bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patients with Diabetic Neuropathy Are at Risk of a Greater Intraoperative Reduction in Core Temperature
Authors: Kitamura Akira , Hoshino Takeshi , Kon Tadashi , Ogawa Ryo 
Published: August 2004

Background
Core hypothermia develops after the induction of general anesthesia, but intraoperative vasoconstriction usually prevents its progression. However, diabetes mellitus is often associated with autonomic neuropathy, which leads to abnormal peripheral neurovascular function. Accordingly, we tested the hypothesis that diabetic patients experience a greater reduction in core temperature during general anesthesia than nondiabetic patients.

Methods
We studied 36 nondiabetic patients (control group) and 27 diabetic patients (diabetic group) undergoing elective abdominal surgery. Both groups were divided into young (< 60 yr) and older age (>/= 60 yr) groups. Standard noninvasive autonomic tests (heart rate variation at deep periodical breathing, Valsalva maneuver, and head-up tilt) were carried out for each patient. The relation between the results of these tests of autonomic function and the tympanic membrane temperature during general anesthesia was assessed in relation to peripheral vasoconstriction.

Results
Thirteen patients in the diabetic group showed abnormal responses to two or more of the basal autonomic function tests (patients with autonomic dysfunction). Changes in core temperature among the groups were similar at 90 min after the induction of anesthesia. However, the core temperature of the diabetic patients with autonomic dysfunction was lower from 120 min (35.1 degrees C) onward compared with the young or older nondiabetic patients and the diabetic patients with normal autonomic function. Peripheral vasoconstriction, evaluated using the forearm-fingertip skin surface temperature gradient, was delayed in patients with autonomic dysfunction compared with the others.

Conclusions
The current results indicate that diabetic autonomic neuropathy is associated with more severe intraoperative hypothermia. We postulate that diabetic patients become more hypothermic because their peripheral neuropathy delays the onset of thermoregulatory vasoconstriction and reduces its efficacy once triggered. These patients may therefore fail to develop a normal core temperature plateau.
Predictors of Hypothermia during Spinal Anesthesia
Authors: Frank Steven M. , El-Rahmany Hossam K. , Cattaneo Christine G. , Barnes Rachel A. 
Published: August 2004

Background
Body temperature often is ignored during regional anesthesia, despite evidence that hypothermia occurs commonly. Because hypothermia is associated with adverse clinical outcomes, it is important to recognize predictors of hypothermia and to monitor and control body temperature in patients at risk. The current study was designed to determine the predictors of core hypothermia in patients receiving spinal anesthesia for radical retropubic prostatectomy.

Methods
Forty-four patients undergoing radical retropubic prostatectomy were studied. A lumbar intrathecal injection of 18-22 mg bupivacaine, 0.75%, with 20 microg fentanyl was given. No active warming measures were used other than intravenous fluid warming. The following clinical variables were assessed as potential predictors of core (tympanic) temperature at admission to the postanesthesia care unit: duration of surgery, average ambient operating room temperature, body habitus, age, and spinal blockade level.

Results
The mean core temperature at admission to the postanesthesia care unit was 35.1 +/- 0.6 degrees C (range, 33.6-36.3 degrees C). Duration of surgery, ambient operating room temperature, and body habitus were not predictors of hypothermia. A high level of spinal blockade and increasing age were predictors of hypothermia. For each incremental increase in block level, core temperature decreased by 0.15 degrees C, and for each increase in age, core temperature decreased by 0.3 degrees C.

Conclusions
Although high-level spinal blockade has been associated with decreased thermoregulatory thresholds, no previous study has shown that a higher level of blockade is associated with a greater magnitude of core hypothermia in the clinical setting. As with general anesthesia, advanced age is associated with hypothermia during spinal anesthesia.
The Action of Sevoflurane on Vascular Smooth Muscle of Isolated Mesenteric Resistance Arteries (Part 2)
Authors: Akata Takashi , Izumi Kaoru , Nakashima Mikio 
Published: August 2004

Background
The precise mechanisms behind the direct inhibitory action of sevoflurane on vascular smooth muscle have not been fully elucidated.

Methods
Endothelium-denuded smooth muscle strips were prepared from rat small mesenteric arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips. In another series of experiments, only isometric force was measured in the beta-escin-membrane-permeabilized strips.

Results
Sevoflurane (3-5%) inhibited the increases in both the [Ca2+]i and the force induced by either norepinephrine (0.5-10 microm) or 40 mm K+. Sevoflurane still inhibited the increase in [Ca2+]i induced by norepinephrine after depletion of intracellular Ca2+ stores with ionomycin, although it little influenced the increase in [Ca2+]i induced by norepinephrine after treatment with verapamil. In the fura-2-loaded membrane-intact muscle, sevoflurane caused a rightward shift of Ca2+-force relation during force development to stepwise increment of extracellular Ca2+ concentration during 40-mm K+ depolarization in either the presence or the absence of norepinephrine. In contrast, sevoflurane did not influence Ca2+-activated contraction in the beta-escin-permeabilized muscle, in which alpha-adrenergic receptor coupling was not retained.

Conclusions
The inhibitory effects of sevoflurane on both norepinephrine- and potassium chloride (KCl)-induced contractions are caused by reduction of [Ca2+]i in vascular smooth muscle and inhibition of the myofilament Ca2+ sensitivity. The [Ca2+]i-reducing effect of sevoflurane observed in both the norepinephrine- and the K+-stimulated muscle is mainly caused by inhibition of voltage-gated Ca2+ influx. The inhibitory effect of sevoflurane on Ca2+ activation of contractile proteins seems to be mediated by the cell membrane or by some diffusible substances that are lost in the beta-escin-permeabilized cells.
Magnesium Increases Morphine Analgesic Effect in Different Experimental Models of Pain
Authors: Begon Sophie , Pickering Gisèle , Eschalier Alain , Dubray Claude 
Published: August 2004

Background
An excess of excitatory pathway activation via N-methyl-D-aspartate (NMDA) receptors has been described in neuropathic pain that responds poorly to morphine. However, in this situation, several published data sets show that coadministration of NMDA receptor antagonists restores the efficacy of opioids. Considering that magnesium behaves like an NMDA receptor antagonist, we investigated the effect of the combination of magnesium and morphine in experimental models of chronic and tonic pain.

Methods
Mechanical hyperalgesia was assessed with the paw-pressure test in mononeuropathic (chronic constrictive injury model) and diabetic rats. Behavioral reactions were scored in a model of inflammation induced by formalin. The animals were assigned to one of three groups according to the intraperitoneal pretreatment: magnesium (30 mg/kg x 3), magnesium (30 mg/kg), and saline. Before testing, morphine was injected intravenously in mononeuropathic (0.3 mg/kg) and diabetic rats (1 mg/kg) and by the subcutaneous route in rats with the formalin test (1.5 mg/kg).

Results
Magnesium alone induced a significant antihyperalgesic effect in mononeuropathic and diabetic rats after a cumulative dose of 90 mg/kg. Furthermore, it significantly increased morphine analgesia, regardless of the loading dose used (30 or 90 mg/kg) in the two models of neuropathic pain. In the formalin test, magnesium alone did not have a significant effect. However, in combination with morphine, it revealed the analgesic effect of this opiate.

Conclusions
These data show that magnesium amplifies the analgesic effect of low-dose morphine in conditions of sustained pain. Considering the good tolerability of magnesium, these findings may have clinical applications in neuropathic and persistent pain.
Comparison of the Effects of Racemic Bupivacaine, Levobupivacaine, and Ropivacaine on Ventricular Conduction, Refractoriness, and Wavelength
Authors: Aya Antoine G. M. , de La Coussaye Jean E. , Robert Emmanuelle , Ripart Jacques , Cuvillon Philippe , Mazoit Jean Xavier , Jeannes Pascal , Fabbro-Péray Pascale , Eledjam Jean-Jacques 
Published: August 2004

Background
The study was designed to compare the effects of equimolar concentrations of racemic bupivacaine, levobupivacaine, and ropivacaine on ventricular conduction, anisotropy, duration and homogeneity of refractoriness, and wavelengths, and to provide a potency ratio for effects on conduction velocity.

Methods
Isolated frozen rabbit hearts (which leave a thin layer of surviving epicardial muscle) were treated with 0.1, 1, and 10 mum racemic bupivacaine, levobupivacaine, or ropivacaine. Left ventricular longitudinal and transverse conduction velocities, anisotropic ratio, minimum pacing cycle length, use dependency, duration and dispersion of ventricular effective refractory period, and wavelengths were studied. A high-resolution mapping system was used for data acquisition. In addition to two-way analysis of variance for repeated measures, data for conduction velocities were fitted simultaneously using a nonlinear mixed-effect modeling program to allow intergroup comparison.

Results
Each agent induced a concentration- and use-dependent slowing of conduction velocities, with no change of the anisotropic ratio. The use-dependent effect of levobupivacaine is similar to that of racemic bupivacaine concerning longitudinal conduction velocity. Fitting of conduction velocities provided a racemic bupivacaine to levobupivacaine and to ropivacaine ratio of 1:1.38 for concentration effect at 1,000-ms pacing cycle length, and 1:0.74 for use-dependent effect at 600-ms pacing cycle length. Racemic bupivacaine and levobupivacaine prolonged the ventricular effective refractory period, whereas ropivacaine did not. No dispersion in ventricular effective refractory period values occurred. All three agents induced significant decreases in wavelengths. This effect was not different among groups.

Conclusions
Differences among racemic bupivacaine, levobupivacaine, and ropivacaine at equimolar concentrations are mainly caused by the use-dependent effects on conduction velocities and the concentration-dependent effects on ventricular effective refractory period. Therefore, one must take into account the corresponding pacing rates when comparing the potency ratios of local anesthetics.
Effects of Dantrolene on Extracellular Glutamate Concentration and Neuronal Death in the Rat Hippocampal CA1 Region Subjected to Transient Ischemia
Authors: Nakayama Ryosuke , Yano Toshiyuki , Ushijima Kazuo , Abe Eiji , Terasaki Hidenori 
Published: August 2004

Background
Excessive extracellular glutamate produced by cerebral ischemia has been proposed to initiate the cascade toward neuronal cell death. Changes in extracellular glutamate concentration are closely linked to changes in intracellular calcium ion concentration. Dantrolene inhibits calcium release from intracellular calcium stores. In this study, the authors investigated the effects of dantrolene on extracellular glutamate accumulation and neuronal degeneration in a rat model of transient global forebrain ischemia.

Methods
Male Wistar rats weighing 230-290 g were anesthetized with halothane in nitrous oxide-oxygen and were subjected to 10 min of transient forebrain ischemia using a four-vessel occlusion technique. Fifteen minutes before ischemic injury, dantrolene sodium (5 mm), dimethyl sulfoxide as a vehicle for dantrolene, or artificial cerebrospinal fluid as a control was intracerebroventricularly administered (n = 8 in each group). In the hippocampal CA1 subfield, the extracellular glutamate concentration in vivo was measured during the periischemic period with a microdialysis biosensor, and the number of intact neurons was evaluated on day 7 after reperfusion.

Results
Both dantrolene and dimethyl sulfoxide significantly reduced the ischemia-induced increase in glutamate concentration to a similar extent, i.e., by 53 and 51%, respectively, compared with artificial cerebrospinal fluid (P < 0.01). The number of intact hippocampal CA1 neurons (mean +/- SD; cells/mm) in dantrolene-treated rats (78 +/- 21) was significantly higher than that in artificial cerebrospinal fluid- (35 +/- 14; P < 0.001) and dimethyl sulfoxide-treated (56 +/- 11; P < 0.05) animals. Dimethyl sulfoxide also significantly increased the number of preserved neurons in comparison with artificial cerebrospinal fluid (P < 0.05).

Conclusions
Intracerebroventricular dantrolene prevents delayed neuronal loss in the rat hippocampal CA1 region subjected to transient ischemia; however, this neuroprotection cannot be accounted for only by the reduced concentrations of extracellular glutamate during ischemia.
Effects of Recruiting Maneuvers in Patients with Acute Respiratory Distress Syndrome Ventilated with Protective Ventilatory Strategy
Authors: Grasso Salvatore , Mascia Luciana , Del Turco Monica , Malacarne Paolo , Giunta Francesco , Brochard Laurent , Slutsky Arthur S. , Marco Ranieri V. 
Published: August 2004

Background
A lung-protective ventilatory strategy with low tidal volume (VT) has been proposed for use in acute respiratory distress syndrome (ARDS). Alveolar derecruitment may occur during the use of a lung-protective ventilatory strategy and may be prevented by recruiting maneuvers. This study examined the hypothesis that the effectiveness of a recruiting maneuver to improve oxygenation in patients with ARDS would be influenced by the elastic properties of the lung and chest wall.

Methods
Twenty-two patients with ARDS were studied during use of the ARDSNet lung-protective ventilatory strategy: VT was set at 6 ml/kg predicted body weight and positive end-expiratory pressure (PEEP) and inspiratory oxygen fraction (Fio2) were set to obtain an arterial oxygen saturation of 90-95% and/or an arterial oxygen partial pressure (Pao2) of 60- 80 mmHg (baseline). Measurements of Pao2/Fio2, static volume-pressure curve, recruited volume (vertical shift of the volume-pressure curve), and chest wall and lung elastance (EstW and EstL: esophageal pressure) were obtained on zero end-expiratory pressure, at baseline, and at 2 and 20 min after application of a recruiting maneuver (40 cm H2O of continuous positive airway pressure for 40 s). Cardiac output (transesophageal Doppler) and mean arterial pressure were measured immediately before, during, and immediately after the recruiting maneuver. Patients were classified a priori as responders and nonresponders on the basis of the occurrence or nonoccurrence of a 50% increase in Pao2/Fio2 after the recruiting maneuver.

Results
Recruiting maneuvers increased Pao2/Fio2 by 20 +/- 3% in nonresponders (n = 11) and by 175 +/- 23% (n = 11; mean +/- standard deviation) in responders. On zero end-expiratory pressure, EstL (28.4 +/- 2.2 vs. 24.2 +/- 2.9 cm H2O/l) and EstW (10.4 +/- 1.8 vs. 5.6 +/- 0.8 cm H2O/l) were higher in nonresponders than in responders (P < 0.01). Nonresponders had been ventilated for a longer period of time than responders (7 +/- 1 vs. 1 +/- 0.3 days; P < 0.001). Cardiac output and mean arterial pressure decreased by 31 +/- 2 and 19 +/- 3% in nonresponders and by 2 +/- 1 and 2 +/- 1% in responders (P < 0.01).

Conclusions
Application of recruiting maneuvers improves oxygenation only in patients with early ARDS who do not have impairment of chest wall mechanics and with a large potential for recruitment, as indicated by low values of EstL.
Perioperative Visual Changes
Authors: Warner Mary E. , Fronapfel Paul J. , Hebl James R. , Herman David C. , Warner David O. , Decker Paul , Warner Mark A. 
Published: August 2004

Background
The goal of this project was to describe the frequency and natural history of perioperative changes in vision.

Methods
The authors performed a prospective evaluation of changes in visual accommodation and acuity in adult patients undergoing various surgical procedures. Patients were evaluated preoperatively and at 1 and 3 days postoperatively. For patients who had persistent blurring of vision on the third postoperative day, surveillance was extended to 1.5 yr to determine how long the visual changes persisted and if the patients required eye-care provider attention for the condition.

Results
Twenty-eight of 671 patients (4.2%) reported new onset of blurred vision lasting at least 3 days after surgery. Seven of these 28 patients (1% of total) required either new corrective lens or changes in eyeglass or contact prescriptions because of persistent blurry vision. Most of the remaining patients reported resolution of blurry vision within 1 to 2 months. No significant risk factors for this problem were identified.

Conclusions
In this surgical population, changes in visual acuity manifest primarily by blurred vision were reported at a surprisingly high frequency. For many of these patients, the blurring resolved within 2 months without complication, but 25% of patients who had blurred vision for 3 days or longer required visits to eye-care providers and either new corrective lens or changes in existing prescriptions.
Peripheral Antinociceptive Action of Morphine and the Synergistic Interaction with Lamotrigine
Authors: Argüelles Carlos F. , Torres-López Jorge E. , Granados-Soto Vinicio 
Published: August 2004

Background
Lamotrigine inhibits glutamate release through the preferential blockade of voltage-dependent Na+ channels. In contrast, morphine reduces release of excitatory amino acids through the activation of opioid receptors and also inhibits tetrodotoxin-resistant Na+ channels on peripheral afferent neurons. The current study was designed to investigate the antinociceptive effects of locally administered morphine and lamotrigine. The interaction between morphine and lamotrigine at the periphery was also examined.

Methods
Morphine, lamotrigine, or a combination of morphine and lamotrigine was administered locally to female Wistar rats, and the antinociceptive effect was determined in the formalin test. Isobolographic analyses were used to define the nature of the functional interactions between morphine and lamotrigine.

Results
Peripheral administration of either morphine or lamotrigine produced a dose-related antinociceptive effect. Isobolographic analyses revealed that peripheral morphine and lamotrigine interacted synergistically in the formalin test.

Conclusions
The study shows a functional interaction between lamotrigine and morphine at the peripheral level.
Radical Scavengers Protect Murine Lungs from Endotoxin-induced Hyporesponsiveness to Inhaled Nitric Oxide
Authors: Raveh Yehuda , Ichinose Fumito , Orbach Pini , Bloch Kenneth D. , Zapol Warren M. 
Published: August 2004

Background
Sepsis is associated with an impaired pulmonary vasodilator response to inhaled nitric oxide (NO). A combination of NO and other inflammatory mediators appears to be responsible for endotoxin-induced pulmonary vascular hyporesponsiveness to inhaled NO. The authors investigated whether scavengers of reactive oxygen species could preserve inhaled NO responsiveness in endotoxin-challenged mice.

Methods
The vasorelaxation to inhaled NO was studied in isolated, perfused, and ventilated lungs obtained from mice 16 h after an intraperitoneal challenge with saline or 50 mg/kg Escherichia coli lipopolysaccharide. In some mice, challenge with saline or lipopolysaccharide was followed by intraperitoneal administration of N-acetylcysteine, dimethylthiourea, EUK-8, or polyethylene glycol-conjugated catalase.

Results
The pulmonary vasodilator response of U46619-preconstricted isolated lungs to ventilation with 0.4, 4, and 40 ppm inhaled NO in lipopolysaccharide-challenged mice was reduced to 32, 43, and 60%, respectively, of that observed in saline-challenged mice (P < 0.0001). Responsiveness to inhaled NO was partially preserved in lipopolysaccharide-challenged mice treated with a single dose of N-acetylcysteine (150 or 500 mg/kg) or 20 U/g polyethylene glycol-conjugated catalase (all P < 0.05 vs. lipopolysaccharide alone). Responsiveness to inhaled NO was fully preserved by treatment with either dimethylthiourea, EUK-8, two doses of N-acetylcysteine (150 mg/kg administered 3.5 h apart), or 100 U/g polyethylene glycol-conjugated catalase (all P < 0.01 vs. lipopolysaccharide alone).

Conclusions
When administered to mice concurrently with lipopolysaccharide challenge, reactive oxygen species scavengers prevent impairment of pulmonary vasodilation to inhaled NO. Therapy with scavengers of reactive oxygen species may provide a means to preserve pulmonary vasodilation to inhaled NO in sepsis-associated acute lung injury.
Modeling of the Sedative and Airway Obstruction Effects of Propofol in Patients with Parkinson Disease undergoing Stereotactic Surgery
Authors: Fábregas Neus , Rapado Javier , Gambús Pedro L. , Valero Ricard , Carrero Enrique , Salvador Lydia , Nalda-Felipe Miguel A. , Trocóniz Iñaki F. 
Published: August 2004

Background
Functional stereotactic surgery requires careful titration of sedation since patients with Parkinson disease need to be rapidly awakened for testing. This study reports a population pharmacodynamic model of propofol sedation and airway obstruction in the Parkinson disease population.

Methods
Twenty-one patients with advanced Parkinson disease undergoing functional stereotactic surgery were included in the study and received propofol target-controlled infusion to achieve an initial steady state concentration of 1 microg/ml. Sedation was measured using the Ramsay Sedation Scale. Airway obstruction was measured using a four-category score. Blood samples were drawn for propofol measurement. Individual pharmacokinetic profiles were constructed nonparametrically using linear interpolation. Time course of sedation and respiratory effects were described with population pharmacodynamic models using NONMEM. The probability (P) of a given level of sedation or airway obstruction was related to the estimated effect-site concentration of propofol (Ce) using a logistic regression model.

Results
The concentrations predicted by the target-controlled infusion system generally exceeded the measured concentrations. The estimates of C(50) for Ramsay scores 3, 4, and 5 were 0.1, 1.02, and 2.28 microg/ml, respectively. For airway obstruction scores 2 and 3, the estimates of C(50) were 0.32 and 2.98 microg/ml, respectively. Estimates of k(e0) were 0.24 and 0.5 1/min for the sedation and respiratory effects, respectively.

Conclusions
The pharmacokinetic behavior of propofol in patients with Parkinson disease differs with respect to the population from which the model used by the target-controlled infusion device was developed. Based on the results from the final models, a typical steady state plasma propofol concentration of 0.35 microg/ml eliciting a sedation score of 3 with only minimal, if any, airway obstruction has been defined as the therapeutic target.