bluuebunny/crossref_metadata_2025 huggingface dataset:
Epileptiform Electroencephalogram during Mask Induction of Anesthesia with Sevoflurane
Authors: Yli-Hankala Arvi , Vakkuri Anne , Särkelä Mika , Lindgren Leena , Korttila Kari , Jäntti Ville
Published: November 2003

Background

Sevoflurane is suggested as a suitable anesthetic agent for mask induction in adults. The authors recently found that hyperventilation during sevoflurane-nitrous oxide-oxygen mask induction is associated with cardiovascular hyperdynamic response. We tested the hypothesis that the hyperdynamic response can be explained by electroencephalography (EEG) findings.

Methods

Thirty women were randomly allocated to receive sevoflurane-nitrous oxygen-oxygen mask induction using a single-breath method, followed by either spontaneous breathing (n = 15) or controlled hyperventilation (n = 15) for 6 min. EEG was recorded. Blood pressure and heart rate were recorded at 1-min intervals.

Results

Epileptiform EEG activity (spikes or polyspikes) was seen in all patients with controlled hyperventilation, and in seven patients with spontaneous breathing (P < 0.01). Jerking movements were seen in three patients with controlled hyperventilation. In the controlled hyperventilation group, heart rate increased 54% from baseline at 4 min after induction (P < 0.001). Mean arterial pressure increased 17% (P < 0.05), peaking at 3 min. In the spontaneous breathing group, heart rate showed no change, and mean arterial pressure decreased by 14% (P < 0.01) at 6 min. Heart rate and mean arterial pressure differed significantly between the groups from 2 min after beginning of the induction to the end of the trial. An increase in heart rate of more than 30% from baseline always was associated with epileptiform EEG activity.

Conclusions

Sevoflurane mask induction elicits epileptiform EEG patterns. These are associated with an increase in heart rate in patients with controlled hyperventilation and also during spontaneous breathing of sevoflurane.
Efficiency of a New Fiberoptic Stylet Scope in Tracheal Intubation
Authors: Kitamura Takayuki , Yamada Yoshitsugu , Du Hong-Lin , Hanaoka Kazuo
Published: November 2003

Background

Failed or difficult tracheal intubation is an important cause of morbidity and mortality during anesthesia. Although a number of fiberoptic devices are available to circumvent this problem, many do not allow manual control of the flexion of the tip and necessitate time-consuming preparation, special training, or the use of an external light source. To improve these limitations, the authors designed a new fiberoptic stylet scope (FSS) that has a simple form of a standard stylet with the fiberoptic view and maneuverability of its tip. This study was undertaken to prospectively evaluate the effectiveness of the FSS in tracheal intubation.

Methods

Thirty-two patients undergoing general surgery participated in this study. The authors used a standard laryngoscope only to elevate the tongue, then tracheal intubation was attempted with the glottic opening being viewed only through the FSS. The success rate, time necessary for intubation, hemodynamics, and adverse effects were recorded.

Results

The success rate of tracheal intubation on the first attempt using the FSS was 94% (30 of 32 patients), and the remaining two patients were intubated successfully on the second attempt. The mean time necessary for the intubation procedure was 29+/-14 s in all patients (mean +/- SD). Changes in hemodynamics during intubation were well within acceptable ranges. There were no major adverse effects, but minor sore throat (28%) and minor hoarseness (25%) on the first postoperative day.

Conclusions

Tracheal intubation using the FSS proved to be a simple and effective technique for airway management.
Rapid Opioid Detoxification during General Anesthesia
Authors: Gold Carl G. , Cullen David J. , Gonzales Scott , Houtmeyers Deirdre , Dwyer Mary Jo
Published: November 2003

Background

Opioid addiction therapy includes successful detoxification, rehabilitation, and sometimes methadone maintenance. However, the patient may have physical, mental, and emotional pain while trying to achieve abstinence. A new detoxification technique that incorporates general anesthesia uses a high-dose opioid antagonist to compress detoxification to within 6 h while avoiding the withdrawal.

Methods

After Institutional Review Board approval and detailed informed consent, 20 patients, American Society of Anesthesiologists status I-II, addicted to various opioids underwent anesthesia-assisted rapid opioid detoxification. After baseline hemodynamics and withdrawal scores were obtained, anesthesia was induced. After testing with 0.4 mg intravenous naloxone, 4 mg nalmefene, was infused over 2 to 3 h. After emergence, severity of withdrawal was scored before and after administration of 0.4 mg intravenous naloxone. After 24 h, patients began outpatient follow-up treatment while taking oral naltrexone.

Results

All 20 patients were successfully detoxified with no adverse anesthetic events. After the first post-treatment test dose of 0.4 mg naloxone, 13 of 20 patients had no signs of withdrawal and hemodynamic changes were minimal. Withdrawal scores were always very low and similar before and after detoxification. Three of 17 patients (18%) available for follow-up have remained abstinent from opioids since treatment (< or = 18 months). Four other patients are clean after brief relapses.

Conclusions

Anesthesia-assisted opioid detoxification is an alternative to conventional detoxification.
Evaluation of Neuromuscular and Cardiovascular Effects of Two Doses of Rapacuronium (ORG 9487) versus Mivacurium and Succinylcholine
Authors: Miguel Rafael , Witkowski Thomas , Nagashima Hideo , Fragen Robert , Bartkowski Richard , Foldes Francis F. , Shanks Colin
Published: November 2003

Background

This study compares the neuromuscular blocking and cardiovascular effects of rapacuronium (ORG 9487), a new aminosteroid nondepolarizing muscle relaxant, to recommended intubating doses of succinylcholine and mivacurium.

Methods

Adult patients were randomized in an open-label fashion to receive 1-5 microg/kg fentanyl before 1.5 mg/kg propofol induction followed by 1.5 or 2.5 mg/kg rapacuronium, 1.0 mg/kg succinylcholine, or 0.25 mg/kg mivacurium (i.e., 0.15 mg/kg followed by 0.1 mg/kg 30 s later).

Results

Patient neuromuscular blockade status was monitored by measuring the train-of-four response to a supramaximal stimulus at the ulnar nerve every 12 s. Percentage of the first twitch of the train-of-four (T1) at 60 s was similar in patients receiving 1.5 mg/kg rapacuronium, 2.5 mg/kg rapacuronium, and succinylcholine and was significantly less than in patients in the mivacurium group (26, 16, and 18%, respectively, vs. 48%; P < 0.01). Times to 80% T1 depression were also similar among patients in the 1.5 mg/kg rapacuronium, 2.5 mg/kg rapacuronium, and succinylcholine groups and significantly longer in the mivacurium group (62, 54, and 54 s, respectively, vs. 112 s; P < 0.01). Clinical duration was longer in all groups compared with the succinylcholine group; however, clinical duration in the 1.5 mg/kg rapacuronium group was shorter compared with the mivacurium group (15 vs. 21 min, respectively; P < 0.01). Heart rate changes were mild in the 1.5 mg/kg rapacuronium, succinylcholine, and mivacurium groups. The patients in the 2.5 mg/kg rapacuronium group had significantly higher heart rates compared with patients in the mivacurium group. No differences were found in blood pressure changes among patients in the four groups.

Conclusions

Rapacuronium, 1.5 and 2.5 mg/kg, produced neuromuscular blockade as rapidly as succinylcholine and significantly faster than mivacurium. Although succinylcholine continued to show the shortest duration, 1.5 mg/kg rapacuronium used a rapid onset and a relatively short duration and may be considered an alternative to succinylcholine.
A New Anterior Approach to the Sciatic Nerve Block
Authors: Chelly Jacques E. , Delaunay Laurent
Published: November 2003

Background

Although several anterior approaches to sciatic nerve block have been described, they are used infrequently. The authors describe a new anterior approach that allows access to the sciatic nerve with the patient in the supine position.

Method

Sciatic nerve blocks were performed in 22 patients. A line was drawn between the inferior border of the anterosuperior iliac spine and the superior angle of the pubic symphysis tubercle. Next, a perpendicular line bisecting the initial line was drawn and extended 8 cm caudad. The needle was inserted perpendicularly to the skin, and the sciatic nerve was identified at a depth of 10.5 cm (9.5-13.5 cm; median and range) using a nerve stimulator and a 15-cm b-beveled insulated needle. After appropriate localization, either 30 ml mepivacaine, 1.5% (group 1 = knee arthroscopy; n = 16), or 15 ml mepivacaine, 1.5%, plus 15 ml ropivacaine, 0.75%, (group 2 = other procedures; n = 6) was injected.

Results

Appropriate landmarks were determined within 1.3 min (0.5-2.0 min). The sciatic nerve was identified in all patients within 2.5 min (1.2-5 min), starting from the beginning of the appropriate landmark determination to the stimulation of its common peroneal nerve component in 13 cases and its tibial nerve component in 9 cases. A complete sensory block in the distribution of both the common peroneal nerve component and the tibial nerve component was obtained within 15 min (5-30 min). A shorter onset was observed in patients who received mepivacaine alone compared with those who received a mixture of mepivacaine plus ropivacaine (10 min [5-25 min] vs. 20 min [10-30 min]; P < 0.05). Recovery time was 4.6 h (2.5-5.5 h) after mepivacaine administration. The addition of ropivacaine produced a block of a much longer duration 13.8 h (5.2-23.6 h); P < 0.05. No complications were observed.

Conclusions

This approach represents an easy and reliable anterior technique for performing sciatic nerve blocks.
Alfentanil Causes Less Postoperative Nausea and Vomiting than Equipotent Doses of Fentanyl or Sufentanil in Outpatients
Authors: Langevin Stephan , Lessard Martin R. , Trépanier Claude A. , Baribault Jean-Pierre
Published: November 2003

Background

The relative potencies of alfentanil, fentanyl, and sufentanil as a risk factor for postoperative nausea and vomiting have not been determined. They were compared in a randomized study designed to obtain equipotent plasma concentrations of these three opioids at the beginning of the recovery period.

Methods

The study included 274 patients treated on an outpatient basis. The steady state opioid plasma concentration providing a predicted 50% reduction of the minimum alveolar concentration of isoflurane was used to determine the relative potency of the opioids. The opioids were prepared in equal volumes at concentrations of alfentanil 150 microg/ml, fentanyl 50 microg/ml, and sufentanil 5 microg/ml and were administered in vol/kg. Anesthesia was induced in a blinded fashion with a bolus of the study opioid (0.05 ml/kg) and 4-6 mg/kg thiopental and was maintained with isoflurane (0.6-1%) in a nitrous oxide-oxygen mixture with a continuous infusion of the study opioid (0.06 ml x kg(-1) x h(-1)). If necessary, up to five additional boluses of opioid (0.02 ml/kg) could be given. This opioid administration protocol was tested by pharmacokinetic simulations.

Results

The incidence of postoperative nausea and vomiting was not different in the postanesthesia care unit, but in the ambulatory surgery unit it was significantly lower for alfentanil compared with fentanyl and sufentanil (12, 34, and 35%, respectively P < 0.005). Pharmacokinetic modeling showed that the end-anesthesia opioid plasma concentrations were approximately equipotent in the three groups. However, modeling does not support that the difference between groups in the postoperative period can be explained by a more rapid disappearance of alfentanil from the plasma.

Conclusions

Alfentanil, compared with approximately equipotent doses of fentanyl and sufentanil, is associated with a lower incidence of postoperative nausea and vomiting in outpatients.
Pharmacokinetics of Thiopental Enantiomers during and following Prolonged High-dose Therapy
Authors: Cordato Dennis J. , Mather Laurence E. , Gross Annette S. , Herkes Geoffrey K.
Published: November 2003

Background

Thiopental is used as a racemate; however, this is not generally recognized. During conditions of prolonged high-dose therapy, the pharmacokinetics of thiopental may become nonlinear, but whether this derives from one or both enantiomers has not been evaluated. The authors determined the pharmacokinetics of R- and S-thiopental and serum concentrations of R- and S-pentobarbital from prolonged high-dose infusion of thiopental for neuroprotection.

Methods

Twenty patients received a mean thiopental dose of 41.2 g over a mean duration of 95 h. R- and S-thiopental enantiomer serum concentration-time data from 18 patients were fitted with two models: a linear one-compartment model with first-order output, and a nonlinear one-compartment model with Michaelis-Menten output.

Results

Nonlinear models were preferred in 16 of 18 patients. Paired analysis indicated that steady state clearance (Clss) and volume of distribution (Vd) were higher for R-thiopental (0.108 vs. 0.096 l/min, P < 0.0001; and 313 vs. 273 l, P < 0.0005, respectively); maximal rate of metabolism (Vm) was higher for S- than for R-thiopental (1.01 vs. 0.86 mg x l(-1) x h(-1), P = 0.02); elimination half-lives did not differ (14.6 vs. 14.7 h, P = 0.8); unbound fractions (f(u)) of R- and S-thiopental were 0.20 and 0.18, respectively, P < 0.0001). The differences in mean Clss, Vd and Vm were not significant when adjusted by f(u). Plasma concentrations of R- and S-pentobarbital were relatively small and unlikely to be of clinical significance.

Conclusion

The pharmacokinetics of R- and S-thiopental became nonlinear at these doses. The pharmacokinetic differences between R- and S-thiopental, although small, were statistically significant and were influenced by the higher f(u) of R-thiopental.
Propofol-induced Depression of Cultured Rat Ventricular Myocytes Is Related to the M2-acetylcholine Receptor–NO–cGMP Signaling Pathway
Authors: Yamamoto Shuji , Kawana Shin , Miyamoto Atsushi , Ohshika Hideyo , Namiki Akiyoshi
Published: November 2003

Background

It is well-known that propofol sometimes causes bradycardia or asystole during anesthesia; however, the direct effect of propofol on the myocardium remains unclear. Previous reports showed the contribution of muscarinic acetylcholine receptors to propofol-induced bradycardia. Conversely, it was suggested recently that nitric oxide (NO) plays an important role in mediating the effect of vagal stimulation in the autonomic regulation of the heart. Therefore, the authors investigated the effects of propofol on spontaneous contraction and NO production in cultured rat ventricular myocytes.

Methods

The authors measured chronotropic responses of cultured rat ventricular myocytes induced by propofol stimulation with a sensor, a fiber-optic displacement measurement instrument. The authors also quantitatively analyzed NO metabolite production in cultured myocytes by measuring the levels of nitrite and nitrate in a high-performance liquid chromatography reaction system. The influence of propofol on muscarinic acetylcholine receptors of myocyte membranes was also measured with a competitive binding assay using [3H]quinuclidinyl benzilate ([3H]QNB).

Results

Propofol caused negative chronotropy in a dose-dependent manner. Propofol (IC50) also caused the enhancement of nitrite production in cultured myocytes. Eighty percent of the enhancement of nitrite production induced by propofol (IC50) stimulation was abolished by pretreatment with atropine, methoctramine, or N(G)-monomethyl-L-arginine acetate (L-NMMA). The negative chronotropy induced by propofol (IC50) stimulation was reduced to 40-50% by pretreatment with atropine, methoctramine, L-NMMA, or 1H[1,2,4]oxadiazolo[4,3-alpha]quanoxalin-1-one, a selective inhibitor of guanylyl cyclase. Propofol displaced [3H]QNB binding to the cell membrane of myocytes in a concentration-dependent manner.

Conclusion

These results suggest that the negative chronotropy induced by propofol is mediated in part by M2-acetylcholine receptor activation, which involves the enhancement of NO production in cultured rat ventricular myocytes.
Local Coupling of Cerebral Blood Flow to Cerebral Glucose Metabolism during Inhalational Anesthesia in Rats
Authors: Lenz Christian , Frietsch Thomas , Fütterer Carsten , Rebel Annette , van Ackern Klaus , Kuschinsky Wolfgang , Waschke Klaus F.
Published: November 2003

Background

It is not known whether the effects of desflurane on local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) are different from those of other volatile anesthetics.

Methods

Using the autoradiographic iodoantipyrine and deoxyglucose methods, LCGU, LCBF, and their overall means were measured in 60 Sprague-Dawley rats (10 groups, n = 6 each) during desflurane and isoflurane anesthesia and in conscious controls.

Results

During anesthesia, mean cerebral glucose utilization was decreased compared with conscious controls: 1 minimum alveolar concentration (MAC) desflurane: -52%; 1 MAC isoflurane: -44%; 2 MAC desflurane: -62%; and 2 MAC isoflurane: -60%. Local analysis showed a reduction of LCGU in the majority of the 40 brain regions analyzed. Mean cerebral blood flow was increased: 1 MAC desflurane: +40%; 1 MAC isoflurane: +43%; 2 MAC desflurane and 2 MAC isoflurane: +70%. LCBF was increased in all brain structures investigated except in the auditory cortex. No significant differences (P < 0.05) could be observed between both anesthetics for mean values of cerebral glucose use and blood flow. Correlation coefficients obtained for the relation between LCGU and LCBF were as follows: controls: 0.95; 1 MAC desflurane: 0.89; 2 MAC desflurane: 0.60; 1 MAC isoflurane: 0.87; and 2 MAC isoflurane: 0.68.

Conclusion

Differences in the physicochemical properties of desflurane compared with isoflurane are not associated with major differences in the effects of both volatile anesthetics on cerebral glucose utilization, blood flow, and the coupling between LCBF and LCGU.
Congenital NOS2 Deficiency Protects Mice from LPS-induced Hyporesponsiveness to Inhaled Nitric Oxide
Authors: Weimann Jörg , Bloch Kenneth D. , Takata Masao , Steudel Wolfgang , Zapol Warren M.
Published: November 2003

Background

In animal models, endotoxin (lipopolysaccharide) challenge impairs the pulmonary vasodilator response to inhaled nitric oxide (NO). This impairment is prevented by treatment with inhibitors of NO synthase 2 (NOS2), including glucocorticoids and L-arginine analogs. However, because these inhibitors are not specific for NOS2, the role of this enzyme in the impairment of NO responsiveness by lipopolysaccharide remains incompletely defined.

Methods

To investigate the role of NOS2 in the development of lipopolysaccharide-induced impairment of NO responsiveness, the authors measured the vasodilator response to inhalation of 0.4, 4, and 40 ppm NO in isolated, perfused, and ventilated lungs obtained from lipopolysaccharide-pretreated (50 mg/kg intraperitoneally 16 h before lung perfusion) and untreated wild-type and NOS2-deficient mice. The authors also evaluated the effects of breathing NO for 16 h on pulmonary vascular responsiveness during subsequent ventilation with NO.

Results

In wild-type mice, lipopolysaccharide challenge impaired the pulmonary vasodilator response to 0.4 and 4 ppm NO (reduced 79% and 45%, respectively, P < 0.001), but not to 40 ppm. In contrast, lipopolysaccharide administration did not impair the vasodilator response to inhaled NO in NOS2-deficient mice. Breathing 20 ppm NO for 16 h decreased the vasodilator response to subsequent ventilation with NO in lipopolysaccharide-pretreated NOS2-deficient mice, but not in lipopolysaccharide-pretreated wild-type, untreated NOS2-deficient or untreated wild-type mice.

Conclusions

In response to endotoxin challenge, NO, either endogenously produced by NOS2 in wild-type mice or added to the air inhaled by NOS2-deficient mice, is necessary to impair vascular responsiveness to inhaled NO. Prolonged NO breathing, without endotoxin, does not impair vasodilation in response to subsequent NO inhalation. These results suggest that NO, plus other lipopolysaccharide-induced products, are necessary to impair responsiveness to inhaled NO in a murine sepsis model.
Diaspirin Cross-linked Hemoglobin Effectively Restores Pancreatic Microcirculatory Failure in Hemorrhagic Shock
Authors: von Dobschuetz Ernst , Hoffmann Tomas , Messmer Konrad
Published: November 2003

Background

Microvascular reperfusion failure of splanchnic organs is a crucial hallmark in organ damage induced by hemorrhagic shock, which should be prevented by a resuscitation solution. Because the vasoactive properties of the hemoglobin-based oxygen carrier diaspirin cross-linked hemoglobin (DCLHb) could adversely influence restoration of pancreatic capillary perfusion during resuscitation, the authors investigated its effects on the microcirculation of the rat pancreas in comparison with whole blood and 6% hydroxyethylstarch resuscitation from severe hemorrhagic shock.

Methods

Twenty-eight pentobarbital-anaesthetized rats were bled to a mean arterial pressure (MAP) of 40 mmHg and maintained at this level for 1 h. Using an intravital microscope, mean arterial pressure, the length of erythrocyte-perfused pancreatic capillaries per observation area (functional capillary density), the adherence of leukocytes in postcapillary venules, and pancreatic lipid peroxidation, measured as thiobarbituric acid-reactive material in pancreatic tissue, were determined in animals resuscitated by volumes of hydroxyethylstarch, DCLHb, and whole blood (WB) equivalent to the shed blood volume or in control animals without shock induction for a period of 2 h after resuscitation.

Results

Compared with control animals (366+/-28 cm(-1)), animals resuscitated with DCLHb (294+/-45 cm(-1)), WB (306+/-11 cm(-1)), and hydroxyethylstarch (241+/-34 cm(-1)) showed a significant reduction of functional capillary density after 2 h of resuscitation. DCLHb was as effective as WB and superior to hydroxyethylstarch in restoring functional capillary density and mean arterial pressure. Leukocyte adherence in postcapillary venules was not enhanced by DCLHb (369+/-148/mm2) infusion when compared with hydroxyethylstarch- (615+/-283/mm2) and WB-treated (510+/-415/mm2) animals. Lipid peroxidation of pancreatic tissue was significantly elevated after treatment with both oxygen-carrying solutions compared with hydroxyethylstarch.

Conclusion

DCLHb is as effective as WB for preservation of the pancreatic microcirculation.
Isoflurane Blunts Electroencephalographic and Thalamic–Reticular Formation Responses to Noxious Stimulation in Goats
Authors: Antognini Joseph F. , Carstens E.
Published: November 2003

Background

Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action.

Methods

Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC.

Results

At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus.

Conclusions

Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.
Colchicine Inhibits Isoflurane-induced Preconditioning
Authors: Ismaeil Mohamed S. , Tkachenko Igor , Hickey Robert F. , Cason Brian A.
Published: November 2003

Background

When administered before prolonged myocardial ischemia and reperfusion, isoflurane exerts potent cardioprotective effects similar to those inferred by ischemic preconditioning. To determine whether an intact cytoskeleton is critically important in isoflurane-induced preconditioning, the authors used a rabbit model in which isoflurane-induced myocardial preconditioning decreases myocardial infarct size (IS) substantially. In this model, the authors tested whether the microtubule depolymerizing agent, colchicine, would inhibit isoflurane-induced myocardial preconditioning.

Methods

Myocardial IS was measured in four groups of propofol-anesthetized rabbits, each subjected to 30 min of anterolateral coronary occlusion followed by 3 h of reperfusion. Groups differed only in the pretreatments given, and only the control group received no pretreatment. An isoflurane-preconditioned group was pretreated with 15 min of end-tidal isoflurane, 1.1%, and then 15 min of washout. An isoflurane-plus-colchicine group was administered 2 mg/kg colchicine intravenously before isoflurane pretreatment. A colchicine-control group was administered 2 mg/kg colchicine but no isoflurane pretreatment. Myocardial IS and area at risk (AR) were defined by staining. Data were analyzed by analysis of variance or covariance.

Results

Infarct size, expressed as a percentage of AR (IS:AR) was 33.6%+/-8.8% (SD) in the control group. Isoflurane preexposure reduced myocardial IS:AR significantly, to 11.8%+/-9.1%. Colchicine pretreatment eliminated the preconditioning-like effect of isoflurane (IS:AR = 32.6%+/-8.7%). Colchicine alone did not alter IS (IS:AR = 27.6%+/-7.1%; P = not significant).

Conclusions

Colchicine abolished the preconditioning effect of isoflurane but did not increase IS when administered alone. An intact microtubular cytoskeleton is critically important in the process of volatile anesthetic-induced preconditioning.
Exposure to Cigarette Smoke Impairs Alveolar Macrophage Functions during Halothane and Isoflurane Anesthesia in Rats
Authors: Kotani Naoki , Hashimoto Hiroshi , Sessler Daniel I. , Yatsu Yuichi , Muraoka Masatoshi , Matsuki Akitomo
Published: November 2003

Background

Smoking alters numerous alveolar macrophage functions and is an important risk factor for postoperative pulmonary complications. The authors therefore tested the hypothesis that smoke exposure impairs antimicrobial and proinflammatory responses in alveolar macrophages during halothane and isoflurane anesthesia with mechanical ventilation.

Methods

Thirty control rats and 30 rats exposed to cigarette smoke were mechanically ventilated with 1.5 minimum alveolar concentration halothane and isoflurane. Ten smoke-exposed and control animals were assigned to one of three different anesthetic durations (0, 2, and 6 h). The fraction of aggregated cells and cell distribution were determined. Opsonized and unopsonized phagocytosis was measured. Microbicidal activity was determined as the ability to kill Listeria monocytogenes. The expression of interleukin (IL)-1alpha, IL-1beta, IL-6, macrophage inflammatory protein-2, interferon-gamma, and tumor necrosis factor-alpha was measured by semiquantitative reverse-transcription polymerase chain reaction. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunosorbent assay.

Results

During both halothane and isoflurane anesthesia, the fraction of aggregated macrophages increased, whereas unopsonized and opsonized phagocytosis and microbicidal activity decreased significantly over time in both groups. Responses observed in smoke-exposed rats were almost twice as great as those observed in the control rats. Gene expression and production of all proinflammatory cytokines except IL-6 increased 2-20-fold during anesthesia. The increases in IL-1beta, interferon-gamma, and tumor necrosis factor-alpha in the control rats were 1.5-8 times greater than those in the smoke-exposed rats.

Conclusion

Antimicrobial and proinflammatory responses of alveolar macrophages during anesthesia were markedly suppressed by smoke exposure. Our data suggest that smoke exposure reduces the efficacy of immune defenses during anesthesia.
Different Ventilation Strategies Affect Lung Function but Do Not Increase Tumor Necrosis Factor-α and Prostacyclin Production in Lavaged Rat Lungs In Vivo
Authors: Verbrugge Serge J. C. , Uhlig Stefan , Neggers Sebastian J. C. M. M. , Martin Christian , Held Heinz-Dieter , Haitsma Jack J. , Lachmann Burkhard
Published: November 2003

Background

Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma.

Methods

In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls.

Results

Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls.

Conclusions

Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.
Tissue Factor Expression in Vital Organs during Murine Traumatic Shock
Authors: Armstead Valerie E. , Opentanova Irina L. , Minchenko Alexander G. , Lefer Allan M.
Published: November 2003

Background

Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats.

Methods

Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1.

Results

TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively).

Conclusions

These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.
Effects of Halothane and Enflurane on Ventricular Conduction, Refractoriness, and Wavelength
Authors: Aya Antoine G. , de La Coussaye Jean E. , Robert Emmanuelle , Ripart Jacques , Lefrant Jean-Yves , Fabbro-Péray Pascale , Eledjam Jean-Jacques
Published: November 2003

Background

Effects of halothane and enflurane on ventricular conduction, anisotropy, duration and dispersion of refractory periods, and wavelengths were studied, and putative antiarrhythmic or arrhythmogenic properties on ventricles were discussed.

Methods

High-resolution epicardial mapping system was used to study the effects of 1, 3, and 5 vol% halothane and enflurane in 30 isolated rabbit hearts. Ten hearts were kept intact to study the effects on spontaneous sinus cycle length (RR interval), perfusion pressure, and the occurrence of spontaneous dysrhythmias. In 20 other hearts, a thin epicardial layer was obtained (frozen hearts) to study ventricular conduction velocity, ventricular effective refractory period (VERP in four sites) and wavelengths.

Results

Halothane induced a concentration-dependent lengthening of RR interval, whereas enflurane did not. Both agents slowed longitudinal and transverse ventricular conduction velocity with no anisotropic change. Ventricular effective refractory period was prolonged at 1 vol% and was shortened at higher concentrations, with no significant increase in dispersion. Ventricular longitudinal and transverse wavelengths decreased in a concentration-dependent manner. Although changes in wavelengths could express proarrhythmic effects of volatile anesthetics, no arrhythmia occurred in spontaneously beating hearts or in frozen hearts.

Conclusions

The ventricular electrophysiologic effects of halothane and enflurane were slight, suggesting that both agents are unable per se to induce functional conduction block and therefore reentrant ventricular arrhythmias.
Incidence of Venous Air Embolism during Craniectomy for Craniosynostosis Repair
Authors: Faberowski Lisa W. , Black Susan , Mickle J. Parker
Published: November 2003

Background

Investigations to determine the incidence of venous air embolism in children undergoing craniectomy for craniosynostosis repair have been limited, although venous air embolism has been suspected as the cause of hemodynamic instability and sometimes death. A precordial Doppler ultrasonic probe is an accepted method for detection of venous air embolism and is readily available at most institutions.

Methods

A prospective study was conducted using a precordial Doppler ultrasonic probe in children undergoing craniectomy for craniosynostosis repair. The Doppler signal was continuously monitored intraoperatively for characteristic changes of venous air embolism. A recording was made of the precordial Doppler probe pulses, which was later reviewed by a neuroanesthesiologist, blinded to the intraoperative events. This information was correlated with the intraoperative events and episodes of venous air embolism were graded.

Results

Twenty-three patients were enrolled in the study during the 2-yr study period. Nineteen patients (82.6%) demonstrated 64 episodes of venous air embolism; six patients (31.6%) had hypotension associated with venous air embolism. Thirty-two episodes of hypotension were demonstrated in eight patients (34.7%). None of the patients developed cardiovascular collapse.

Conclusion

The incidence of venous air embolism in our study of 23 children undergoing craniectomy for craniosynostosis was 82.6%. Though most episodes of venous air embolism during craniosynostosis repair are without hemodynamic consequences, the preemptive placement of a precordial Doppler ultrasonic probe is a noninvasive, economic, and safe method for the detection of venous air embolism. Prompt recognition may allow for the early initiation of therapy, thereby decreasing morbidity and mortality rates related to venous air embolism.
Hemodynamic Effects of Synchronized High-frequency Jet Ventilation Compared with Low-frequency Intermittent Positive-pressure Ventilation after Myocardial Revascularization
Authors: Romand Jacques-Andre , Treggiari-Venzi Miriam M. , Bichel Thierry , Suter Peter M. , Pinsky Michael R.
Published: November 2003

Background

The purpose of this prospective study was to examine the effect on cardiac performance of selective increases in airway pressure at specific points of the cardiac cycle using synchronized high-frequency jet ventilation (sync-HFJV) delivered concomitantly with each single heart beat compared with controlled mechanical ventilation in 20 hemodynamically stable, deeply sedated patients immediately after coronary artery bypass graft.

Methods

Five 30-min sequential ventilation periods were used interspersing controlled mechanical ventilation with sync-HFJV twice to control for time and sequencing effects. Sync-HFJV was applied using a driving pressure, which generated a tidal volume resulting in gas exchanges close to those obtained on controlled mechanical ventilation and associated with the maximal mixed venous oxygen saturation. Hemodynamic variables including cardiac output, mixed venous oxygen saturation and vascular pressures were recorded at the end of each ventilation period.

Results

The authors found that in 20 patients, hemodynamic changes induced by controlled mechanical ventilation and by sync-HFJV were similar. Cardiac index did not change (mean +/- SD for controlled mechanical ventilation: 2.6 +/- 0.7 l x min(-1) x m(-2); for sync-HFJV: 2.7 +/- 0.7 l x min(-1) x m(-2); P value not significant). This observation persisted after stratification according to baseline left-ventricular contractility, as estimated by ejection fraction.

Conclusions

The authors conclude that after coronary artery bypass graft, if gas-exchange values are maintained within normal range, sync-HFJV does not result in more favorable hemodynamic support than controlled mechanical ventilation. These findings contrast with the beneficial effects of sync-HFJV, resulting in marked hypocapnia, on cardiac performance observed in patients with terminal left-ventricular failure.
Left-molar Approach Improves the Laryngeal View in Patients with Difficult Laryngoscopy
Authors: Yamamoto Ken , Tsubokawa Tsunehisa , Ohmura Shigeo , Itoh Hironori , Kobayashi Tsutomu
Published: November 2003

Background

The molar approach of laryngoscopy is reported to improve glottic view in sporadic cases of difficult laryngoscopy. The authors studied the effect of molar approaches and optimal external laryngeal manipulation (OELM) using the Macintosh blade.

Methods

A series of 1,015 adult patients who underwent general anesthesia and tracheal intubation was studied. Laryngoscopy was carried out using a Macintosh no. 3 or 4 standard blade. Three consecutive trials of direct laryngoscopy using the midline and left- and right-molar approaches were carried out under full muscle relaxation with optimal head and neck positioning. The best glottic views were recorded for each approach with and without OELM.

Results

Difficult laryngoscopy with a midline approach accounted for 6.5% (66 cases) before OELM and 1.97% (20 cases) after OELM. A left-molar approach with OELM further reduced difficult laryngoscopy to seven cases (P < 0.001 vs. midline approach with OELM); a right-molar approach with OELM reduced difficult laryngoscopy to 18 cases (P = 0.48).

Conclusions

The left-molar approach with OELM improves the laryngeal view in patients with difficult laryngoscopy.
Concentration–Effect Relationship of Intravenous Lidocaine on the Allodynia of Complex Regional Pain Syndrome Types I and II
Authors: Wallace Mark S. , Ridgeway Beri M. , Leung Albert Y. , Gerayli Afshin , Yaksh Tony L.
Published: November 2003

Background

Several lines of evidence suggest that neuropathic pain (including Complex Regional Pain Syndrome [CRPS] I and CRPS II) is mediated in part by an increase in the density of voltage-sensitive sodium channels in injured axons and the dorsal root ganglion of injured axons. This study sought to characterize the effects of intravenous lidocaine (a sodium channel blocker) on acute sensory thresholds within the painful area and the size of the painful area in patients suffering from CRPS I and II.

Methods

This study used a randomized, double-blind, placebo-controlled design in 16 subjects suffering from CRPS I and II with a prominent allodynia. Each subject received an intravenous infusion of lidocaine and diphenhydramine separated by 1 week. A computer-controlled infusion pump targeted stair-step increases in plasma levels of lidocaine of 1, 2, and 3 microg/ml. At baseline and at each plasma level, spontaneous and evoked pain scores and neurosensory testing within the painful area were measured. The neurosensory testing consisted of thermal thresholds, tactile thresholds and the area of allodynia to punctate, and stroking and thermal stimuli.

Results

Intravenous lidocaine and diphenhydramine had no significant effect on the cool, warm, or cold pain thresholds. However, lidocaine caused a significant elevation of the hot pain thresholds in the painful area. Intravenous lidocaine caused a significantly decreased response to stroking and cool stimuli in the allodynic area. There was also a significant decrease in pain scores to cool stimuli at all plasma levels and the spontaneous pain at the highest plasma level.

Conclusions

This study demonstrates that intravenous lidocaine affects pain in response to cool stimuli more than mechanical pain in subjects with neuropathic pain. There is a lesser effect on spontaneous pain and pain induced by stroking stimuli and no effect on the pain induced by punctate stimuli.
Stellate Ganglion Block Modifies the Distribution of Lymphocyte Subsets and Natural-killer Cell Activity
Authors: Yokoyama Masataka , Nakatsuka Hideki , Itano Yoshitaro , Hirakawa Masahisa
Published: November 2003

Background

Recent investigations suggest that the sympathetic nervous system affects the immune system. This study examined whether stellate ganglion block (SGB) affects the immune response, specifically the distribution of lymphocyte subsets and natural-killer (NK) cell activity.

Methods

Ten volunteers received three different treatments in random order at 7-day intervals: (1) SGB with 7 ml of 1% lidocaine; (2) an identical volume of normal saline injected at the same site as SGB; and (3) an identical volume of 1% lidocaine injected intramuscularly. Blood samples were drawn before and 30 min after treatment. The distribution of lymphocyte subsets was analyzed, and NK cell activity was measured. Plasma concentrations of epinephrine, norepinephrine, adrenocorticotropic hormone, and cortisol were measured.

Results

Any value in the normal saline and intramuscular treatments did not change significantly. After SGB, the plasma concentrations of epinephrine and norepinephrine decreased significantly (P < 0.01), but adrenocorticotropic hormone and cortisol values were unchanged. Increases were observed in the proportion of B cells (from 18.4 +/- 3.0% to 20.0 +/- 3.8%; P < 0.01) and T cells (from 64.2 +/- 4.1% to 67.1 +/- 4.2%; P < 0.01). A decrease in the proportion of NK cells was observed (from 13.4 +/- 2.7% to 9.8 +/- 2.2%; P < 0.01). The proportion of CD4+ cells increased (P < 0.01), and that of CD8+ cells decreased (P < 0.01), so that the CD4+ cell/CD8+ cell ratio increased (P < 0.01). The proportion of CD29+ (helper-inducer T) cells increased (P < 0.05), but that of CD45RA+ (suppressor-inducer T) cells did not change. NK cell activity decreased significantly (from 33.6 +/- 8.3% to 29.1 +/- 7.6%; P < 0.01).

Conclusions

A small but significant alteration in lymphocyte subsets and in NK cell activity by SGB indicates that local sympathetic nerve block may modulate the immune response.
Tonic Blocking Action of Meperidine on Na+and K+Channels in Amphibian Peripheral Nerves
Authors: Bräu Michael E. , Koch E. Dietlind , Vogel Werner , Hempelmann Gunter
Published: November 2003

Background

Among opioids, meperidine (pethidine) also shows local anesthetic activity when applied locally to peripheral nerve fibers and has been used for this effect in the clinical setting for regional anesthesia. This study investigated the blocking effects of meperidine on different ion channels in peripheral nerves.

Methods

Experiments were conducted using the outside-out configuration of the patch-clamp method applied to enzymatically prepared peripheral nerve fibers of Xenopus laevis. Half-maximal inhibiting concentrations were determined for Na+ channels and different K+ channels by nonlinear least-squares fitting of concentration-inhibition curves, assuming a one-to-one reaction.

Results

Externally applied meperidine reversibly blocked all investigated channels in a concentration-dependent manner, i.e., voltage-activated Na+ channel (half-maximal inhibiting concentration, 164 microM), delayed rectifier K+ channels (half-maximal inhibiting concentration, 194 microM), the calcium-activated K+ channel (half-maximal inhibiting concentration, 161 microM), and the voltage-independent flicker K+ channel (half-maximal inhibiting concentration, 139 microM). Maximal block in high concentrations of meperidine reached 83% for delayed rectifier K+ channels and 100% for all other channels. Meperidine blocks the Na+ channel in the same concentration range as the local anesthetic agent lidocaine (half-maximal inhibiting concentration, 172 microM) but did not compete for the same binding site as evaluated by competition experiments. Low concentrations of meperidine (1 nM to 1 microM) showed no effects on Na+ channels. The blockade of Na+ and delayed rectifier K+ channels could not be antagonized by the addition of naloxone.

Conclusions

It is concluded that meperidine has a nonselective inhibitory action on Na+ and K+ channels of amphibian peripheral nerve. For tonic Na+ channel block, neither an opioid receptor nor the the local anesthetic agent binding site is the target site for meperidine block.