyridine-sensitive transient outward K(+) current (I(to)) which in many species, including humans, plays an important role in determining action potential duration. As I(to) is greater in the ventricular subepicardium than subendocardium, halothane may have differential effects on action potential duration and, therefore, contraction in cells isolated from these two regions.

Methods
Myocytes were isolated from the subendocardium and subepicardium of the rat left ventricle. Myocytes from each region were electrically stimulated at 1 Hz to measure contractions and action potentials and exposed to 0.6 mm halothane (approximately 2 x minimum alveolar concentration(50) for the rat) for 1 min. The time from the peak of the action potential to repolarization at 0 and -50 mV was measured to assess the effects of halothane on action potential duration.

Results
Halothane inhibited contraction to a significantly (P = 0.002) greater extent in subendocardial myocytes than in subepicardial myocytes: the amplitude of contraction during control conditions was 3.6 +/- 0.4 microm and 3.2 +/- 0.7 microm in subendocardial and subepicardial cells, respectively, and this was reduced to 1.1 +/- 0.2 microm (29 +/- 2% of control, P < 0.0001, n = 10) and 1.4 +/- 0.3 microm (46 +/- 3% of control, P = 0.007, n = 7), respectively, after a 1-min exposure to 0.6 mm halothane. Control action potential duration (at -50 mV) was 67 +/- 10 and 28 +/- 4 ms in subendocardial and subepicardial myocytes, respectively, and these values were reduced to 39 +/- 6 ms (58 +/- 3% of control, P < 0.001) and 20 +/- 3 ms (73 +/- 5% of control, P = 0.009) by halothane, respectively.

Conclusions
Action potential duration was reduced to a greater extent in subendocardial than subepicardial myocytes, which would contribute to the greater negative inotropic effect of halothane in the subendocardium. Furthermore, the transmural difference in action potential duration was reduced by halothane, which could contribute to its arrhythmogenic properties.
Consumption of Soy Diet before Nerve Injury Preempts the Development of Neuropathic Pain in Rats
Authors: Shir Yoram , Raja Srinivasa N. , Weissman Charles S. , Campbell James N. , Seltzer Ze’ev 
Published: November 2003

Background
A previous report using a partial sciatic nerve ligation (PSL) model for neuropathic pain in rats demonstrated that consumption of soy-containing diets preoperatively and postoperatively suppressed development of mechanical and heat allodynia, as well as hyperalgesia. The current study examined whether dietary soy suppresses these neuropathic sensory disorders when consumed either before or after PSL injury.

Methods
Male Wistar rats were grouped into seven different feeding regimens. These rats were fed SOY (RMH-1000, PMI Feeds, St. Louis, MO), a diet containing 85% soy protein since weaning, and were then switched to noSOY (Bio-Serv Co., Frenchtown, NJ), a diet devoid of soy at certain time points before PSL injury (14, 7, 1 days, or 15 and 0 h). Postoperatively, these rats were fed SOY or noSOY diets. Levels of mechanical and heat allodynia and hyperalgesia were determined preoperatively and 3, 8, and 14 days after PSL injury.

Results
Compared with groups fed preoperative noSOY, consumption of SOY before PSL injury significantly blunted postoperative levels of allodynia and hyperalgesia. Administering the SOY diet both before and after PSL injury provided no additional suppression of neuropathic pain. No pain suppression was noted in rats fed a noSOY diet preoperatively and SOY diet after PSL injury. Switching from SOY to noSOY feeding within 15 h of PSL injury was sufficient to allow for the full development of allodynia and hyperalgesia.

Conclusions
Consumption of a soy-containing diet suppressed the development of neuropathic pain after PSL injury. The pain-suppressing properties of dietary soy were the result of a preemptive effect (i.e., when consumed preoperatively), but not a palliative effect (i.e., when consumed postoperatively). This effect of soy-containing diets appears to be short-lived, since switching to a noSOY diet 15 h before ligation abrogated the suppressive effect of soy.
Are Estimates of MAC Reliable?
Authors: Paul Matthias , Fisher Dennis M. 
Published: November 2003

Background
Potency of inhaled anesthetics (minimum alveolar concentration [MAC]) is typically studied in humans using an "up-down" approach in which the (quantal) response to skin incision is assessed only once for each individual, so that each individual's MAC is never determined. The authors examined the influence of interindividual variability and study design issues (e.g., the number of patients enrolled in a study) on the accuracy of MAC estimates.

Methods
The typical sequence of a MAC study was simulated. The authors varied and tested the impact of several factors: anesthetic concentration used to start a study; number of "crossovers" (successive patients having different responses to skin incision) to terminate a study; concentration increment between consecutive patients; interindividual variability; and "measurement error." For each factor, simulations were replicated 500 times, and the resulting estimates were summarized.

Results
Starting an experiment below or above the "true" value led to slightly biased MAC estimates; in contrast, variability was underestimated with starting concentrations close to the true value. More than six crossovers improved MAC estimates minimally but increased variability estimates toward true values. A larger increment size affected MAC minimally and increased variability estimates toward true values. A larger interindividual variability led to more "outlier" estimates for MAC. Under many conditions, several of 500 replicates yielded MAC estimates that deviated more than 10% or even more than 25% from the "true" value.

Conclusion
Individual experiments may yield inaccurate MAC estimates. This inaccuracy is minimized as the number of crossovers increases; however, improvement diminishes as the number of crossovers exceeds six.
Effect of Clonidine on Lidocaine Clearance In Vivo
Authors: Kopacz Dan J. , Bernards Christopher M. 
Published: November 2003

Background
The addition of clonidine to local anesthetics has been shown to prolong both peripheral and central neuraxial local anesthetic blocks. Whether clonidine prolongs local anesthetic block by a pharmacokinetic effect or a pharmacodynamic effect is unclear. By directly measuring lidocaine tissue concentrations at the site of injection in the presence and absence of clonidine, this study was designed to address this question.

Methods
Microdialysis probes were placed adjacent to the superficial peroneal nerve in both feet of seven volunteers. Plain lidocaine (1%) was injected along one nerve, and lidocaine with clonidine (10 microg/ml) was injected along the other nerve in a double-blind, randomized manner. The extracellular fluid was then sampled for lidocaine concentration at 5-min intervals using microdialysis, cutaneous blood flow was assessed by laser Doppler at 10-min intervals, and sensory block was assessed every 10 min until resolution.

Results
Consistent with previous studies, clonidine prolonged lidocaine sensory block. Blood flow increased in both groups but was significantly lower in the clonidine group, especially during the first 60 min. Consistent with the lower blood flow, the area under the lidocaine concentration-versus-time curve was significantly greater in the clonidine group during the first 60 min.

Conclusion
When added to lidocaine, clonidine prolonged peripheral nerve block. The pharmacokinetic data suggest that the mechanism of prolongation is at least in part pharmacokinetic.
Isoflurane and Sevoflurane Anesthesia in Pigs with a Preexistent Gas Exchange Defect
Authors: Kleinsasser Axel , Lindner Karl H. , Hoermann Christoph , Schaefer Andreas , Keller Christian , Loeckinger Alexander 
Published: November 2003

Background
Decreased arterial partial pressure of oxygen (PaO2) during volatile anesthesia is well-known. Halothane has been examined with the multiple inert gas elimination technique and has been shown to alter the distribution of pulmonary blood flow and thus PaO2. The effects of isoflurane and sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesized that sevoflurane with a relatively high minimum alveolar concentration (MAC) would result in significantly more gas exchange disturbances in comparison with isoflurane or control.

Methods
This study was performed in a porcine model with an air pneumoperitoneum that generates a reproducible gas exchange defect. After a baseline measurement of pulmonary gas exchange (multiple inert gas elimination technique) during propofol anesthesia, 21 pigs were randomly assigned to three groups of seven animals each. One group received isoflurane anesthesia, one group received sevoflurane anesthesia, and one group was continued on propofol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or propofol anesthesia, a second measurement (multiple inert gas elimination technique) was performed.

Results
At the second measurement, inert gas shunt was 15 +/- 3% (mean +/- SD) during sevoflurane anesthesia versus 9 +/- 1% during propofol anesthesia (P = 0.02). Blood flow to normal ventilation/perfusion (V(A)/Q) lung areas was 83 +/- 5% during sevoflurane anesthesia versus 89 +/- 1% during propofol anesthesia (P = 0.04). This resulted in a PaO2 of 88 +/- 11 mmHg during sevoflurane anesthesia versus 102 +/- 15 mmHg during propofol anesthesia (P = 0.04). Inert gas and blood gas variables during isoflurane anesthesia did not differ significantly from those obtained during propofol anesthesia.

Conclusions
In pigs with an already existent gas exchange defect, sevoflurane anesthesia but not isoflurane anesthesia causes significantly more gas exchange disturbances than propofol anesthesia does.
Unventilated Airway Is Time-dependently Constricted in Paralyzed Dogs
Authors: Hirota Kazuyoshi , Hashiba Eiji , Kabara Shizuko , Yoshioka Hideki , Ishihara Hironori , Matsuki Akitomo 
Published: November 2003

Background
Apnea has been reported to produce bronchoconstriction and to cause hypoxia, hypercapnia, and modulation of vagal afferent nerves, which also change airway tone. In this study, the authors determined the mechanism of apnea-induced bronchoconstriction.

Methods
Twenty-eight dogs anesthetized and paralyzed were assigned to four groups (n = 7 each): apnea after artificial ventilation with 50% and 100% O2 groups (apnea-50% O2 and apnea-100% O2 groups, respectively), an apnea plus vagotomy group (fraction of inspired oxygen [FiO2] = 1.0), and a one-lung ventilation group (FiO2 = 1.0). The trachea was intubated with a single- or double-lumen tube in the three apnea groups or the one-lung ventilation group, respectively. The bronchial cross-sectional area (BCA) was assessed by the authors' bronchoscopic method. In the apnea-100% O2 and apnea plus vagotomy groups, a respirator was turned off for 5 min to produce apnea. In the apnea-50% O2 group, apnea was produced for 3 min. In the one-lung ventilation group, the right lumen was blocked for 5 min, and 15 min later, the left lumen was blocked for 5 min. BCA, arterial oxygen tension (PaO2), and arterial carbon dioxide tension (PaCO2) were assessed every minute.

Results
The BCA in intact dogs time-dependently decreased by approximately 20% and 40% at 3 and 5 min after apnea started, respectively, whereas they did not in vagotomized dogs. In the apnea-50% O2 and apnea-100% O2 groups, bronchoconstriction could occur without hypoxemia, although hypercapnia was observed in all dogs. In the one-lung ventilation group, despite the fact that PaCO2 increased by only 2 mmHg without hypoxemia, unventilated BCA time-dependently decreased by 33.6 +/- 10.3%, whereas ventilated BCA did not.

Conclusion
The current study suggests that the unventilated airway may constrict spontaneously. In addition, the airway constriction could be vagally mediated but not due to hypoxia and hypercapnia.
Cardiopulmonary Bypass Induces Neurologic and Neurocognitive Dysfunction in the Rat
Authors: Mackensen G. Burkhard , Sato Yukie , Nellgård Bengt , Pineda Jose , Newman Mark F. , Warner David S. , Grocott Hilary P. 
Published: November 2003

Background
Neurocognitive dysfunction is a common complication of cardiac surgery using cardiopulmonary bypass (CPB). Elucidating injury mechanisms and developing neuroprotective strategies have been hampered by the lack of a suitable long-term recovery model of CPB. The purpose of this study was to investigate neurologic and neurocognitive outcome after CPB in a recovery model of CPB in the rat.

Methods
Fasted rats (n = 10) were subjected to 60 min of normothermic (37.5 degrees C) nonpulsatile CPB using a roller pump and a membrane oxygenator. Sham-operated controls (n = 10) were not subjected to CPB. Neurologic outcome was assessed on days 1, 3, and 12 after CPB using standardized functional testing. Neurocognitive outcome, defined as the time (or latency) to finding a submerged platform in a Morris water maze (an indicator of visual-spatial learning and memory), was evaluated daily from post-CPB days 3-12. Histologic injury in the hippocampus was also evaluated.

Results
Neurologic outcome was worse in the CPB versus the sham-operated controls at all three measurement intervals (P < 0.001). The CPB group also had longer water maze latencies compared with the sham-operated controls (P = 0.004), indicating significant neurocognitive dysfunction after CPB. No difference in histologic injury between groups was observed.

Conclusions
CPB caused both neurologic and neurocognitive impairment in a rodent recovery model. This model could potentially facilitate the investigation of CPB-related injury mechanisms and possible neuroprotective interventions.
The Effectiveness of Video Technology As an Adjunct to Teach and Evaluate Epidural Anesthesia Performance Skills
Authors: Birnbach David J. , Santos Alan C. , Bourlier Remi A. , Meadows Warner E. , Datta Sanjay , Stein Deborah J. , Kuroda Maxine M. , Thys Daniel M. 
Published: November 2003

Background
Although video review has been used in teaching, it has not been reported for use as an adjunct to teaching anesthesiology residents. The purpose of the prospective, randomized, blinded study was to determine whether teaching with video review improves epidural anesthesia skills of anesthesiology residents.

Methods
Twenty-two second-year (CA-2) anesthesiology residents beginning their first obstetric anesthesia rotation were assigned to video or non-video groups. All residents were filmed daily as they placed epidural analgesia. Residents assigned to the video group reviewed their tapes twice a week with an attending anesthesiologist, whereas residents assigned to the non-video group never saw their films. Four experienced attending anesthesiologists independently judged videotapes taken on days 1, 15, and 30 and scored the residents for "overall" skill (range of summed overall grades, 0-40), as well as on 13 predetermined criteria.

Results
As determined by kappa coefficients, interrater reliability was high among the judges (k = 0.7-0.8). Residents in the video group improved to a greater degree than residents in the non-video group. On day 1, the median overall grades for the video and non-video groups were 21 and 12, respectively. By day 15, the corresponding grades had increased to 32 and 24, respectively (P < 0.01). However, overall median grades continued to improve between days 15 and 30 in the video group only (P < 0.01).

Conclusions
Review of resident videotapes resulted in greater improvement in overall and predetermined performance criteria. In addition, video review was helpful in identifying skills that were inadequately learned, thus allowing for specific teaching in those areas.
Simulation Technology
Authors: Morgan Pamela J. , Cleave-Hogg Doreen , McIlroy Jodi , Devitt James Hugh 
Published: November 2003

Background
The availability of simulator technology at the University of Toronto (Toronto, Ontario, Canada) provided the opportunity to compare the efficacy of video-assisted and simulator-assisted learning.

Methods
After ethics approval from the University of Toronto, all final-year medical students were invited to participate in the current randomized trial comparing video-based to simulator-based education using three scenarios. After an introduction to the simulator environment, a 5-min performance-based pretest was administered in the simulator operating room requiring management of a critical event. A posttest was administered after students had participated in either a faculty-facilitated video or simulator teaching session. Standardized 12-point checklist performance protocols were used for assessment purposes. As well, students answered focused questions related to the educational sessions on a final examination. Student opinions regarding the value of the teaching sessions were obtained.

Results
One hundred forty-four medical students participated in the study (scenario 1, n = 43; scenario 2, n = 48; scenario 3, n = 53). There was a significant improvement in posttest scores over pretest scores in all scenarios. There was no statistically significant difference in scores between simulator or video teaching methods. There were no differences in final examination marks when the two educational methods were compared. Student opinions indicated that the experiential simulator sessions were more enjoyable and valuable than the video teaching sessions.

Conclusions
Both simulator and video types of faculty-facilitated education offer a valuable learning experience. Future work is needed that addresses the long-term effects of experiential learning in the retention of knowledge and acquired skills.
Phase I Safety Assessment of Intrathecal Injection of an American Formulation of Adenosine in Humans
Authors: Eisenach James C. , Hood David D. , Curry Regina 
Published: November 2003

Background
Preclinical studies of intrathecal adenosine suggest it may be effective in the treatment of acute and chronic pain in humans. A phase I safety trial of the intrathecal injection of a mannitol-containing formulation of adenosine in Sweden showed a considerable incidence of backache. We performed a phase I safety trial of intrathecal injection of the American formulation of adenosine, which lacks mannitol.

Methods
Following US Food and Drug Administration and institutional review board approval and written informed consent, 65 volunteers were studied in two trials: an open-label, dose-escalating trial with intrathecal adenosine doses of 0.25-2.0 mg (25 subjects) and a double-blind, placebo-controlled trial of adenosine, 2 mg (40 subjects). Blood pressure, heart rate, end-tidal carbon dioxide, and sensory, motor, and reflex neurologic functions were systematically examined for 24 h after injection, and volunteers were contacted by telephone at times up to 6 months after injection.

Results
Intrathecal adenosine did not affect blood pressure, heart rate, end-tidal carbon dioxide, or neurologic function. Headache was reported by 10 and back pain was reported by 8 of 30 subjects exposed to adenosine in the second double-blind trial, whereas none of these symptoms was reported by the 10 saline-treated subjects.

Conclusion
These data support further investigation of intrathecal adenosine for analgesia in humans and suggest that this agent does not produce a high incidence of severe side effects.
Preliminary Efficacy Assessment of Intrathecal Injection of an American Formulation of Adenosine in Humans
Authors: Eisenach James C. , Hood David D. , Curry Regina 
Published: November 2003

Background
Preclinical studies of intrathecal adenosine suggest it may be effective in the treatment of acute and chronic pain in humans, and preliminary studies in volunteers and patients with a Swedish formulation of adenosine suggests it may be effective in hypersensitivity states but not with acute noxious stimulation. The purpose of this study was to screen for efficacy of a different formulation of adenosine marketed in the US, using both acute noxious stimulation and capsaicin-evoked mechanical hypersensitivity.

Methods
Following Food and Drug Administration and institutional review board approval and written informed consent, 65 volunteers were studied in two trials: an open-label, dose-escalating trial with intrathecal adenosine doses of 0.25-2.0 mg and a double-blind, placebo-controlled trial of adenosine, 2 mg. Cerebrospinal fluid was obtained for pharmacokinetic analysis, and pain ratings in response to acute heat stimuli and areas of mechanical hyperalgesia and allodynia after intradermal capsaicin injection were determined.

Results
Adenosine produced no effect on pain report to acute noxious thermal or chemical stimulation but reduced mechanical hyperalgesia and allodynia from intradermal capsaicin injection for at least 24 h. In contrast, residence time of adenosine in cerebrospinal fluid was short (< 4 h).

Conclusions
These results show selective inhibition by intrathecal adenosine of hypersensitivity, presumed to reflect central sensitization in humans after peripheral capsaicin injection. The long-lasting effect is consistent with that observed in preliminary reports of patients with chronic neuropathic pain and is not due to prolonged residence of adenosine in cerebrospinal fluid.