bluuebunny/crossref_metadata_2025_split huggingface dataset:
Combinations of Morphine with Ketamine for Patient-controlled Analgesia
Authors: Sveticic Gorazd , Gentilini Andrea , Eichenberger Urs , Luginbühl Martin , Curatolo Michele 
Published: November 2003

Background
According to previous studies, the addition of ketamine to morphine for intravenous patient-controlled analgesia (PCA) may be beneficial. The authors developed and applied a new model to optimize the combination of morphine, ketamine, and a lockout interval for PCA after lumbar spine and hip surgery.

Methods
One-hundred two patients undergoing lumbar spine or hip surgery participated in the study. The analgesic effect of PCA during 48 h after surgery was optimized under restrictions dictated by side effects. Initially, eight combinations of morphine, ketamine (expressed as drug concentration in the solution administered), and a lockout interval (i.e., minimal allowed time between two consecutive PCA boluses) were empirically chosen and investigated. To determine subsequent combinations, an optimization model was applied until three consecutive steps showed no decrease in pain score.

Results
The authors analyzed 12 combinations with an allowed morphine and ketamine range in a PCA solution of 0-2 mg/ml and a lockout interval range of 5-12 min. During the optimization procedure, a reduction in mean pain scores with a low incidence of side effects was observed. The procedure converged to a morphine-to-ketamine ratio of 1:1 and a lockout interval of 8 min.

Conclusions
Using a novel method to analyze drug combinations, the study supports combinations of morphine with ketamine in a ratio of 1:1 and a lockout interval of 8 min for postoperative PCA following spine and hip surgery.
Piriformis Syndrome
Authors: Benzon Honorio T. , Katz Jeffrey A. , Benzon Hubert A. , Iqbal Muhammad S. 
Published: November 2003

Background
Piriformis syndrome can be caused by anatomic abnormalities. The treatments of piriformis syndrome include the injection of steroid into the piriformis muscle and near the area of the sciatic nerve. These techniques use either fluoroscopy and muscle electromyography to identify the piriformis muscle or a nerve stimulator to stimulate the sciatic nerve.

Methods
The authors performed a cadaver study and noted anatomic variations of the piriformis muscle and sciatic nerve. To standardize their technique of injection, they also noted the distance from the lower border of the sacroiliac joint (SIJ) to the sciatic nerve. They retrospectively reviewed the charts of 19 patients who had received piriformis muscle injections, noting the site of needle insertion in terms of the distance from the lower border of the SIJ and the depth of needle insertion at which the motor response of the foot was elicited. The authors tabulated the response of the patients to the injection, any associated diagnoses, and previous treatments that these patients had before the injection. Finally, they reviewed the literature on piriformis syndrome, a rare cause of buttock pain and sciatica.

Results
In the cadavers, the distance from the lower border of the SIJ to the sciatic nerve was 2.9 +/- 0.6 (1.8-3.7) cm laterally and 0.7 +/- 0.7 (0.0-2.5) cm caudally. In 65 specimens, the sciatic nerve passed anterior and inferior to the piriformis. In one specimen, the muscle was bipartite and the two components of the sciatic nerve were separate, with the tibial nerve passing below the piriformis and the peroneal nerve passing between the two components of the muscle. In the patients who received the injections, the site of needle insertion was 1.5 +/- 0.8 (0.4-3.0) cm lateral and 1.2 +/- 0.6 (0.5-2.0) cm caudal to the lower border of the SIJ as seen on fluoroscopy. The needle was inserted at a depth of 9.2 +/- 1.5 (7.5-13.0) cm to stimulate the sciatic nerve. Patients had comorbid etiologies including herniated disc, failed back surgery syndrome, spinal stenosis, facet syndrome, SIJ dysfunction, and complex regional pain syndrome. Sixteen of the 19 patients responded to the injection, their improvements ranged from a few hours to 3 months.

Conclusions
Anatomic abnormalities causing piriformis syndrome are rare. The technique used in the current study was successful in injecting the medications near the area of the sciatic nerve and into the piriformis muscle.
Large-dose Hydroxyethyl Starch 130/0.4 Does Not Increase Blood Loss and Transfusion Requirements in Coronary Artery Bypass Surgery Compared with Hydroxyethyl Starch 200/0.5 at Recommended Doses
Authors: Kasper Stefan-Mario , Meinert Philipp , Kampe Sandra , Görg Christoph , Geisen Christof , Mehlhorn Uwe , Diefenbach Christoph 
Published: November 2003

Background
Hydroxyethyl starch (HES) 130/0.4 may impair blood coagulation less than other HES solutions and, thus, may be used at larger doses without increasing the risk of postoperative bleeding. This study tested the hypothesis that volume replacement with 6% HES 130/0.4 at a dose of up to 50 ml/kg does not increase blood loss and transfusion requirements in elective coronary artery bypass surgery compared with 6% HES 200/0.5 at a dose of up to 33 ml/kg.

Methods
One hundred twenty adult patients scheduled for elective coronary artery bypass surgery were randomized to receive up to 50 ml/kg of 6% HES 130/0.4 or up to 33 ml/kg of 6% HES 200/0.5 for volume replacement during surgery and until 24 h thereafter. Volume requirements in excess of the respective maximum dose of HES were treated with gelatin. Colloid use was at the discretion of the attending physicians and not dictated by protocol. The primary outcome variable was chest tube drainage volume during the first 24 h after surgery.

Results
The data from 117 patients (HES 130/0.4, 59 patients; HES 200/0.5, 58 patients) who completed the study according to protocol were analyzed. The median volumes of HES administered were 49 and 33 ml/kg in the HES 130/0.4 and HES 200/0.5 groups, respectively (P < 0.001). Consequently, patients in the HES 130/0.4 group required less gelatin in addition to HES than those in the HES 200/0.5 group (medians: 7 ml/kg vs. 20 ml/kg, P < 0.001). The combined volumes of HES and gelatin were similar for both groups (P = 0.21). The 24-h chest tube drainage (medians: 660 ml vs. 705 ml, P = 0.60) did not differ significantly between the groups, nor did transfusion outcome.

Conclusion
Six percent HES 130/0.4 at a median dose of 49 ml/kg did not increase blood loss and transfusion requirements in coronary artery bypass surgery compared with 6% HES 200/0.5 at a median dose of 33 ml/kg.
Translocation of Protein Kinase C Isoforms to Subcellular Targets in Ischemic and Anesthetic Preconditioning
Authors: Uecker Marina , da Silva Rafaela , Grampp Thomas , Pasch Thomas , Schaub Marcus C. , Zaugg Michael 
Published: November 2003

Background
Translocation of protein kinase C (PKC) to subcellular targets is a pivotal signaling step in ischemic preconditioning (IPC). However, to date, it is unknown whether PKC isoforms translocate in anesthetic preconditioning (APC).

Methods
The PKC blockers chelerythrine and rottlerin and the adenosine triphosphate-dependent potassium (K(ATP)) channel blockers HMR-1098 and 5-hydroxydecanoate were used to assess the role of PKC and K(ATP) channels in isolated perfused rat hearts subjected to IPC or APC (1.5 minimum alveolar concentration isoflurane) followed by 40 min of ischemia and 30 min of reperfusion. Immunohistochemical techniques were used to visualize PKC translocation after preconditioning. In addition, the phosphorylation status of PKC isoforms was assessed.

Results
Chelerythrine, rottlerin, and 5-hydroxydecanoate blocked IPC and APC with respect to functional recovery, albeit IPC at higher concentrations. HMR-1098 did not affect IPC or APC. PKCdelta and PKCepsilon translocated to nuclei in both IPC and APC, which was inhibited by chelerythrine and rottlerin. PKCdelta translocated to mitochondria but not to the sarcolemma, and PKCepsilon translocated to the sarcolemma and intercalated disks but not to mitochondria. Interestingly, PKCepsilon was accumulated at the intercalated disks in control and preconditioned hearts. Phosphorylation of PKCdelta on serine643 was increased in IPC and APC and blocked by chelerythrine and rottlerin, whereas phosphorylation of PKCdelta on threonine505 was increased only in IPC and not blocked by chelerythrine or rottlerin. PKCepsilon on serine729 did not change its phosphorylation status.

Conclusions
This study indicates that translocation of PKCdelta plays a pivotal role in IPC and APC and suggests that phosphorylation of PKCdelta on serine643 may be of particular relevance in transferring the APC stimulus to mitochondrial K(ATP) channels.
Laryngeal Resistance before and after Minor Surgery
Authors: Tanaka Atsuko , Isono Shiroh , Ishikawa Teruhiko , Sato Jiro , Nishino Takashi 
Published: November 2003

Background
The placement of an endotracheal tube (ETT) may promote laryngeal swelling, which is an important cause of upper airway obstruction after extubation. The authors hypothesized that laryngeal swelling after ETT placement increases laryngeal resistance and tested that hypothesis by comparing postoperative laryngeal patency between patients with ETT placement and those with a Laryngeal Mask Airway trade mark (LMA).

Methods
Fourteen adult patients who underwent elective minor surgeries were randomly allocated to two groups whose airway would be managed through ETTs (the ETT group) or LMAs (the LMA group) during the surgery. While maintaining at sevoflurane 1 minimum alveolar concentration, the authors measured laryngeal resistance before and after surgery, during both spontaneous breathing and mechanical ventilation under complete paralysis. In addition, they endoscopically measured the vocal cord angle under complete paralysis.

Results
In association with marked swelling of the vocal cords, the vocal cord angle significantly decreased after surgery in the ETT group, whereas the angle did not change in the LMA group. Laryngeal resistance during mechanical ventilation significantly increased only in the ETT group. Laryngeal resistance during spontaneous breathing significantly increased after surgeries in both groups.

Conclusions
Postoperative laryngeal resistance increases at least in part because of laryngeal swelling in patients with ETT placement, whereas alteration of laryngeal neural control mechanisms has been also indicated. The use of the LMA trade mark has an advantage over ETT placement in order to avoid postoperative laryngeal swelling.
Short- and Long-term Prognostic Value of Postoperative Cardiac Troponin I Concentration in Patients Undergoing Coronary Artery Bypass Grafting
Authors: Fellahi Jean-Luc , Gué Xavier , Richomme Xavier , Monier Emmanuel , Guillou Louis , Riou Bruno 
Published: November 2003

Background
The value of postoperative cardiac troponin I (cTnI) has been shown to indicate a higher risk of in-hospital death after cardiac surgery. The authors therefore assessed the long-term prognostic value of cTnI in patients undergoing elective coronary artery bypass grafting.

Methods
Consecutive patients (n = 202) were included and divided into two groups according to the postoperative value of cTnI (< or >/= 13 ng/ml). In-hospital mortality and nonfatal cardiac events (delayed extubation > 24 h; postoperative requirement of inotropic agent; ventricular and supraventricular arrhythmia; postoperative myocardial infarction) were recorded. Survivors were then followed up over a 2-yr period. Data are median and odds ratio (95% confidence interval).

Results
Of all patients, 174 (86%) had a low cTnI (4.1 ng/ml; range, 1.1-12.6) and 28 (14%) had a high cTnI (23.8 ng/ml; range, 13.4-174.6). In-hospital mortality was not significantly different (4 vs. 2%), whereas long-term mortality (18 vs. 3%, P = 0.006) and mortality from cardiac cause (18 vs. 1%, P < 0.001) was greater in patients with a high cTnI. A high cTnI was a significant factor predicting death (odds ratio, 7.3 [2.0-27.1]) or death from cardiac causes (odds ratio, 37.4 [4.2-334.4]). Nonfatal cardiac events were also more frequent in the hospital (64 vs. 41%, P = 0.02) and within the 2-yr follow-up period (39% vs. 16%, P = 0.03) in patients with high cTnI.

Conclusion
A high postoperative peak of cTnI is associated with increased risk of death, death from cardiac causes, and nonfatal cardiac events within 2 yr after coronary artery bypass grafting.
Thiopental Inhibits Tumor Necrosis Factor α–induced Activation of Nuclear Factor κB through Suppression of IκB Kinase Activity
Authors: Loop Torsten , Humar Matjaz , Pischke Soeren , Hoetzel Alexander , Schmidt Rene , Pahl Heike L. , Geiger Klaus K. , Pannen Benedikt H. J. 
Published: November 2003

Background
Thiopental is frequently used for the treatment of intracranial hypertension after severe head injury and is associated with immunosuppressive effects. The authors have recently reported that thiopental inhibits activation of nuclear factor (NF) kappaB, a transcription factor implicated in the expression of many inflammatory genes. Thus, it was the aim of the current study to examine the molecular mechanism of this inhibitory effect.

Methods
The authors tested gamma-aminobutyric acid (GABA), the GABA(A) antagonist bicuculline, and the GABA(B) antagonist dichlorophenyl-methyl-amino-propyl-diethoxymethyl-phosphinic acid (CGP 52432) in combination with thiopental for their influence on the activation of NF-kappaB. In addition, they investigated the direct effect of thiopental on activated NF-kappaB DNA binding activity. These experiments were conducted in Jurkat T lymphocytes using electrophoretic mobility shift assays. The presence of the phosphorylated and dephosphorylated NF-kappaB inhibitor IkappaBalpha (Western blotting) and IkappaB kinase activity were studied in Jurkat T cells and human CD3+ T lymphocytes. In addition, the authors tested the effect of the structural barbiturate analog pairs thiopental-pentobarbital and thiamylal-secobarbital and of thiopental in combination with the thio-group containing chemical dithiothreitol on the activation of NF-kappaB.

Results
GABA did not inhibit NF-kappaB activation, and the GABA(A) and GABA(B) antagonists bicuculline and CGP did not diminish the thiopental-mediated inhibitory effect on NF-kappaB activation. Thiopental did not inhibit activated NF-kappaB directly in a cell-free system. The phosphorylation of IkappaBalpha was prevented after incubation with 1,000 microg/ml thiopental. The same concentration of thiopental also inhibited IkappaB kinase activity in tumor necrosis factor-stimulated Jurkat T cells and human CD3+ T lymphocytes (60% suppression, P < 0.05 vs. tumor necrosis factor alpha alone). Thiobarbiturates (4 x 10(-3) m) inhibited NF-kappaB activity, whereas equimolar concentrations of the structural oxyanalogs did not. Preincubation of thiopental with dithiothreitol diminished the inhibitory effect.

Conclusion
Thiopental-mediated inhibition of NF-kappaB activation is due to the suppression of IkappaB kinase activity and depends at least in part on the thio-group of the barbiturate molecule.
Neuroprotective Effects of Propofol in a Model of Ischemic Cortical Cell Cultures
Authors: Velly Lionel J. , Guillet Benjamin A. , Masmejean Frederique M. , Nieoullon André L. , Bruder Nicolas J. , Gouin François M. , Pisano Pascale M. 
Published: November 2003

Background
During cerebral ischemia, excess of glutamate release and dysfunction of its high affinity transport induce an accumulation of extracellular glutamate, which plays an important role in neuronal death. The authors studied the relationship among propofol neuroprotection, glutamate extracellular concentrations, and glutamate transporter activity in a model of ischemic cortical cell cultures.

Methods
Thirteen-day-old primary cortical neuronal-glial cultures were exposed to a 90-min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber, followed by reoxygenation. Propofol was added only during the OGD period, and its effect was compared to that of the N-methyl-d-aspartate receptor antagonist dizocilpine (MK-801). Twenty-four hours after the injury, cell death was quantified by lactate dehydrogenase release and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). Extracellular concentrations of glutamate in culture supernatants and glutamate uptake were performed at the end of OGD period by high-performance liquid chromatography and incorporation of l-[3H]glutamate into cells, respectively.

Results
At clinically relevant concentrations (0.05-10 microm), propofol offered protection equivalent to that of MK-801. It significantly reduced lactate dehydrogenase release and increased the reduction of MTT. At the end of the ischemic injury, propofol was able to reverse the OGD-induced increase in glutamate extracellular concentrations and decrease of glutamate uptake. The inhibition of the glial GLT1 transporter by 3-methyl-glutamate did not further modify the effect of propofol on glutamate uptake, suggesting that GLT1 was not the major target of propofol.

Conclusion
Propofol showed a neuroprotective effect in this in vitro model of OGD, which was apparently mediated by a GLT1-independent restoration of the glutamate uptake impaired during the injury.
G-protein Activation Decreases Isoflurane Inhibition of N-type Ba2+Currents
Authors: Nikonorov Igor M. , Blanck Thomas J. J. , Recio-Pinto Esperanza 
Published: November 2003

Background
G-protein activation mediates inhibition of N-type Ca2+ currents. Volatile anesthetics affect G-protein pathways at various levels, and activation of G-proteins has been shown to increase the volatile anesthetic potency for inhibiting the electrical-induced contraction in ileum. The authors investigated whether isoflurane inhibition of N-type Ba2+ currents was mediated by G-protein activation.

Methods
N-type Ba2+ currents were measured in the human neuronal SH-SY5Y cell line by using the whole cell voltage-clamp method.

Results
Isoflurane was found to have two effects on N-type Ba2+ currents. First, isoflurane reduced the magnitude of N-type Ba2+ currents to a similar extent (IC50 approximately 0.28 mm) in the absence and presence of GDPbetaS (a nonhydrolyzable GDP analog). Interestingly, GTPgammaS (a nonhydrolyzable GTP analog and G-protein activator) in a dose-dependent manner reduced the isoflurane block; 120 microm GTPgammaS completely eliminated the block of 0.3 mm isoflurane and reduced the apparent isoflurane potency by approximately 2.4 times (IC50 approximately 0.68 mm). Pretreatment with pertussis toxin or cholera toxin did not eliminate the GTPgammaS-induced protection against the isoflurane block. Furthermore, isoflurane reduced the magnitude of voltage-dependent G-protein-mediated inhibition of N-type Ba2+ currents, and this effect was eliminated by pretreatment with pertussis toxin or cholera toxin.

Conclusions
It was found that activation of G-proteins in a neuronal environment dramatically reduced the isoflurane potency for inhibiting N-type Ba2+ currents and, in turn, isoflurane affected the G-protein regulation of N-type Ba2+ currents.
Reactive Oxygen Species Precede the ε Isoform of Protein Kinase C in the Anesthetic Preconditioning Signaling Cascade
Authors: Novalija Enis , Kevin Leo G. , Camara Amadou K.S. , Bosnjak Zeljko J. , Kampine John P. , Stowe David F. 
Published: November 2003

Background
Protein kinase C (PKC) and reactive oxygen species (ROS) are known to have a role in anesthetic preconditioning (APC). Cardiac preconditioning by triggers other than volatile anesthetics, such as opioids or brief ischemia, is known to be isoform selective, but the isoform required for APC is not known. The authors aimed to identify the PKC isoform that is involved in APC and to elucidate the relative positions of PKC activation and ROS formation in the APC signaling cascade.

Methods
Isolated guinea pig hearts were subjected to 30 min of ischemia and 120 min of reperfusion. Before ischemia, hearts were either untreated or treated with sevoflurane (APC) in the absence or presence of the nonspecific PKC inhibitor chelerythrine, the PKC-delta inhibitor PP101, or the PKC-epsilon inhibitor PP149. Spectrofluorometry and the fluorescent probes dihydroethidium were used to measure intracellular ROS, and effluent dityrosine as used to measure extracellular ROS release.

Results
Previous sevoflurane exposure protected the heart against ischemia-reperfusion injury, as previously described. Chelerythrine or PP149 abolished protection, but PP101 did not. ROS formation was observed during sevoflurane exposure and was not altered by any of the PKC inhibitors.

Conclusions
APC is mediated by PKC-epsilon but not by PKC-delta. Furthermore, PKC activation probably occurs downstream of ROS generation in the APC signaling cascade.
Brachial Plexus Examination and Localization Using Ultrasound and Electrical Stimulation
Authors: Perlas Anahi , Chan Vincent W. S. , Simons Martin 
Published: November 2003

Background
Current techniques of brachial plexus block are "blind," and nerve localization can be frustrating and time consuming. Previous studies on ultrasound-assisted brachial plexus blocks are mostly performed with scanning probes of 10 MHz or less. The authors tested the usefulness of a state-of-the-art, high-resolution ultrasound probe (up to 12 MHz) in identifying the brachial plexus in five locations of the upper extremity and in guiding needle advancement to target before nerve stimulation.

Methods
In this prospective observational study, 15 volunteers underwent brachial plexus examination using an L12-L5 MHz probe and a Philips-ATL 5000 ultrasound unit in the interscalene, supraclavicular, infraclavicular, axillary, and midhumeral regions. Thereafter, an insulated block needle was advanced under direct ultrasound guidance to target nerves before confirmation by electrical nerve stimulation in five volunteers in each of the interscalene, supraclavicular, and axillary regions. The quality of brachial plexus images, anatomic variations, and the technique of needle advancement for nerve localization were recorded.

Results
The brachial plexus components were successfully identified in the transverse view as round to oval hypoechoic structures with small internal punctuate echos in all regions examined except the infraclavicular area (visualized in 27% of the cases). The authors' technique of advancing the needle in-line with the ultrasound beam allowed moment-by-moment observation of the needle shaft and tip movement at the time of nerve localization. Hypoechoic structures were stimulated electrically and confirmed to be nerves.

Conclusions
These preliminary data show that the high-resolution L12-L5 probe provides good quality brachial plexus ultrasound images in the superficial locations i.e., the interscalene, supraclavicular, axillary, and midhumeral regions. The needle technique described here for ultrasound-assisted nerve localization provides real-time guidance and is potentially valuable for brachial plexus blocks.