bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebrovascular Carbon Dioxide Reactivity in Carotid Artery Disease
Authors: Thiel A. , Zickmann B. , Stertmann W. A. , Wyderka T. , Hempelmann G. 
Published: November 2003

Background
In patients with carotid artery disease, poor intracerebral collateralization is reflected by impaired cerebrovascular reactivity to carbon dioxide inhalation, which will improve after endarterectomy. The relationship between preoperative reactivity to carbon dioxide using transcranial Doppler sonography (TCD) and intraoperative changes of somatosensory evoked potentials (SEP) and TCD parameters were investigated.

Methods
In 94 patients, preoperative carbon dioxide reactivity was examined and defined impaired if mean blood flow velocity in the middle cerebral artery (Vm-MCA) increased less than 1.5% mmHg during carbon dioxide challenge. Patients then underwent 100 carotid operations under general anesthesia with both SEP and TCD monitoring. Shunts were placed if SEP amplitude decreased to less then 50% of control or central conduction time increased by 20% after clamping (critical SEP changes). TCD changes were defined as critical in case of a postclamping/preclamping Vm-MCA ratio < or = 0.4. The incidence of critical SEP and TCD changes was compared to preoperative carbon dioxide testing using Fisher's exact test with P < 0.05 considered significant. Postoperatively, neurologic state and carbon dioxide responsiveness were re-examined.

Results
Twelve patients showed impaired preoperative carbon dioxide reactivity on the side of operation, which improved markedly after surgery. The incidence of critical SEP changes in these cases (8.3%) was not significantly different from that in the remaining patients (14.8%). Critical SEP changes were significantly correlated with critical TCD changes (P < 0.0001).

Conclusions
Patients with poor carbon dioxide reactivity (preoperative TCD testing) did not have an increased risk of cerebral ischemia during carotid surgery, as assessed by intraoperative SEP recording.
Heat Flow and Distribution during Induction of General Anesthesia
Authors: Matsukawa Takashi , Sessler Daniel I. , Sessler Andrew M. , Schroeder Marc , Ozaki Makoto , Kurz Andrea , Cheng Christi 
Published: November 2003

Background
Core hypothermia after induction of general anesthesia results from an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution.

Methods
Six minimally clothed male volunteers in an approximately 22 degrees C environment were evaluated for 2.5 control hours before induction of general anesthesia and for 3 subsequent hours. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in distal esophageal (core) temperature, leaving the core hypothermia specifically resulting from redistribution.

Results
Core temperature was nearly constant during the control period but decreased 1.6 +/- 0.3 degree C in the first hour of anesthesia. Redistribution contributed 81% to this initial decrease and required transfer of 46 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 1.1 +/- 0.3 degree C, with redistribution contributing only 43%. Thus, only 17 kcal was redistributed during the second and third hours of anesthesia. Redistribution therefore contributed 65% to the entire 2.8 +/- 0.5 degree C decrease in core temperature during the 3 h of anesthesia. Proximal extremity heat content decreased slightly after induction of anesthesia, but distal heat content increased markedly. The distal extremities thus contributed most to core cooling. Although the arms constituted only a fifth of extremity mass, redistribution increased arm heat content nearly as much as leg heat content. Distal extremity heat content increased approximately 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study.

Conclusions
The arms and legs are both important components of the peripheral thermal compartment, but distal segments contribute most. Core hypothermia during the first hour after induction resulted largely from redistribution of body heat, and redistribution remained the major cause even after 3 h of anesthesia.
Effects of Hypothermia, Potassium, and Verapamil on the Action Potential Characteristics of Canine Cardiac Purkinje Fibers
Authors: Sprung Juraj , Laszlo Adam , Turner Lawrence , Kampine John , Bosnjak Zeljko 
Published: November 2003

Background
Hypothermia may induce hypokalemia and increase intracellular Ca2+ by affecting serum K+ and Ca2+ fluxes across the cell membrane. These ionic alterations may significantly change the electrophysiologic characteristics of the cardiac action potential and may induce cardiac arrhythmias. The current study was undertaken to determine whether electrophysiologic changes in Purkinje fibers induced by hypothermia could be reversed by manipulating the extracellular K+ and transmembrane Ca2+ fluxes by Ca2+ channel blockade with verapamil.

Methods
A conventional microelectrode method was used to determine the effects of hypothermia (32 +/- 0.5 degrees C and 28 +/- 0.5 degrees C) and various external K+ concentrations ([K+]o) (2.3, 3.8, and 6.8 mM) on maximum diastolic potential, maximum rate of phase 0 depolarization (Vmax), and action potential duration (APD) at 50% (APD50) and at 95% (APD95) repolarization in isolated canine cardiac Purkinje fibers. To evaluate the contribution of the slow inward Ca2+ current to action potential changes in hypothermia, the experiments were repeated in the presence of the Ca(2+)-channel antagonist verapamil (1 microM).

Results
Variations of [K+]o induced the expected shifts in maximum diastolic potential, and hypothermia (28 degrees C) induced moderate depolarization, but only when [K+]o was > or = 3.9 mM (P < 0.05). Hypothermia decreased Vmax at all [K+]o studied (P < 0.05). Regardless of the temperature, Vmax was not affected by verapamil when [K+]o was < or = 3.9 mM, but at 6.8 mM [K+]o in hypothermia Vmax was significantly lower in the presence of verapamil. Hypothermia increased both the APD50 and the APD95. The effects of verapamil on APD were temperature and [K+]o dependent; between 37 degrees C and 28 degrees C with 2.3 mM [K+]o in the superfusate, verapamil did not affect APD. At 28 degrees C in the presence of verapamil, the APD50 and APD95 decreased only if the [K+]o was > or = 3.9 mM.

Conclusions
Verapamil and K+ supplementation in hypothermia may exert an antiarrhythmic effect, primarily by reducing the dispersion fo prolonged APD.
Comparative Systemic Toxicity of Ropivacaine and Bupivacaine in Nonpregnant and Pregnant Ewes
Authors: Santos Alan C. , Arthur Richard G. , Wlody David , De Armas Pedro , Morishima Hisayo O. , Finster Mieczyslaw 
Published: November 2003

Background
Ropivacaine is a new amide local anesthetic, having therapeutic properties similar to those of bupivacaine but with a wider margin of safety. Bupivacaine is probably the most commonly used drug in obstetric epidural analgesia, even though laboratory studies have suggested that pregnancy increases the cardiotoxicity of bupivacaine but not of other local anesthetics. The current study was designed to reevaluate, in a random and blinded fashion, the systemic toxicity of bupivacaine and ropivacaine in nonpregnant and pregnant sheep.

Methods
Chronically prepared nonpregnant and pregnant ewes were randomized to receive an intravenous infusion of ropivacaine or bupivacaine at a constant rate of 0.5 mg.kg-1.min-1 until circulatory collapse. The investigators were blinded to the identity of local anesthetic. Heart rate, arterial blood pressure, and cardiac rhythm were monitored throughout the study. Arterial blood samples were obtained before infusion and at the onset of toxic manifestations, which appeared in the following sequence: convulsions, hypotension, apnea, and circulatory collapse. Serum drug concentrations and protein binding were determined. Blood pH and gas tensions were measured.

Results
There were no significant differences between non-pregnant and pregnant animals in the doses or serum concentrations of either drug required to elicit toxic manifestations. In nonpregnant animals, similar doses and serum concentrations of ropivacaine and bupivacaine were associated with the onset of convulsions and circulatory collapse. In pregnant ewes, greater doses of ropivacaine as compared to bupivacaine were required to produce convulsions (7.5 +/- 0.5 vs. 5.0 +/- 0.6 mg.kg-1) and circulatory collapse (12.9 +/- 0.8 vs. 8.5 +/- 1.2 mg.kg-1). The corresponding serum concentrations of ropivacaine were similar to those of bupivacaine. Pregnancy did not affect the serum protein binding of either drug. The proportion of animals manifesting a malignant ventricular arrhythmia as the terminal event was similar among all groups.

Conclusions
The systemic toxicity of ropivacaine or bupivacaine is not enhanced by gestation in sheep. This is in contrast to an earlier study in which the cardiotoxicity of bupivacaine was enhanced during ovine pregnancy. Greater doses of ropivacaine, as compared to bupivacaine, are needed to produce toxic manifestations in pregnant animals.
Thermoregulatory Vasoconstriction Impairs Active Core Cooling
Authors: Kurz Andrea MD , Sessler Daniel I. , Birnbauer Franz , Illievich Udo M. , Spiss Christian K. 
Published: November 2003

Background
Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction.

Methods
Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold.

Results
In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01).

Conclusions
Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.
Effects of Propofol or Isoflurane Anesthesia on Cardiac Conduction in Children Undergoing Radiofrequency Catheter Ablation for Tachydysrhythmias
Authors: Lavoie J. , Walsh E. P. , Burrows F. A. , Laussen P. , Lulu J. A. , Hansen D. D. 
Published: November 2003

Background
To determine suitability for ablation procedures in children, two commonly used anesthetic agents were studied: propofol and isoflurane.

Methods
Twenty patients presenting for a radiofrequency catheter ablation procedure were included and randomly assigned to two groups. A baseline electrophysiology study was performed during anesthesia with thiopental, alfentanil, nitrous oxide, and pancuronium in all patients. At the completion of the baseline electrophysiology study (EPS), 0.8-1.2% isoflurane was administered to patients in group 1 and 2 mg/kg propofol bolus plus an infusion of 150 micrograms.kg-1.min-1 was administered to patients in group 2. Nitrous oxide and pancuronium were used throughout the procedure. After 30 min of equilibration, both groups underwent a repeat EPS. The following parameters were measured during the EPS: cycle length, atrial-His interval, His-ventricle interval, corrected sinus node recovery time, AV node effective refractory period, and atrial effective refractory period. Using paired t tests, the electrophysiologic parameters described above measured during propofol or isoflurane anesthesia were compared to those measured during baseline anesthesia. Statistical significance was accepted as P < 0.05.

Results
There was no statistically significant difference in the results obtained during baseline anesthesia when compared with those measured during propofol or isoflurane anesthesia.

Conclusions
Neither propofol nor isoflurane anesthesia alter sinoatrial or atrioventricular node function in pediatric patients undergoing radiofrequency catheter ablation, compared to values obtained during baseline anesthesia with alfentanil and midazolam.
Arterial Oxygenation during One-lung Ventilation
Authors: Slinger P. , Scott W. A. C. 
Published: November 2003

Background
Because maintaining arterial oxygenation (PaO2) during one-lung ventilation (OLV) can be a clinical problem, it is useful to be aware of factors that influence PaO2 in this situation and are under the control of the anesthesiologist. It is unknown whether, among the commonly used volatile anesthetic agents, one is associated with higher PaO2 levels. Clinical studies suggest that isoflurane provides superior PaO2 during OLV than does halothane. These have not been compared to enflurane. The authors studied PaO2 and hemodynamics during OLV with 1 MAC enflurane versus 1 MAC isoflurane.

Methods
Twenty-eight adults who had prolonged periods of OLV anesthesia with minimal trauma to the nonventilated lung (thoracoscopic or esophageal surgery) were studied in a cross-over design. Patients were randomized to two groups: Group 1 received 1 MAC enflurane in oxygen from induction until after the first 30 min of OLV, then were switched to 1 MAC isoflurane. In group 2, the order of the anesthetics was reversed.

Results
Isoflurane was associated with higher PaO2 values during OLV (P < 0.0001). Mean PaO2 (+/- SD) after 30 min OLV isoflurane was 231 (+/- 125) mmHg versus 184 (+/- 106) mmHg after 30 min OLV enflurane. The difference in PaO2 between the two anesthetics was most marked in the patients with the highest PaO2 during OLV: PaO2 isoflurane PaO2 enflurane varies; is directly proportional to PaO2 isoflurane (r = 0.65, P < 0.001). There were no other significant differences between anesthetic gases in the measured hemodynamic or respiratory variables. In the subgroup of patients with pulmonary artery catheters (n = 7), PaO2 correlated with cardiac output during OLV for both anesthetics (r = 0.81, P < 0.001).

Conclusions
During OLV, the PaO2 values with 1 MAC isoflurane were greater than those with enflurane. The dependence of PaO2 on cardiac output does not support the hypothesis that an increase in cardiac output will cause a decrease in hypoxic pulmonary vasoconstriction and a decrease in PaO2 during OLV.
Glycine Receptor Antagonism
Authors: McFarlane Claude , Warner David S. , Nader Antoun , Dexter Franklin 
Published: November 2003

Background
Glycine and glutamate binding sites are allosterically coupled at the N-methyl-D-aspartate (NMDA) receptor complex. Previous studies have shown that antagonism of glutamate at the NMDA receptor reduces the minimum alveolar concentration (MAC) for volatile anesthetics. 5-Nitro-6,7-dichloro-2,3-quinoxalinedione (ACEA-1021) is a competitive antagonist at the glycine recognition site of the NMDA receptor. The purpose of this study was to determine whether glycine receptor antagonism also reduces volatile anesthetic requirements in the rat.

Methods
In experiment 1, Sprague-Dawley rats were anesthetized with halothane in 50% O2-balance N2 and their lungs mechanically ventilated. They were randomly assigned to one of three groups according to the dose of ACEA-1021 administered (0, 20, or 40 mg/kg intravenously; n = 6). The bolus dose of ACEA-1021 was followed by a continuous intravenous infusion of vehicle or ACEA-1021 at 14 mg.kg-1.h-1. Halothane MAC was then determined by the tail-clamp method. In experiment 2, awake rats were randomly assigned to groups according to the same dosages of ACEA-1021 as in experiment 1. Arterial CO2 tension and mean arterial pressure were recorded before and 5 and 30 min after the start of the infusion. The infusion was then stopped, and the time to recovery of the righting reflex was recorded.

Results
In experiment 1, ACEA-1021 decreased halothane MAC (mean +/- SD) in a dose-dependent manner (control, 0.95 +/- 0.15 vol%; ACEA-1021 20 mg/kg, 0.50 +/- 0.14 vol%; ACEA-1021 40 mg/kg, 0.14 +/- 0.16 vol%; P < 0.01). In experiment 2, arterial CO2 tension was increased by ACEA-1021 (control, 38 +/- 3 mmHg; ACEA-1021 20 mg/kg, 43 +/- 3 mmHg; ACEA-1021 40 mg/kg, 48 +/- 2 mmHg; P < 0.01). Mean arterial pressure was not affected by any dose of ACEA-1021. The righting reflex was abolished in rats receiving ACEA-1021 40 mg/kg only and recovered 30 +/- 7 min after discontinuation of the infusion.

Conclusions
Halothane MAC reduction by glycine receptor antagonism was greater than that previously observed for antagonism of glutamate at the NMDA or AMPA receptor. In rats receiving ACEA-1021 only, minimal hemodynamic depression and moderate hypoventilation were observed. Antagonism of glycine at the NMDA receptor recognition site offers a potential mechanism of action of anesthesia.
Masseter Muscle Rigidity Associated with Glycine1306-to- Alanine Mutation in the Adult Muscle Sodium Channel α-Subunit Gene
Authors: Vita Gary M. , Olckers Antonel , Jedlicka Anne E. , George Alfred L. , Heiman-Patterson Terry , Rosenberg Henry , Fletcher Jeffrey E. , Levitt Roy C. 
Published: November 2003

Background
Succinylcholine-induced masseter muscle rigidity (MMR) is a potentially life-threatening complication of anesthesia and is closely correlated with the heterogeneous disorder malignant hyperthermia (MH) susceptibility. MMR also is identified with a variety of neuromuscular disorders, including the myotonias, that are associated with abnormal in vitro contracture test (IVCT) results. Recently, mutations in the adult skeletal muscle sodium channel alpha-subunit gene (SCN4A) have been shown to cause generalized nondystrophic myotonias, some of which are associated with mild nonspecific symptoms. The purpose of the current investigation was to begin to evaluate the molecular genetic relationship between known mutations in the SCN4A gene, MMR, and the results of the IVCT used to diagnose MH-susceptibility.

Methods
A single extended pedigree of 16 individuals was ascertained through a proband who experienced MMR and whole-body rigidity after succinylcholine administration. Subsequently, four individuals were shown to have a mild form of myotonia on clinical and laboratory examination. IVCT was carried out according to standardized protocols. Mutations in the SCN4A gene were sought in exons 22 and 24 using single-strand conformational analyses. Variability in the SCN4A gene sequence was confirmed by direct DNA sequence analyses.

Results
Four individuals with myotonia were shown to carry a guanine-to-cytosine mutation at nucleotide position 3917 of the reported SCN4A sequence. This DNA mutation was coinherited with MMR and an abnormal IVCT result in this family. Previous studies have demonstrated that the glycine1306-to-alanine substitution is associated with a mild clinical syndrome referred to as myotonia fluctuans.

Conclusions
The current report provides direct evidence that succinylcholine-induced MMR, whole-body rigidity, and an abnormal IVCT result are associated with a mutation in the SCN4A gene.
Wheezing during Induction of General Anesthesia in Patients with and without Asthma
Authors: Pizov Reuven , Brown Robert H. , Weiss Yuval S. , Baranov Dimitry , Hennes Hans , Baker Stuart , Hirshman Carol A. 
Published: November 2003

Background
Patients with asthma who require general anesthesia and tracheal intubation are at increased risk for the development of bronchospasm during induction. The incidence of wheezing during induction with different intravenously administered agents is unknown. A randomized, double-blinded prospective study was undertaken to evaluate the incidence of wheezing in asymptomatic asthmatic and nonasthmatic patients receiving three commonly used intravenous anesthetic agents for induction of anesthesia.

Methods
Fifty-nine asymptomatic asthmatic and 96 nonasthmatic patients of ASA physical status 1 and 2 were studied. All patients received 1.5 micrograms/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital or 2.5 mg/kg propofol, 1.5 mg/kg succinylcholine, tracheal intubation, and inhalational anesthesia. Wheezing was assessed by an independent blinded observer, auscultating the lungs at 2 and 5 min postintubation. Data were analyzed by Pearson's chi-squared, Fisher's exact test, and multiple logistic regression with significance set at P < 0.05.

Results
Both asthmatic and nonasthmatic patients who received a thiobarbiturate for induction had a greater incidence of wheezing than did patients receiving propofol. In asthmatic patients, 45% (23, 67) (mean and 95% confidence interval) who received a thiobarbiturate, 26% (8, 44) who received an oxybarbiturate, and none (0, 17) who received propofol wheezed after intubation. In nonasthmatic patients, 16% (3, 28) who received thiobarbiturate and 3% (0, 9) who received propofol wheezed.

Conclusions
This study suggests that propofol should be considered for induction of anesthesia in patients, particularly those with asthma, who require timely intubation.