bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nerve Stimulators Used for Peripheral Nerve Blocks Vary in Their Electrical Characteristics
Authors: Hadzic Admir , Vloka Jerry , Hadzic Nihad , Thys Daniel M. , Santos Alan C. 
Published: November 2003

Background
Nerve stimulation with a low-intensity electrical current has become a vital part of the performance of peripheral nerve blockade. The purpose of this study was to compare the accuracy and characteristics of peripheral nerve stimulators used in clinical practice in the United States.

Methods
Fifteen peripheral nerve stimulators were fitted with fresh batteries and set to deliver currents ranging from 0.1 to 4.0 mA into a series of high-tolerance resistance loads ranging from 1 to 100 komega. The current output, stimulus duration, morphology, frequency, and maximum voltage output were studied using a factory-calibrated oscilloscope.

Results
All peripheral nerve stimulators performed uniformly well when set to deliver currents of 1.0 mA or more into a standard resistance load of 1 or 2 komega. However, at lower currents, the median error (%) increased from 2.4 (-5-144%) at 0.5 mA to 10.4 (-24-180%) at 0.1 mA into a 1 komega load. The morphology of the stimulus was characterized by a regular monophasic square pulse at current outputs of up to 1 mA and at a resistance of 1 komega. The stimulus waveform became particularly distorted as the impedance load was increased. The duration of the default stimulus set by the manufacturer varied from 34.8 to 460 micros among the peripheral nerve stimulators tested. The maximum voltage output ranged from 7.4 to 336 Volts.

Conclusions
Nerve stimulators used for regional anesthesia vary greatly in accuracy of current output and in manufacturer-selected electrical characteristics (e.g., current duration, stimulating frequency, maximum voltage output).
Does the Suggested Lightwand Bent Length Fit Every Patient?
Authors: Chen Tsai-Hsin , Tsai Shen-Kou , Lin Chen-Jung , Lu Cheng-Wei , Tsai Tsung-Po , Sun Wei-Zen 
Published: November 2003

Background
To date, no study has explored the effect of bent length on lightwand intubation. For successful intubation in daily practice, the authors found that bent length should be approximated to the patient's thyroid prominence-to-mandibular angle distance (TMD), but some patients have a TMD much shorter than the suggested bent length range. The purposes of this study were to understand TMD distribution in adults and to test the influence of bent length on lightwand intubation.

Methods
The TMD, airway, and demographic data of 379 patients were collected. To test the bent length influence, patients were enrolled in group A (158 patients, TMD </= 5.5 cm) and group B (131 patients, TMD > 5.5 cm) and were intubated randomly using the lower (6.5 cm) and upper (8.5 cm) limits of the suggested range. Success rate and lightwand search time were compared.

Results
In group A, the success rate was 98.8% with 6.5-cm bent length and 78.2% with 8.5-cm bent length (P < 0.05). Search times were 5.7 +/- 2.90 and 8.9 +/- 5.80 s with 6.5- and 8.5-cm bent length, respectively (P < 0.01). In group B, there was no statistical difference in success rate and search time between 6.5- and 8.5-cm bent length.

Conclusion
The suggested range was suitable for patients in group B (TMD > 5.5 cm). However, in group A (</=5.5 cm), the large discrepancy between the upper limit of the suggested range and this TMD caused difficulty in lightwand intubation. A 6.5-cm bent length is more suitable than an 8.5-cm bent length in these patients.
Neural Mechanism of Propofol Anesthesia in Severe Depression
Authors: Ogawa Kenichi , Uema Takeshi , Motohashi Nobutaka , Nishikawa Masami , Takano Harumasa , Hiroki Masahiko , Imabayashi Etsuko , Ohnishi Takashi , Inoue Tomio , Takayama Yutaka , Takeda Masatoshi , Matsuda Hiroshi , Andoh Tomio , Yamada Yoshitsugu 
Published: November 2003

Background
The precise neural mechanisms of propofol anesthesia in humans are still unknown. The authors examined the acute effects of propofol on regional cerebral blood flow (rCBF) using positron emission tomography in patients with severe depression.

Methods
In six severely depressed patients (mean age, 55.0 yr) scheduled for electroconvulsive therapy, anesthetic levels were monitored by electroencephalography, and rCBF was serially quantified in the awake, sedated, and anesthetized states. The authors used high-resolution positron emission tomography with 15O-labeled water and statistical parametric mapping 99 for imaging and analysis of the data.

Results
Global cerebral blood flow showed sharp decreases from the awake level during the administration of propofol, decreasing 26.8% in the sedated state and 54.4% in the anesthetized state. Moreover, a dose effect was seen in both parietal cortices and the left lateral prefrontal region with larger regions of relative decrease in rCBF at higher propofol doses. At the higher dose, the values of rCBF in the pulvinar nucleus of the thalamus, the pontine tegmentum, and the cerebellar cortex were also affected. Meanwhile, there were few changes of relative rCBF in the basal frontal lobes during both sedated and anesthetized states.

Conclusions
As in earlier studies using normal subjects, pronounced suppression in rCBF in the brain stem reticular formation, the thalamus, and the parietal association cortex occurred even in severely depressed patients. However, previously reported decreases in rCBF in the basal frontal lobe were absent in depressed patients.
Hypothermia Does Not Alter Somatosensory Evoked Potential Amplitude and Global Cerebral Oxygen Extraction during Marked Sodium Nitroprusside–induced Arterial Hypotension
Authors: Kottenberg-Assenmacher Eva , Armbruster Wolf , Bornfeld Norbert , Peters Jürgen 
Published: November 2003

Background
To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia.

Methods
Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo(2)) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32 degrees C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma.

Results
Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 microV, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo(2), arterial-jugular bulb oxygen content difference, or lactate concentration.

Conclusions
Thus, hypothermia to 32 degrees C does not alter MN-SSEP amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension with a mean arterial pressure of 40 mmHg but prolongs MN-SSEP latencies during propofol-remifentanil anesthesia in individuals without cerebrovascular disease.
Peri-MAC Depression of a Nociceptive Withdrawal Reflex Is Accompanied by Reduced Dorsal Horn Activity with Halothane but not Isoflurane
Authors: Jinks Steven L. , Martin John T. , Carstens Earl , Jung Sung-Won , Antognini Joseph F. 
Published: November 2003

Background
Anesthetics act in the spinal cord to suppress movement evoked by a noxious stimulus, although the exact site is unknown.

Methods
This study investigated sensorimotor processing in hind limb withdrawal reflexes, and effects of two general anesthetics, halothane and isoflurane, on simultaneously recorded responses of single dorsal horn neurons and hind limb withdrawal force, elicited by graded noxious thermal hind paw stimulation in rats. Minimum alveolar anesthetic concentration (MAC) needed to block gross movement to a supra-maximal mechanical stimulus was determined for each animal.

Results
Between 0.9 and 1.1 MAC, halothane and isoflurane greatly reduced or abolished withdrawal force (79 and 89% reduction, respectively). Halothane (0.75-1.4 MAC) depressed heat-evoked neuronal responses in a concentration-related manner (41% reduction between 0.9 and 1.1 MAC averaged across all stimulus temperatures, P < 0.05) and decreased stimulus-response function slopes, with corresponding reductions in withdrawal force. In contrast, isoflurane did not reduce neuronal responses in the 0.75-1.4 MAC range and slightly facilitated responses (by 16%) when concentration increased from 0.9 to 1.1 MAC, despite a concurrent withdrawal force reduction. Anesthetic depression of heat-evoked withdrawal force correlated well with MAC determination using a supra-maximal mechanical stimulus. At sub-MAC anesthetic concentrations, some units exhibited firing rate changes that preceded and paralleled moment-to-moment changes in force during a given withdrawal.

Conclusions
Halothane reduces noxious-evoked movement at least partly via depression of dorsal horn neurons, whereas isoflurane suppresses movement by an action at more ventral sites in the spinal cord.
Potentiation of Proopiomelanocortin Gene Expression in Cultured Pituitary Cells by Benzodiazepines
Authors: Fukuda Kazuhiko , Uetsuki Nobuo , Uga Hisatoshi , Hashiguchi Mitsuko , Sato Masami , Hisano Taizo , Segawa Hajime , Iwasaki Yasumasa 
Published: November 2003

Background
Benzodiazepines are frequently used not only as a part of general anesthesia but also for the purpose of sedation during regional anesthesia. Effects of these drugs on the hypothalamic-pituitary-adrenal axis activity have been studied, but are still controversial. It is not known whether benzodiazepines affect expression of proopiomelanocortin, precursor protein of adrenocorticotropic hormone and related peptides.

Methods
AtT20PL cell line, a clone of AtT20/D16v mouse corticotroph tumor cells stably transfected with approximately 0.7 kilobases (kb) of the rat proopiomelanocortin 5' promoter-luciferase fusion gene, was used. In the presence or absence of diazepam or midazolam, cells were stimulated by corticotropin-releasing hormone (CRH) or forskolin. Proopiomelanocortin gene expression was estimated by measurement of luciferase activity. Furthermore, to study the mechanism of benzodiazepine effects, cyclic adenosine 3',5'-monophosphate (cyclic AMP) efflux was measured by enzyme immunoassay.

Results
Diazepam and midazolam dose-dependently increased the proopiomelanocortin gene expression induced by CRH or forskolin. The potentiating effect was not affected by benzodiazepine receptor antagonists flumazenil and PK11195, but was abolished by a cyclic AMP-dependent protein kinase inhibitor H89. Cyclic AMP efflux induced by CRH or forskolin was also enhanced by diazepam and midazolam. In the presence of isobutylmethylxanthine, a nonspecific phosphodiesterase inhibitor, potentiation of proopiomelanocortin gene expression and enhancement of cyclic AMP efflux by benzodiazepines were not observed.

Conclusions
Benzodiazepines potentiate the effect of CRH or forskolin on proopiomelanocortin gene expression. The potentiating effect is not mediated by the benzodiazepine receptors, but its mechanism probably involves inhibition of phosphodiesterase.
Propofol Suppresses Macrophage Functions and Modulates Mitochondrial Membrane Potential and Cellular Adenosine Triphosphate Synthesis
Authors: Chen Ruei-Ming , Wu Chih-Hsiung , Chang Huai-Chia , Wu Gong-Jhe , Lin Yi-Ling , Sheu Joen-Rong , Chen Ta-Liang 
Published: November 2003

Background
Propofol is an intravenous anesthetic agent that may impair host defense system. The aim of this study was to evaluate the effects of propofol on macrophage functions and its possible mechanism.

Methods
Mouse macrophage-like Raw 264.7 cells were exposed to propofol, at 3, 30 (a clinically relevant concentration), and 300 microm. Cell viability, lactate dehydrogenase, and cell cycle were analyzed to determine the cellular toxicity of propofol to macrophages. After administration of propofol, chemotactic, phagocytic, and oxidative ability and interferon-gamma mRNA production were carried out to validate the potential effects of propofol on macrophage functions. Mitochondrial membrane potential and cellular adenosine triphosphate levels were also analyzed to evaluate the role of mitochondria in propofol-induced macrophage dysfunction.

Results
Exposure of macrophages to 3 and 30 microm propofol did not affect cell viability. When the administered concentration reached 300 microm, propofol would increase lactate dehydrogenase release, cause arrest of cell cycle in G1/S phase, and lead to cell death. In the 1-h-treated macrophages, propofol significantly reduced macrophage functions of chemotactic and oxidative ability in a concentration-dependent manner. However, the suppressive effects were partially or completely reversed after 6 and 24 h. Propofol could reduce phagocytic activities of macrophages in concentration- and time-dependent manners. Exposure of macrophages to lipopolysaccharide induced the mRNA of interferon-gamma, but the induction was significantly blocked by propofol. Propofol concentration-dependently decreased the membrane potential of macrophage mitochondria, but the effects were descended with time. The levels of cellular adenosine triphosphate in macrophages were also reduced by propofol.

Conclusions
A clinically relevant concentration of propofol can suppress macrophage functions, possibly through inhibiting their mitochondrial membrane potential and adenosine triphosphate synthesis instead of direct cellular toxicity.
GABAergic Interneurons at Supraspinal and Spinal Levels Differentially Modulate the Antinociceptive Effect of Nitrous Oxide in Fischer Rats
Authors: Orii Ryo , Ohashi Yoko , Halder Sunil , Giombini Mariangela , Maze Mervyn , Fujinaga Masahiko 
Published: November 2003

Background
The study hypothesizes that nitrous oxide (N(2)O) releases opioid peptide in the brain stem, which results in inhibition of gamma-aminobutyric acid-mediated (GABAergic) neurons that tonically inhibit the descending noradrenergic inhibitory neurons (DNIN), resulting in activation of DNIN. In the spinal cord, activation of DNIN leads to the release of norepinephrine, which inhibits nociceptive processing through direct activation of alpha2 adrenoceptor and indirect activation of GABAergic neurons through alpha1 adrenoceptor. Arising from this hypothesis, it follows that GABAergic neurons will modulate the antinociceptive effect of N(2)O in diametrically opposite directions at supraspinal and spinal levels. The authors have tested this tenet and further examined the effect of midazolam, a GABA-mimetic agent, on N(2)O-induced antinociceptive effect.

Methods
Adult male Fischer rats were administered muscimol (GABA(A) receptor agonist) intracerebroventricularly (icv), gabazine (GABA(A) receptor antagonist) intrathecally (intrathecal), or midazolam intraperitoneally (intraperitoneal). Fifteen minutes later, they were exposed to air or 75% N(2)O and were subjected to the plantar test after 30 min of gas exposure. In some animals administered with midazolam, gas exposure was continued for 90 min, and the brain and spinal cord were examined immunohistochemically.

Results
The N(2)O-induced antinociceptive effect, which was attenuated by icv muscimol, intrathecal gabazine, and intraperitoneal midazolam. Midazolam inhibited N(2)O-induced c-Fos expression (a marker of neuronal activation) in the pontine A7 and spinal cord.

Conclusions
The GABAergic neurons modulate the antinociceptive effect of N(2)O in opposite directions at supraspinal and spinal levels. The pronociceptive effects of enhancement at the supraspinal GABAergic site predominate in response to systemically administered midazolam.
Preconditioning by Sevoflurane Decreases Biochemical Markers for Myocardial and Renal Dysfunction in Coronary Artery Bypass Graft Surgery: A Double-blinded, Placebo-controlled, Multicenter Study
Authors: Julier Karine , da Silva Rafaela , Garcia Carlos , Bestmann Lukas , Frascarolo Philippe , Zollinger Andreas , Chassot Pierre-Guy , Schmid Edith R. , Turina Marko I. , von Segesser Ludwig K. , Pasch Thomas , Spahn Donat R. , Zaugg Michael 
Published: November 2003

Background
Preconditioning by volatile anesthetics is a promising therapeutic strategy to render myocardial tissue resistant to perioperative ischemia. It was hypothesized that sevoflurane preconditioning would decrease postoperative release of brain natriuretic peptide, a biochemical marker for myocardial dysfunction. In addition, several variables associated with the protective effects of preconditioning were evaluated.

Methods
Seventy-two patients scheduled for coronary artery bypass graft surgery under cardioplegic arrest were randomly assigned to preconditioning during the first 10 min of complete cardiopulmonary bypass with either placebo (oxygen-air mixture only) or sevoflurane 4 vol% (2 minimum alveolar concentration). No other volatile anesthetics were administered at any time during the study. Treatment was strictly blinded to anesthesiologists, perfusionists, and surgeons. Biochemical markers of myocardial dysfunction and injury (brain natriuretic peptide, creatine kinase-MB activity, and cardiac troponin T), and renal dysfunction (cystatin C) were determined. Results of Holter electrocardiography were recorded perioperatively. Translocation of protein kinase C was assessed by immunohistochemical analysis of atrial samples.

Results
Sevoflurane preconditioning significantly decreased postoperative release of brain natriuretic peptide, a sensitive biochemical marker of myocardial contractile dysfunction. Pronounced protein kinase C delta and epsilon translocation was observed in sevoflurane-preconditioned myocardium. In addition, postoperative plasma cystatin C concentrations increased significantly less in sevoflurane-preconditioned patients. No differences between groups were found for perioperative ST-segment changes, arrhythmias, or creatine kinase-MB and cardiac troponin T release.

Conclusions
Sevoflurane preconditioning preserves myocardial and renal function as assessed by biochemical markers in patients undergoing coronary artery bypass graft surgery under cardioplegic arrest. This study demonstrated for the first time translocation of protein kinase C isoforms delta and epsilon in human myocardium in response to sevoflurane.
Auricular Acupressure as a Treatment for Anxiety in Prehospital Transport Settings
Authors: Kober Alexander , Scheck Thomas , Schubert Barbara , Strasser Helmut , Gustorff Burkhard , Bertalanffy Petra , Wang Shu-Ming , Kain Zeev N. , Hoerauf Klaus 
Published: November 2003

Background
Auricular acupuncture at the relaxation point has been previously shown to be an effective treatment for anxiety in the preoperative setting. The purpose of this prospective, randomized, blinded study was to determine whether auricular acupressure can reduce stress and anxiety during ambulance transport.

Methods
Patients who required ambulance transport secondary to medical conditions were randomized to receive auricular acupressure at the relaxation point (n = 17) or at a sham point (n = 19). A visual analog scale was used to assess state anxiety as well as patient anticipation of hospital medical treatment (estimated waiting period for treatment, anticipated pain during treatment, attitude toward the physicians, and treatment outcomes). These variables were assessed at baseline and on arrival to the hospital.

Results
Patients in the relaxation group reported significantly less anxiety than patients in the sham group on arrival to the hospital (visual analog scale mean +/- SD: 37.6 +/- 20.6 to 12.4 +/- 7.8 mm vs. 42.5 +/- 29.9 to 46.7 +/- 25.9 mm, respectively; P = 0.002). Similarly, patient perception of pain during treatment (mean visual analog scale +/- SD: 32.7 +/- 27.7 to 14.5 +/- 8.1 mm vs. 17.2 +/- 26.1 to 28.8 +/- 21.9 mm, respectively; P = 0.006) and treatment outcomes of their illnesses (mean visual analog scale +/- SD: 46.7 +/- 29.4 to 19.1 +/- 10.4 mm vs. 35.0 +/- 25.7 to 31.5 +/- 20.5 mm, respectively; P = 0.014) were significantly more positive in the relaxation group than in the sham group. No differences were found in the other variables assessed.

Conclusion
It was concluded that auricular acupressure is an effective treatment for anxiety in prehospital emergency settings.
Terlipressin Versus Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors
Authors: Boccara Gilles , Ouattara Alexandre , Godet Gilles , Dufresne Eric , Bertrand Michèle , Riou Bruno , Coriat Pierre 
Published: November 2003

Background
Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients.

Methods
Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval).

Results
Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively.

Conclusions
In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.