bluuebunny/crossref_metadata_2025_split huggingface dataset:
Addition of Sodium Bicarbonate to Lidocaine Decreases the Duration of Peripheral Nerve Block in the Rat
Authors: Sinnott Catherine J. , Garfield Joseph M. , Thalhammer Johannes G. , Strichartz Gary R. 
Published: November 2003

Background
Adding sodium bicarbonate to lidocaine to enhance its efficacy during peripheral nerve block is controversial. The authors studied the effect of adding sodium bicarbonate to lidocaine with and without epinephrine versus equivalent alkalinization by sodium hydroxide (NaOH) on onset, degree, and duration of peripheral nerve block.

Methods
Part I examined alkalinization by sodium bicarbonate versus NaOH to pH 7.8 on 0.5% lidocaine, with and without epinephrine (1:100,000), prepared from crystalline salt. Part II examined 0.5% and 1.0% commercial lidocaine solutions, with and without epinephrine, either unalkalinized or alkalinized with sodium bicarbonate or NaOH. With NaOH, pH was adjusted to 7.8, but with sodium bicarbonate, no pH adjustments were made to simulate clinical conditions.

Results
In part I, addition of either NaOH or sodium bicarbonate to 0.5% lidocaine without epinephrine produced a faster onset than did unalkalinized lidocaine, without effecting degree or duration of block. In solutions with epinephrine there were no differences in onset, degree, or duration between lidocaine alkalinized with sodium bicarbonate versus NaOH. In part II, addition of sodium bicarbonate or NaOH to 1.0% commercial lidocaine without epinephrine did not accelerate onset compared with the unalkalinized solution. However, adding sodium bicarbonate decreased the degree and duration of block by 25% and more than 50%, respectively, compared with lidocaine unalkalinized and alkalinized with NaOH. With epinephrine, sodium bicarbonate hastened onset without effecting degree and duration compared with the unalkalinized solution.

Conclusions
With 1% commercial lidocaine without epinephrine, sodium bicarbonate decreases the degree and duration of block. However, in solutions with epinephrine, sodium bicarbonate hastens onset, without effecting degree or duration.
Activation of μ- and δ-Opioid Receptors Causes Presynaptic Inhibition of Glutamatergic Excitation in Neocortical Neurons
Authors: Ostermeier Andreas M. , Schlösser Beate , Schwender Dirk , Sutor Bernd 
Published: November 2003

Background
The mechanism underlying the depressant effect of opioids on neuronal activity within the neocortex is still not clear. Three modes of action have been suggested: (1) inhibition by activation of postsynaptic potassium channels, (2) interaction with postsynaptic glutamate receptors, and (3) presynaptic inhibition of glutamate release. To address this issue, the authors investigated the effects of mu- and delta-receptor agonists on excitatory postsynaptic currents (EPSCs) and on membrane properties of neocortical neurons.

Methods
Intracellular recordings were performed in rat brain slices. Stimulus-evoked EPSCs mediated by different glutamate receptor subtypes were pharmacologically isolated, and opioids were applied by addition to the bathing medium. Possible postsynaptic interactions between glutamate and opioid receptors were investigated using microiontophoretic application of glutamate on neurons functionally isolated from presynaptic input.

Results
delta-Receptor activation by d-Ala2-d-Leu5-enkephalin (DADLE) reduced the amplitudes of EPSCs by maximum 60% in a naltrindole-reversible manner (EC50: 6-15 nm). In 30-40% of the neurons investigated, higher concentrations (0.1-1 micrometer) of DADLE activated small outward currents. The mu-receptor selective agonist d-Ala2-N-MePhe5-Gly5-ol-enkephalin (0.1-1 micrometer) depressed the amplitudes of EPSCs by maximum 30% without changes in postsynaptic membrane properties. In the absence of synaptic transmission, inward currents induced by microiontophoretic application of glutamate were not affected by DADLE.

Conclusions
Activation of mu- and delta-opioid receptors depresses glutamatergic excitatory transmission evoked in neocortical neurons by presynaptic inhibition. A weak activation of a postsynaptic potassium conductance becomes evident only at high agonist concentrations. There is no evidence for a postsynaptic interaction between glutamate and opioid receptors.
In Vitro Compound A Formation in a Computer-controlled Closed-circuit Anesthetic Apparatus
Authors: Versichelen Linda F. M. , Rolly Georges , Bouche Marie-Paule L. A. , Van Bocxlaer Jan F. P. , Struys Michel M. R. F. , Van der herten Catherine , De Leenheer André P. , Mortier Eric P. 
Published: November 2003

Background
Few data exist on compound A during sevoflurane anesthesia when using closed-circuit conditions and sodalime with modern computer-controlled liquid injection.

Methods
A PhysioFlex apparatus (Dräger, Lübeck, Germany) was connected to an artificial test lung (inflow approximately 160 ml/min carbon dioxide, outflow approximately 200 ml/min, simulating oxygen consumption). Ventilation was set to obtain an end-tidal carbon dioxide partial pressure (Petco2) approximately 40 mmHg. Canister inflow (T degrees in) and outflow (T degrees out) temperatures were measured. Fresh sodalime and charcoal were used. After baseline analysis, sevoflurane concentration was set at 2.1% end-tidal for 120 min. At baseline and at regular intervals thereafter, Petco2, end-tidal sevoflurane, T degrees in, and T degrees out were measured. For inspiratory and expiratory compound A determination, samples of 2-ml gas were taken. These data were compared with those of a classical valve-containing closed-circuit machine. Ten runs were performed in each set-up.

Results
Inspired compound A concentrations increased from undetectable to peak at 6.0 (SD 1.3) and 14.3 (SD 2.5) ppm (P < 0.05), and maximal temperature in the upper outflow part of the absorbent canister was 24.3 degrees C (SD 3.6) and 39.8 degrees C (SD 1.2) (P < 0.05) in the PhysioFlex and valve circuit machines, respectively. Differences between the two machines in compound A concentrations and absorbent canister temperature at the inflow and outflow regions were significantly different (P < 0.05) at all times after 5 min.

Conclusion
Compound A concentrations in the high-flow (70 l/min), closed-circuit PhysioFlex machine were significantly lower than in conventional, valve-based machines during closed-circuit conditions. Lower absorbent temperatures, resulting from the high flow, appear to account for the lower compound A formation.
Enflurane Directly Depresses Glutamate AMPA and NMDA Currents in Mouse Spinal Cord Motor Neurons Independent of Actions on GABAAor Glycine Receptors
Authors: Cheng Gong , Kendig Joan J. 
Published: November 2003

Background
The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors.

Methods
Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography.

Results
Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively.

Conclusions
Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.
Periischemic Cerebral Blood Flow (CBF) Does Not Explain Beneficial Effects of Isoflurane on Outcome from Near-complete Forebrain Ischemia in Rats
Authors: Mackensen G. Burkhard , Nellgård Bengt , Kudo Masaya , Sheng Huaxin , Pearlstein Robert D. , Warner David S. 
Published: November 2003

Background
Isoflurane improves outcome from near-complete forebrain ischemia in rats compared with fentanyl-nitrous oxide (N2O). Sympathetic ganglionic blockade with trimethaphan abolishes this beneficial effect. To evaluate whether anesthesia-related differences in cerebral blood flow (CBF) may explain these findings, this study compared regional CBF before, during, and after near-complete forebrain ischemia in rats anesthetized with either isoflurane (with and without trimethaphan) or fentanyl-nitrous oxide.

Methods
Fasted, normothermic isoflurane anesthetized Sprague-Dawley rats were prepared for near-complete forebrain ischemia (10 min of bilateral carotid occlusion and mean arterial pressure = 30 mmHg). After surgery, rats were anesthetized with either 1.4% isoflurane (with or without 2.5 mg of trimethaphan intravenously at onset of ischemia) or fentanyl-nitrous oxide (25 microgram. kg-1. h-1. 70% N2O-1). Regional CBF was determined (14C-iodoantipyrine autoradiography) before ischemia, 8 min after onset of ischemia, and 30 min after onset of reperfusion.

Results
Regional CBF did not differ significantly among groups at any measurement interval. Ischemia caused a marked flow reduction to 5% or less of baseline (P < 0.001) in selectively vulnerable regions, such as the cortex, caudoputamen and hippocampus, whereas flow in the brain stem and cerebellum was preserved. Reperfusion at 30 min was associated with partial restoration of flow to 35-50% of baseline values in ischemic structures.

Conclusions
The results indicate that improved histologic-behavioral outcome provided by isoflurane anesthesia cannot be explained by differential vasodilative effects of the anesthetic states before, during, or after severe forebrain ischemia. This study also shows severe postischemic delayed hypoperfusion that was not affected by choice of anesthetic or the presence of trimethaphan. Mechanisms other than effects on periischemic CBF must be responsible for beneficial effects of isoflurane in this model.
Statistical Method for Predicting When Patients Should Be Ready on the Day of Surgery
Authors: Dexter Franklin , Traub Rodney D. 
Published: November 2003

Background
Previously, mathematical theory was developed for determining when a patient should be ready for surgery on the day of surgery. To apply this theory, a method is needed to predict the earliest start time of the case.

Methods
The authors calculated a time estimate such that the probability is 0.05 that the preceding case in the patient's operating room (OR) will be finished before the patient is ready for surgery. This implies there will be a 5% risk of OR personnel being idle and waiting for the patient. This 0. 05 value was chosen by considering the relative cost valuation of an average patient's time to that of an average surgical team based on national salary data. Case duration data from a surgical services information system were used to test different statistical methods to estimate earliest start times.

Results
Simulations found that 0.05 prediction bounds, calculated assuming case durations followed log-normal distributions, achieved actual risks for the OR staff to wait for patients of 0.050 to 0.053 (SEM = 0.001). Nonparametric prediction bounds performed no better than the parametric method. Having patients ready a fixed number of hours before the scheduled starts of their operations is not reliable. If the preceding case in an OR had been underway for 0.5 to 1.5 h, the parametric 0.05 prediction bounds for the time remaining achieved actual risks for OR staff waiting of 0.055 to 0.058 (SEM = 0.001).

Conclusion
The earliest start time of a case can be estimated using the 0.05 prediction bound for the duration of the preceding case. The authors show 0.05 prediction bounds can be estimated accurately assuming that case durations follow log-normal distributions.
Dilutional Acidosis following Hetastarch or Albumin in Healthy Volunteers
Authors: Waters Jonathan H. , Bernstein Clifford A. 
Published: November 2003

Background
The intent of this study was to evaluate the impact of the commonly used colloids-hetastarch and albumin-on in vivo acid-base balance. From this evaluation, a better understanding of the mechanism of dilutional acidosis was expected.

Methods
In a prospective, randomized fashion, 11 healthy volunteers were administered 15 ml/kg hetastarch solution, 6%, or 15 ml/kg albumin, 5%, intravenously over 30 min. Four weeks later, the study subjects were administered the other colloid. Arterial blood gas and electrolyte parameters were measured at baseline and at 30, 60, 90, 120, 210, and 300 min after colloid administration. Pre- and postlaboratory values were compared within groups using a paired t test and a Wilcoxon signed rank test and between groups using repeated-measures analysis of variance and a Wilcoxon rank sum test.

Results
Thirty min after infusion, subjects who were administered hetastarch showed statistically significant changes (P < 0.05) in base excess (from 2.5 +/- 0.9 mEq/l to 0.7 +/- 1.1 mEq/l), HCO3- concentration (from 27 +/- 1.0 mEq/l to 25 +/- 1.3 mEq/l), Cl- concentration (from 108 +/- 2 mEq/l to 112 +/- 2 mEq/l), albumin concentration (from 4.4 +/- 0.2 g/dl to 3.5 +/- 0.5 g/dl), and arterial carbon dioxide tension (Paco2; from 40.8 +/- 2.3 mmHg to 39. 2 +/- 3.2 mmHg), whereas only the albumin concentration (from 4.4 +/- 0.2 g/dl to 4.8 +/- 0.6 g/dl) changed significantly in the albumin-treated group.

Conclusions
Decreases in base excess were observed for 210 min after hetastarch administration but not after albumin. The mechanism for this difference is discussed.
Inhaled Albuterol, but Not Intravenous Lidocaine, Protects Against Intubation-induced Bronchoconstriction in Asthma
Authors: Maslow Andrew D. , Regan Meredith M. , Israel Elliot , Darvish Amir , Mehrez Mary , Boughton Robert , Loring Stephen H. 
Published: November 2003

Background
The ability of intravenous lidocaine to prevent intubation-induced bronchospasm is unclear. The authors performed a prospective, randomized, double-blind, placebo-controlled trial to test the ability of intravenous lidocaine and inhaled albuterol to attenuate airway reactivity after tracheal intubation in asthmatic patients undergoing general anesthesia.

Methods
Sixty patients were randomized to receive either 1.5 mg/kg intravenous lidocaine or saline, 3 min before tracheal intubation. An additional 50 patients were randomized to receive 4 puffs of inhaled albuterol or placebo 15-20 min before tracheal intubation. Anesthesia was induced with propofol. Immediately after intubation and at 5-min intervals, transpulmonary pressure and airflow were recorded, and lower pulmonary resistance (RL) was calculated. Isoflurane was administered after the initial two measurements to assess reversibility of bronchoconstriction. A bronchoconstrictor response to intubation was defined as RL greater than or equal to 5 cm H2O. l-1. s-1 in the first two measurements after intubation and RL subsequently decreasing by 50% or more after isoflurane.

Results
The lidocaine and placebo groups were not different in the peak RL before administration of isoflurane (8.2 cm H2O. l-1. s-1 vs. 7.6 cm H2O. l-1. s-1) or frequency of airway response to intubation (lidocaine 6 of 30 vs. placebo 5 of 27). In contrast, the albuterol group had lower peak RL (5.3 cm H2O. l-1. s-1 vs. 8.9 cm H2O. l-1. s-1; P < 0.05) and a lower frequency of airway response (1 of 25 vs. 8 of 23; P < 0.05) than the placebo group.

Conclusions
Inhaled albuterol blunted airway response to tracheal intubation in asthmatic patients, whereas intravenous lidocaine did not.
Ventilator-associated Sinusitis
Authors: Souweine Bertrand , Mom Thierry , Traore Ousmane , Aublet-Cuvelier Bruno , Bret Laurent , Sirot Jacques , Deteix Patrice , Gilain Laurent , Boyer Louis 
Published: November 2003

Background
The efficacy of systemic antibiotics on the treatment of ventilator-associated infectious maxillary sinusitis (VAIMS) is debated. The objective of this study was to determine the etiologic diagnosis of VAIMS in patients receiving antibiotics.

Methods
Patients mechanically ventilated for more than or equal to 72 h, who had persistent fever while on antibiotics for more than or equal to 48 h, underwent computed tomography scan followed by transnasal puncture of involved maxillary sinuses. VAIMS was defined as follows: fever greater than or equal to 38 degrees C, radiographic signs (air fluid level or opacification of maxillary sinuses on computed tomography scan), and a quantitative culture of sinus aspirate yielding more than or equal to 103 colony-forming units/ml.

Results
Twenty-four patients had radiographic signs of sinusitis. The mean +/- SD prior durations of mechanical ventilation and antibiotic exposure were 9.5 +/- 4.7 days and 6 +/- 4 days, respectively. Six unilateral and nine bilateral VAIMS were diagnosed in 15 patients. The median number of etiologic organisms per patient was two (range, one to four). The bacteriologic cultures yielded gram-positive bacteria (n = 21), gram-negative bacteria (n = 22), and yeasts (n = 5). Forty percent of causative agents were susceptible to the antibiotics prescribed. Seven patients with VAIMS developed 10 concomitant infections: ventilator-associated pneumonia (n = 5), urinary tract infection (n = 3), catheter infections (n = 2). In all cases of ventilator-associated pneumonia, the implicated agents were the causative agents of VAIMS.

Conclusion
In VAIMS patients on antibiotics, quantitative cultures of sinus aspirates may contribute to establish the diagnosis. The frequent recovery of microorganisms susceptible to the antimicrobial treatment administered suggests that therapy of VAIMS with systemic antibiotics may not be sufficient.
Compatibility of Different Colloid Plasma Expanders with Perflubron Emulsion
Authors: Nolte Dirk , Pickelmann Sven , Lang Michael , Keipert Peter , Messmer Konrad 
Published: November 2003

Background
Perfluorocarbon-based oxygen carriers have been proposed as an adjunct to autologous blood conservation techniques during elective surgery. To date, the effects of perfluorocarbon emulsions at the microcirculatory level have not been studied extensively. In this study the effects of perflubron emulsion on the microcirculation after acute normovolemic hemodilution (ANH) were investigated using different colloid plasma expanders.

Methods
The dorsal skin fold chamber model and intravital fluorescence microscopy were used for analysis of the microcirculation in the thin striated skin muscle of conscious hamsters (body weight, 40-60 g). Measurements of microvascular perfusion and leukocyte adhesion (n = 6 animals per experimental group) were made before and at 10, 30, and 60 min after ANH (to hematocrit 0.3) with either 6% hydroxyethyl starch 200/0.6 (HES), 3.5% gelatin, 5% human serum albumin (HSA), or 6% dextran 60 (DX-60) followed by intravenous injection of 3 ml/kg body weight of a 60% weight/volume perfluorocarbon emulsion based on perflubron (perfluorooctyl bromide) emulsified with egg yolk lecithin.

Results
Acute normovolemic hemodilution with HES, gelatin, or HSA followed by injection of perflubron emulsion elicited no alterations of local microvascular perfusion or leukocyte-endothelium interaction as assessed in arterioles and postcapillary venules. However, ANH with DX-60 followed by injection of perflubron emulsion led to a significant reduction of erythrocyte velocity in postcapillary venules and an increase in venular leukocyte sticking that was never observed with DX-60 alone.

Conclusions
Hydroxyethyl starch, gelatin, and HSA are compatible with perflubron emulsion in the setting of ANH. Only DX-60 appeared to be incompatible with perflubron emulsion, as evidenced by impairment of capillary perfusion.
Protection of Sensory Function and Antihyperalgesic Properties of a Prosaposin-derived Peptide in Diabetic Rats
Authors: Calcutt Nigel A. , Freshwater Jason D. , O’Brien John S. 
Published: November 2003

Background
Short-term diabetes causes sensory disorders in rats ranging from thermal hypoalgesia to exaggerated behavioral responses to other sensory stimuli. As impaired neurotrophic support may promote sensory nerve disorders during diabetes, the authors investigated whether TX14(A), a neurotrophic peptide derived from prosaposin, was able to ameliorate nerve disorders in diabetic rats.

Methods
TX14(A) was delivered by intraperitoneal or intrathecal injection to control or streptozotocin-diabetic rats in either single or multiple (three times weekly) dose regimens. Efficacy was measured against diabetes-induced disorders of sensory nerve conduction velocity, paw withdrawal latency to radiant heat, tactile response thresholds to von Frey filaments, and flinching after paw formalin injection.

Results
Prolonged TX14(A) treatment of diabetic rats prevented the progressive decline in large sensory fiber conduction velocity in the sciatic nerve, development of paw thermal hypoalgesia, and increased flinching after paw formalin injection. The effect on formalin hyperalgesia persisted for 48 h but not 72 h after injection. No effects were noted in control rats. A single injection of TX14(A) 30 min before testing did not alter thermal response latencies in control or diabetic rats but prevented formalin hyperalgesia in diabetic rats. Tactile allodynia and the prolonged paw thermal hyperalgesia to radiant heat after intrathecal delivery of substance P were also dose-dependently ameliorated in diabetic rats by a single injection of TX14(A), whereas no effects were observed on the responses to these tests in control rats.

Conclusions
TX14(A) exhibits both neuroprotective and acute antihyperalgesic properties in diabetic rats without altering normal nociceptive function.