bluuebunny/crossref_metadata_2025_split huggingface dataset:
Uterine Cervical Afferents in Thoracolumbar Dorsal Root Ganglia Express Transient Receptor Potential Vanilloid Type 1 Channel and Calcitonin Gene–related Peptide, but Not P2X3 Receptor and Somatostatin
Authors: Tong Chuanyao , Conklin Dawn , Clyne Brittany B. , Stanislaus Jennifer D. , Eisenach James C. 
Published: March 2006

Background
Little is known regarding the phenotype of afferents that innervate the uterine cervix. Chronic estrogen sensitizes uterine cervical afferents to mechanical distension, but whether this reflects changes in afferent neurotransmitter or excitatory ion channel expression is unknown. The authors used immunocytochemistry to characterize uterine cervical afferents and the effects of estrogen on them.

Methods
Fluorogold was injected into the uterine cervix of intact rats (n = 7) and those with ovariectomy alone (n = 9) or with estrogen supplementation (n = 8). Bilateral dorsal root ganglia at T12-L2 were removed and immunostained for transient receptor potential vanilloid type 1 (TRPV1), P2X3 receptor, calcitonin gene-related peptide, and somatostatin. The proportion of fluorogold-traced dorsal root ganglion neurons expressing each of these markers was compared with untraced neurons.

Results
Most fluorogold-traced cells were found at L1 (> 55%) and were of small diameter (24 microm). TRPV1 expression was similar between traced and untraced cells, except the estrogen treatment increased TRPV1 expression in traced cells. Calcitonin gene-related peptide expression was greater in traced than in untraced cells, with no effect of experimental treatment. No traced cells expressed the P2X3 receptor or somatostatin, although each of these was present in untraced cells.

Conclusion
Uterine cervical afferents in the hypogastric nerve express TRPV1, an important nociceptive channel, which may play a role in estrogen-induced sensitization of cervical afferents. High expression of calcitonin gene-related peptide suggests a sensory and efferent role for this peptide. In contrast to other viscera, these afferents do not express somatostatin or P2X3 receptor, indicating a unique phenotype of these C fibers.
Prognosis Value of Plasma S100B Protein Levels after Subarachnoid Aneurysmal Hemorrhage
Authors: Weiss Nicolas , Sanchez-Peña Paola , Roche Sabine , Beaudeux Jean L. , Colonne Chantal , Coriat Pierre , Puybasset Louis 
Published: March 2006

Background
S100B has been described as a biologic marker of neuronal damage. The purpose of this study was to assess its prognostic value in patients with subarachnoid aneurysmal hemorrhage.

Methods
Seventy-four patients (32 men and 42 women; age, 48 +/- 11 yr) admitted within 48 h after subarachnoid hemorrhage onset and treated by surgical clipping or coiling within 2 days after admission were included. World Federation of Neurological Surgeons, Fisher, and Glasgow outcome scores at intensive care unit discharge and at 6 months were evaluated. Blood concentrations of S100B were determined at admission and daily up to day 8.

Results
The time course of S100B was increased in patients with high World Federation of Neurological Surgeons and Fisher scores. Patients who underwent surgical clipping had an S100B time course longer than that of those who underwent coiling. This difference remained true after stratification for World Federation of Neurological Surgeons and Fisher scores. The threshold of mean daily value of S100B predicting a poor outcome at 6 months was 0.4 microg/l (sensitivity = 0.50 [95% confidence interval (CI), 0.29-0.71], specificity = 0.87[corrected] [95% CI, 0.76-0.95]). In multivariate analysis, high World Federation of Neurological Surgeons score (odds ratio = 9.5 [95% CI, 3.1-29.4]), mean daily S100B value above 0.4 microg/l (odds ratio = 7.3 [95% CI, 2.3-23.6]), and age (odds ratio = 1.08 per year [95% CI, 1.01-1.15]) were independent predictors of a poor 6-month outcome (Glasgow outcome score 1-3).

Conclusion
Mean daily value of S100B assessed during the first 8 days is a prognostic tool complementary to initial clinical evaluation in subarachnoid hemorrhage patients.
Reversal of Rocuronium-induced Neuromuscular Block by the Selective Relaxant Binding Agent Sugammadex
Authors: Sorgenfrei Iben F. , Norrild Kathrine , Larsen Per Bo , Stensballe Jakob , Østergaard Doris , Prins Martine E. , Viby-Mogensen Jørgen 
Published: March 2006

Background
Sugammadex (Org 25969) forms a complex with steroidal neuromuscular blocking agents, thereby reversing neuromuscular block. This study investigated the dose-response relation, safety, and pharmacokinetics of sugammadex to reverse rocuronium-induced block.

Methods
Twenty-seven male surgical patients aged 18-64 yr were randomly assigned to receive placebo or sugammadex (0.5, 1.0, 2.0, 3.0, or 4.0 mg/kg) for reversal of 0.6 mg/kg rocuronium-induced neuromuscular block. Anesthesia was induced and maintained using intravenous fentanyl and propofol. Neuromuscular function was assessed using acceleromyography. Sugammadex or placebo was administered at reappearance of T2 of the train-of-four. The primary efficacy variable was the time required for recovery to a train-of-four ratio of 0.9.

Results
Sugammadex decreased median recovery time in a dose-dependent manner from 21.0 min in the placebo group to 1.1 min in the group receiving 4.0 mg/kg sugammadex. Doses of sugammadex of 2.0 mg/kg or greater reversed rocuronium-induced neuromuscular block within 3 min. A median of 59-77% of sugammadex was excreted unchanged in the urine within 16 h, mostly in the first 8 h. Sugammadex increased the proportion of the rocuronium dose excreted unchanged in the urine (from a median of 19% in the placebo group to 53% in the 4.0-mg/kg group within 16 h). Sugammadex was safe and well tolerated. No evidence of recurarization was observed in any patient.

Conclusion
At doses of 2.0 mg/kg or greater, sugammadex safely reversed 0.6 mg/kg rocuronium-induced neuromuscular block in a dose-dependent manner. Sugammadex enhanced renal excretion of rocuronium and was excreted unchanged by the kidneys.
Atlantoaxial Subluxation in Different Intraoperative Head Positions in Patients with Rheumatoid Arthritis
Authors: Tokunaga Daisaku , Hase Hitoshi , Mikami Yasuo , Hojo Tatsuya , Ikoma Kazuya , Hatta Yoichiro , Ishida Masashi , Sessler Daniel I. , Mizobe Toshiki , Kubo Toshikazu 
Published: March 2006

Background
Disorders of the cervical spine are often observed in patients with rheumatoid arthritis (RA). However, the best head position for RA patients with atlantoaxial subluxation in the perioperative period is unknown. This study investigated head position during general anesthesia for the patients with RA and proven atlantoaxial subluxation.

Methods
During anesthesia of patients with RA and proven atlantoaxial subluxation, the authors used fluoroscopy to obtain a lateral view of the upper cervical spine in four different positions: the mask position, the intubation position, the flat pillow position, and the protrusion position. Copies of the still fluoroscopic images were used to determine the anterior atlantodental interval, the posterior atlantodental interval, and the angle of atlas and axis (C1-C2 angle).

Results
The anterior atlantodental interval was significantly smaller in the protrusion position (2.3 mm) than in the flat pillow position (5.1 mm) (P < 0.05). The posterior atlantodental interval was significantly greater in the protrusion position (18.9 mm) than in the flat pillow position (16.2 mm) (P < 0.05). The C1-C2 angle was, on average, 9.3 degrees greater in the protrusion position than in the flat pillow position (P < 0.05).

Conclusion
This study showed that the protrusion position using a flat pillow and a donut-shaped pillow during general anesthesia reduced the anterior atlantodental interval and increased the posterior atlantodental interval in RA patients with atlantoaxial subluxation. This suggests that the protrusion position, which involves support of the upper cervical spine and extension at the craniocervical junction, might be advantageous for these patients.
Preoperative Evaluation of Extension Capacity of the Occipitoatlantoaxial Complex in Patients with Rheumatoid Arthritis
Authors: Takenaka Ichiro , Iwagaki Tamao , Aoyama Kazuyoshi , Ishimura Hiroshi , Kadoya Tatsuo 
Published: March 2006

Background
The authors devised a new method, the hyomental distance ratio (HMDR), for preoperatively identifying patients with a reduced occipitoatlantoaxial extension capacity, which was defined as the ratio of the hyomental distance in head extension position to that in the neutral position. They compared the accuracy of the HMDR with that of the Bellhouse test in 40 patients with rheumatoid arthritis.

Methods
Each patient wearing goggles on which a goniometer was mounted sat upright with the head in the neutral position and then extended the head maximally. The angle of the goggles and the hyomental distance were measured in the two head positions, and a lateral cervical radiograph was taken simultaneously. The Bellhouse angle was defined as a difference in the angles of the goggles between these positions.

Results
Median values of the radiologic occipitoatlantoaxial extension angle and the Bellhouse angle were 11.2 degrees and 24.9 degrees , respectively. In 21 of 40 patients, the radiologic occipitoatlantoaxial extension angle was less than 12 degrees (reduced occipitoatlantoaxial extension capacity). In these patients, extension of the median angle of 16.4 degrees occurred at the subaxial regions and was greater than that of 8.5 degrees in patients with a radiologic occipitoatlantoaxial extension angle of 12 degrees or more (P < 0.01). As a result, a strong relation between the Bellhouse angle and radiologic occipitoatlantoaxial extension angle was not established (P < 0.01, r = 0.48). In contrast, the HMDR correlated well with the radiologic occipitoatlantoaxial extension angle (P < 0.0001, r = 0.88). The areas under the receiver operating characteristic curve of the Bellhouse test and the HMDR were 0.72 and 0.95, respectively.

Conclusions
The HMDR was a good predictor of a reduced occipitoatlantoaxial extension capacity in patients with rheumatoid arthritis, but the Bellhouse test was not a clinically reliable method.
An Evaluation of Transcutaneous Carbon Dioxide Partial Pressure Monitoring during Apnea Testing in Brain-dead Patients
Authors: Vivien Benoîit , Marmion Frédéric , Roche Sabine , Devilliers Catherine , Langeron Olivier , Coriat Pierre , Riou Bruno 
Published: March 2006

Background
Diagnosis of brain death usually requires an arterial carbon dioxide partial pressure (Paco2) of 60 mmHg during the apnea test, but the increase in Paco2 is unpredictable. The authors evaluated whether transcutaneous carbon dioxide partial pressure (Ptcco2) monitoring during apnea test can predict that a Paco2 of 60 mmHg has been reached.

Methods
The authors compared Ptcco2 measured with a transcutaneous ear sensor (V-Sign Sensor, Sentec Digital Monitoring System; SENTEC-AG, Therwil, Switzerland) and Paco2 obtained from arterial blood gas measurements in 32 clinically brain-dead patients.

Results
In the first 20 patients, the mean Paco2-Ptcco2 gradient was 0.7 +/- 3.6 mmHg at baseline and 8.7 +/- 7.1 mmHg after 20 min of apnea. Using receiver operating characteristic curve analysis (area under the curve: 0.983 +/- 0.013), the best threshold value of Ptcco2 to predict that a Paco2 of 60 mmHg had been reached was 60 mmHg (positive predictive value: 1.00 [0.93-1.00]). In the following 12 patients investigated with use of this Ptcco2 target value of 60 mmHg, the mean duration of the apnea test (11 +/- 4 vs. 20 +/- 0 min; P < 0.001), hypercapnia (74.0 +/- 4.9 vs. 98.3 +/- 20.0 mmHg; P < 0.001), acidosis (pH: 7.18 +/- 0.06 vs. 7.11 +/- 0.08; P < 0.001), and decrease in arterial oxygen partial pressure (-47 +/- 44 vs. -95 +/- 89; P < 0.05) at the end of the test were reduced as compared with the 20-min apnea test group.

Conclusion
During the apnea test in brain-dead patients, a Ptcco2 of 60 mmHg accurately predicts that a Paco2 of 60 mmHg has been reached. This may allow a reduction in the duration of the apnea test and consecutively limit occurrence of complications.
Reversal of Profound Rocuronium Neuromuscular Blockade by Sugammadex in Anesthetized Rhesus Monkeys
Authors: de Boer Hans D. , van Egmond Jan , van de Pol Francien , Bom Anton , Booij Leo H. D. J. 
Published: March 2006

Background
Reversal of neuromuscular blockade can be accomplished by chemical encapsulation of rocuronium by sugammadex, a synthetic gamma-cyclodextrin derivative. The current study determined the feasibility of reversal of rocuronium-induced profound neuromuscular blockade with sugammadex in the anesthetized rhesus monkey using train-of-four stimulation.

Methods
Four female rhesus monkeys each underwent three experiments. In each experiment, first, a 100-microg/kg dose of rocuronium was injected and spontaneous recovery was monitored. After full recovery, a 500-microg/kg dose of rocuronium was injected. Up to this point, all three experiments in a single monkey were identical. One minute after this rocuronium injection, either one of the two tested dosages of sugammadex (1.0 or 2.5 mg/kg) was injected or saline was injected.

Results
Injection of 100 microg/kg rocuronium resulted in a mean neuromuscular blockade of 93.0% (SD = 4%), and profound blockade was achieved by injection of 500 microg/kg. In all experiments, a 100% neuromuscular blockade was achieved at this dose. After injection of the high rocuronium dose, the 90% recovery of the train-of-four ratio took 28 min (SD = 7 min) after saline, 26 min (SD = 9.5 min) after 1 mg/kg sugammadex, and 8 min (SD = 3.6 min) after 2.5 mg/kg sugammadex. Signs of residual blockade or recurarization were not observed. Injection of sugammadex had no significant effects on blood pressure or heart rate.

Conclusions
Chemical encapsulation of rocuronium by sugammadex is a new therapeutic mechanism allowing effective and rapid reversal of profound neuromuscular blockade induced by rocuronium in anesthetized rhesus monkeys.
Activation and Inhibition of Human Muscular and Neuronal Nicotinic Acetylcholine Receptors by Succinylcholine
Authors: Jonsson Malin , Dabrowski Michael , Gurley David A. , Larsson Olof , Johnson Edwin C. , Fredholm Bertil B. , Eriksson Lars I. 
Published: March 2006

Background
Succinylcholine is one of the most widely used muscle relaxants in clinical anesthesia and emergency medicine. Although the clinical advantages and cardiovascular side effects are well known, its mechanism of action within the human nicotinic cholinergic receptor system remains to be understood. The aim of this study was to investigate the effect of succinylcholine on human muscle and neuronal nicotinic acetylcholine receptor (nAChR) subtypes.

Methods
Xenopus laevis oocytes were injected with human messenger RNA for muscle and neuronal nAChR subunits. Receptor activation, desensitization, and inhibition induced by the natural ligand acetylcholine or by succinylcholine was studied using a multichannel two-electrode voltage clamp setup. Responses were measured as peak current and net charge.

Results
Succinylcholine concentration-dependently activated the muscle-type nAChR with an EC50 value of 10.8 microm (95% confidence interval, 9.8-11.9 microm), and after the initial activation, succinylcholine desensitized the muscle-type nAChR. Succinylcholine did not activate the neuronal nAChR subtypes alpha3beta2, alpha3beta4, alpha4beta2, or alpha7 at concentrations up to 1 mm and was a poor inhibitor at these receptor subtypes, with IC50 values above 100 microm.

Conclusion
Succinylcholine activates the muscle-type nAChR followed by desensitization. The observation that succinylcholine does not inhibit the presynaptic alpha3beta2 autoreceptor at clinically relevant concentrations provides a possible mechanistic explanation for the typical lack of tetanic fade in succinylcholine-induced neuromuscular blockade. Finally, cardiovascular side effects (e.g., tachyarrhythmias) of succinylcholine are not mediated via direct activation of the autonomic ganglionic alpha3beta4 subtype because succinylcholine does not activate the neuronal nAChRs.
Comparison of Arginine Vasopressin, Terlipressin, or Epinephrine to Correct Hypotension in a Model of Anaphylactic Shock in Anesthetized Brown Norway Rats
Authors: Dewachter Pascale , Jouan-Hureaux Valérie , Lartaud Isabelle , Bello Gaëlle , de Talancé Nicole , Longrois Dan , Mertes Paul Michel 
Published: March 2006

Background
Arginine vasopressin (AVP) and terlipressin were proposed as alternatives to catecholamines in shock states characterized by decreased plasma AVP concentrations. The endogenous plasma AVP profile in anaphylactic shock is unknown. In an ovalbumin-sensitized anesthetized anaphylactic shock rat model, the authors investigated (1) plasma AVP concentrations and (2) the dose versus mean arterial pressure response for exogenous AVP and terlipressin and compared them with those of epinephrine.

Methods
In a first series of rats (n = 12), endogenous plasma AVP concentrations were compared with a model of pharmacologically induced hypotension (nicardipine, n = 12). A second series was randomly assigned to three groups (AVP, n = 7; terlipressin, n = 7; epinephrine, n = 7) and dose (AVP: 8 doses, 0.03-100 U/kg; terlipressin: 7 doses, 0.03-30 microg/kg; epinephrine: 7 doses, 0.3-300 microg/kg)-response mean arterial pressure curves were plotted. Data are expressed as mean +/- SD.

Results
Endogenous plasma AVP concentrations were significantly lower in anaphylactic shock (57 +/- 26 pg/ml) than in the nicardipine group (91 +/- 43 pg/ml; P < 0.05). The ED50 was 10.6 microg/kg (95% confidence interval, 7.1-15.9) for epinephrine and 4.1 U/kg (95% confidence interval, 3.0-5.6) for AVP. Terlipressin did not change mean arterial pressure, regardless of the dose used.

Conclusions
In a rat model, anaphylactic shock is associated with inadequately low plasma AVP concentrations. For clinically relevant doses, AVP and epinephrine had comparable effects on mean arterial pressure and heart rate values, whereas, unexpectedly, terlipressin was ineffective. These results are consistent with reports in humans experiencing anaphylaxis where AVP injection restored arterial pressure.
The Well-being Model
Authors: Zanderigo Eleonora , Sartori Valentina , Sveticic Gorazd , Bouillon Thomas , Schumacher Peter , Morari Manfred , Curatolo Michele 
Published: March 2006

Background
Drugs are routinely combined in anesthesia and pain management to obtain an enhancement of the desired effects. However, a parallel enhancement of the undesired effects might take place as well, resulting in a limited therapeutic usefulness. Therefore, when addressing the question of optimal drug combinations, side effects must be taken into account.

Methods
By extension of a previously published interaction model, the authors propose a method to study drug interactions considering also their side effects. A general outcome parameter identified as patient's well-being is defined by superposition of positive and negative effects. Well-being response surfaces are computed and analyzed for varying drugs pharmacodynamics and interaction types. In particular, the existence of multiple maxima and of optimal drug combinations is investigated for the combination of two drugs.

Results
Both drug pharmacodynamics and interaction type affect the well-being surface and the deriving optimal combinations. The effect of the interaction parameters can be explained in terms of synergy and antagonism and remains unchanged for varying pharmacodynamics. For all simulations performed for the combination of two drugs, the presence of more than one maximum was never observed.

Conclusions
The model is consistent with clinical knowledge and supports previously published experimental results on optimal drug combinations. This new framework improves understanding of the characteristics of drug combinations used in clinical practice and can be used in clinical research to identify optimal drug dosing.
Propofol Inhibits Phosphorylation of N -methyl-d-aspartate Receptor NR1 Subunits in Neurons
Authors: Kingston Seth , Mao Limin , Yang Lu , Arora Anish , Fibuch Eugene E. , Wang John Q. 
Published: March 2006

Background
Anesthetics may interact with ionotropic glutamate receptors to produce some of their biologic actions. Cellular studies reveal that the ionotropic glutamate receptors, N-methyl-D-aspartate receptors (NMDARs), can be phosphorylated on their NR1 subunits at the C-terminal serine residues, which is a major mechanism for the regulation of NMDAR functions. It is currently unknown whether anesthetics have any modulatory effects on NMDAR NR1 subunit phosphorylation.

Methods
The possible effect of a general anesthetic propofol on phosphorylation of NR1 subunits at serine 897 (pNR1S897) and 896 (pNR1S896) was detected in cultured rat cortical neurons.

Results
Propofol consistently reduced basal levels of pNR1S897 and pNR1S896 in a concentration-dependent manner. This reduction was rapid as the reliable reduction of pNR1S896 developed 1 min after propofol administration. Pretreatment of cultures with the protein phosphatase 2A inhibitors okadaic acid or calyculin A blocked the effect of propofol on the NR1 phosphorylation, whereas okadaic acid or calyculin A alone did not alter basal pNR1S897 and pNR1S896 levels. In addition, propofol decreased tyrosine phosphorylation of protein phosphatase 2A at tyrosine 307, resulting in an increase in protein phosphatase 2A activity. In the presence of propofol, the NMDAR agonist-induced intracellular Ca2+ increase was impaired in neurons with dephosphorylated NR1 subunits.

Conclusions
Together, these data indicate an inhibitory effect of a general anesthetic propofol on NMDAR NR1 subunit phosphorylation in neurons. This inhibition was mediated through a signaling mechanism involving activation of protein phosphatase 2A.
Xenon Impairs Neurocognitive and Histologic Outcome after Cardiopulmonary Bypass Combined with Cerebral Air Embolism in Rats
Authors: Jungwirth Bettina , Gordan M Lucia , Blobner Manfred , Schmehl Wolfgang , Kochs Eberhard F. , Mackensen G Burkhard 
Published: March 2006

Background
The neuroprotective properties of xenon may improve cerebral outcome after cardiac surgery using cardiopulmonary bypass (CPB). However, its disposition to expand gaseous bubbles that during CPB present as cerebral air emboli (CAE) could abolish any beneficial effect or even worsen cerebral outcome. Therefore, the authors studied the impact of xenon on neurologic, cognitive, and histologic outcome after CPB combined with CAE in rats.

Methods
With institutional review board approval, 40 rats were assigned to four groups (n = 10). In two CPB-CAE groups, rats were subjected to 90 min of normothermic CPB with 10 repetitively administered CAEs (0.3 microl/bolus). Rats in two sham groups were not exposed to CPB and CAE. Groups were further subdivided into xenon (56%; 20 min before, during, and 30 min after CPB) and nitrogen groups. Neurologic and cognitive function was tested until postoperative day 14, when cerebral infarct volumes were determined.

Results
Animals of the CPB-CAE groups showed transient deficits in gross neurologic function. Further, rats of the CPB-CAE-xenon group demonstrated impaired fine motor and cognitive performance persisting until postoperative day 14. Consistently, infarct volumes were larger in the CPB-CAE-xenon group compared with the CPB-CAE-nitrogen group (P = 0.03).

Conclusions
This is the first demonstration in which the neurologic effects of CAE have been examined in a rat model of CPB. Xenon exposure aggravated the neurologic dysfunction that is produced by CAE during CPB; potential neuroprotective effects of xenon may have been masked by the effects of xenon on CAE.