bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thiopental Uncouples Hippocampal and Cortical Synchronized Electroencephalograpbic Activity
Authors: MacIver Bruce M. , Mandema Jaap W. , Stanski Donald R. , Bland Brian H. 
Published: November 2003

Background
Thiopental produces a concentration-dependent continuum of effects on the cortical electroencephalogram (EEG) that has been linked to behavioral measures of anesthetic depth. The complexity of the response, however, limits a clear insight into the neurophysiologic actions of thiopental. The current study investigated thiopental actions on cortical EEG and hippocampal electrical activity, to determine whether similar effects occur on both structures and to compare synchronized activity between these structures.

Methods
Thiopental was administered intravenously via an implanted catheter in freely moving rats. Arterial blood oxygen/carbon dioxide concentration, thiopental concentrations, and temperature were monitored and controlled. Neocortical EEG was recorded from implanted dural surface electrodes and hippocampal neuron electrical activity was recorded from stereotaxically placed microelectrodes. Pharmacokinetic models were used to determine effect site concentrations.

Results
Thiopental produced an increase in EEG frequency and amplitude at low concentrations (15-20 micrograms/ml total plasma, approximately 10 microM unbound), which produced a loss of righting reflex. This was followed by a frequency decrease and burst suppression activity at higher concentrations (50-80 micrograms/ml, approximately 60 microM), which produced a loss of tail pinch and corneal reflexes. Higher concentrations of thiopental ( > 60 micrograms/ml) uncoupled synchronized burst discharges recorded in hippocampus and cortex. Isoelectric EEG activity was associated with concentrations of 70-90 micrograms/ml (approximately 80 microM) and a deep level of anesthesia; motor reflexes were abolished, although cardiovascular reflexes remained. In all frequency bands, similar concentration-EEG effect relationships were observed for cortical and hippocampal signals, only differing in the magnitude of response. A reversed progression of effects was observed on recovery.

Conclusions
The results confirm earlier findings in humans and animals and demonstrate that both the hippocampus and neocortex exhibit burst suppression and isoelectric activity during thiopental anesthesia. Thiopental-induced synchronized burst activity was depressed by progressively higher concentrations. The lost synchronization suggests a depression of synaptic coupling between cortical structures contributes to anesthesia.
Differential Nerve Block
Authors: Jaffe Richard A. , Rowe Michael A. 
Published: November 2003

Background
Clinically, differential block is manifested by the loss of small fiber mediated sensation (e.g., temperature) two or more dermatomes beyond the sensory limit for large fiber mediated sensations. These observations support the belief that sensitivity to local anesthetics is inversely proportional to axon diameter. This study reports the first measurements of differential sensitivity to lidocaine in individual myelinated and unmyelinated mammalian dorsal root axons.

Methods
Lumbar dorsal roots and vagus nerves were isolated from anesthetized adult rats and maintained in vitro in a perfusion/recording chamber at 37 +/- 0.3 degrees C. Using single fiber techniques, evoked action potentials in individual myelinated and unmyelinated axons were digitized and recorded for subsequent analysis. Axons were exposed to lidocaine at 150, 260, or 520 microM. Sensitivity to local anesthetic was assessed by measuring the incidence of conduction block and the magnitude of conduction velocity slowing under steady-state conditions.

Results
Data were obtained from 77 dorsal root axons and 41 vagal axons. The estimated steady-state EC50 lidocaine concentration for myelinated dorsal root axons (232 microM) was comparable to that for unmyelinated axons (228 microM). Similarly, the incidence of conduction block was not significantly different among dorsal root axon groups. However, unmyelinated dorsal root axons were significantly less sensitive to the conduction velocity slowing effect of lidocaine than their myelinated counterparts (P < 0.01). The incidence of conduction block in short (mean length 13.5 mm) dorsal root axons was not significantly different from that in long (mean length 22.4 mm) axons. Compared with dorsal root axons, the estimated EC50s for vagal myelinated and unmyelinated axons (345 and 285 microM, respectively), while lower were not significantly different. However, the incidence of conduction block at 260 microM lidocaine was significantly lower (16.7% vs. 56.7%; P < 0.05) in vagal myelinated axons.

Conclusions
Although no difference in sensitivity to the conduction blocking effects of lidocaine could be demonstrated among dorsal root axons, myelinated axons were more sensitive to the conduction velocity slowing effects of lidocaine. This differential effect cannot explain clinical observations of differential nerve block. Differential sensory block with lidocaine may depend on factors (e.g., physiologic function) related only indirectly to individual axon conduction velocity (diameter).
Effect of Volatile Anesthetics with and without Verapamil on Intracellular Activity in Vascular Smooth Muscle
Authors: Namba Hitoshi , Tsuchida Hideaki 
Published: November 2003

Background
Although halothane and isoflurane inhibit receptor agonist-induced smooth muscle contraction by inhibiting Ca2+ influx via the L-type voltage-dependent Ca2+ channels, their effects on pharmacomechanical coupling remained to be clarified. The intracellular action of both anesthetics was studied during agonist-induced contractions using the Ca2+ channel blocker verapamil.

Methods
Isolated spiral strips of rat thoracic aorta with endothelium removed were suspended for isometric tension recordings in physiologic salt solution. Cytosolic concentration of Ca2+ ([Ca2+]i) was measured concomitantly using fura-2-Ca2+ fluorescence. Muscle contraction was evoked by the receptor agonists with 30 nm norepinephrine or 10 microM prostaglandin F2 alpha (PGF2 alpha), followed by exposure to halothane, at 0%, 1%, 2%, and 3% or isoflurane, at 2% and 4%. The effects of the anesthetics were compared with those of 0.1-1 microM verapamil (n = 8 for each condition). To clarify the intracellular action of the volatile anesthetics on agonist-induced contractions, this procedure was repeated for the anesthetics only in the presence of 1 microM verapamil (n = 8 for each condition). The effects of both anesthetics were also examined in nonreceptor-mediated contractions evoked with a 1-microM dose of the protein kinase C activator, 12-deoxyphorbol 13-isobutylate, which increases the Ca2+ sensitivity of the contractile elements (n = 8 for each).

Results
Halothane, isoflurane, and verapamil suppressed norepinephrine-and PGF2 alpha-induced increases in muscle tension and [Ca2+]i in a concentration-dependent manner. The Ca2+-tension regression lines suggested that the volatile anesthetics reduced Ca2+ sensitivity of the contractile elements during PGF2 alpha-induced contraction. Pretreatment of the muscle strip with verapamil revealed that halothane and isoflurane released Ca2+ during norepinephrine-induced contraction and that [Ca2+]i-tension relationship was modulated during PGF2 alpha-induced contractions. Halothane at 2% and 3% and isoflurane at 4% suppressed 12-deoxyphorbol 13-isobutylate-induced increases in muscle tension, whereas they enhanced increases in [Ca2+]i, indicating that both anesthetics suppressed Ca2+ sensitivity during 12-deoxyphorbol 13-isobutylate-induced contraction.

Conclusions
Verapamil pretreatment unmasked the intracellular action of the anesthetics. Halothane and isoflurane influenced pharmacomechanical coupling during agonist-induced contraction.
Electroencephalographic Burst Suppression Is Not Required to Elicit Maximal Neuroprotection from Pentobarbital in a Rat Model of Focal Cerebral Ischemia
Authors: Warner David S. , Takaoka Seiji , Wu Bo , Ludwig Paula S. , Pearlstein Robert D. , Brinkhous Ann D. , Dexter Franklin MD 
Published: November 2003

Background
Barbiturates have previously been demonstrated to reduce focal cerebral ischemic brain damage. However, the dose of drug required to elicit maximal neuroprotection has not been defined. The authors' hypothesized that doses of pentobarbital substantially lower than those required to cause electroencephalographic burst suppression would result in maximal magnitudes of reduction of cerebral infarct volume.

Methods
Wistar rats underwent 90 min of filament occlusion of the middle cerebral artery while either awake (control), or anesthetized with intravenous sodium pentobarbital administered to preserve an active electroencephalogram (15-23 mg.kg-1.h-1) or a pattern of burst suppression (45-60 mg.kg-1.h-1; n = 17). During ischemia and for the first 6 h of recirculation, brain temperature was rigorously controlled at 38.0 +/- 0.2 degrees C. Rats were allowed a recovery interval of 7 days after which neurologic function and cerebral infarct volume were assessed. In nonischemic rats undergoing a similar anesthetic protocol, the cerebral metabolic rate of glucose utilization was measured at each anesthetic depth.

Results
Relevant physiologic values were similar between groups. Total infarct volume (mean +/- SD) was smaller in the active electroencephalogram group than in the control group (124 +/- 68 mm3 versus 163 +/- 66 mm3; P < 0.05). Increasing the dose of pentobarbital (burst suppression) did not further decrease infarct volume (128 +/- 54 mm3). Neurologic score and infarct volume were positively correlated (P < 0.001). Cerebral metabolic rate of glucose utilization was reduced by 56% in the burst suppression group versus 43% in the active electroencephalogram pentobarbital group (P < 0.001).

Conclusions
Sodium pentobarbital administered at either dose (active electroencephalogram or burst suppression) resulted in an approximately equal to 25% reduction of cerebral infarct size, indicating that burst suppression is not required to elicit maximal neuroprotective efficacy.
Etomidate and Thiopental Inhibit the Release of Endothelium-derived Hyperpolarizing Factor in the Human Renal Artery
Authors: Kessler Paul , Lischke Volker , Hecker Markus 
Published: November 2003

Background
Endothelium-derived hyperpolarizing factor is thought to be a cytochrome P450-derived arachidonic acid metabolite that hyperpolarizes vascular smooth muscle cells by opening Ca(2+)-activated K+ channels (K+Ca channels). In the rabbit carotid artery both volatile and intravenous anesthetics inhibit the acetylcholine-stimulated release of endothelium-derived hyperpolarizing factor. Because the release of this factor may help to maintain vascular tone in humans under conditions of a failing nitric oxide synthesis, e.g., in atherosclerosis, the effects of two intravenous anesthetics, thiopental and etomidate, on the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine were investigated in human isolated renal artery segments.

Methods
The segments were suspended in Krebs-Henseleit solution (37 degrees C) containing the cyclooxygenase inhibitor diclofenac (1 microM) and preconstricted with norepinephrine (6 microM). Relaxations caused by acetylcholine (1 microM) were compared in the presence and absence of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine (0.1 mM) in control segments and in segments exposed to etomidate or thiopental (0.03-0.3 mM). In addition, the effects of the two anesthetics on the relaxant response to the nitric oxide donors glyceryl trinitrate (3 microM) and sodium nitroprusside (0.1 microM) were examined.

Results
The relaxant response to acetylcholine, which was resistant to both nitric oxide synthase and cyclooxygenase blockade, was markedly reduced by the K+Ca channel antagonist tetrabutyl ammonium (3 mM) and the cytochrome P450 inhibitor clotrimazole (30 microM). Both etomidate and thiopental, at a concentration of 0.3 mM, selectively attenuated the relaxant response to acetylcholine in N(G)-nitro-L-arginine-treated segments, but did not affect relaxations elicited by glyceryl trinitrate or sodium nitroprusside.

Conclusions
Etomidate and thiopental inhibit the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine in the human renal artery, an effect that appears to be attributable to the cytochrome P450-inhibiting properties of these anesthetics.
Mass Spectrometry Provides Warning of Carbon Monoxide Exposure Via Trifluoromethane
Authors: Woehlck Harvey J. , Dunning Marshall , Nithipatikom Kasem , Kulier Alexander H. , Henry Daniel W. 
Published: November 2003

Background
The chemical breakdown of isoflurane, enflurane, or desflurane in dried carbon dioxide absorbents may produce carbon monoxide. Some mass spectrometers can give false indications of enflurane during anesthetic breakdown.

Methods
During clinical anesthesia with isoflurane or desflurane, the presence of carbon monoxide in respiratory gas was confirmed when enflurane was inappropriately indicated by a clinical mass spectrometer that identified enflurane at mass to charge ratio = 69. In vitro, isoflurane, enflurane, or desflurane in oxygen was passed through dried carbon dioxide absorbents at 35, 45, and 55 degrees C. Gases were analyzed by gas chromatography and by mass spectrometry.

Results
Mass spectrometry identified several clinical incidents in which 30-410 ppm carbon monoxide was measured in respiratory gas. Trifluoromethane was produced during in vitro breakdown of isoflurane or desflurane. Although these inappropriately indicated quantities of "enflurane" correlated (r2 > 0.95) to carbon monoxide concentrations under a variety of conditions, this ratio varied with temperature, anesthetic agent, absorbent type, and water content.

Conclusions
Trifluoromethane causes the inappropriate indication of enflurane by mass spectrometry, and indicates isoflurane and desflurane breakdown. Because the ratio of carbon monoxide to trifluoromethane varies with conditions, this technique cannot be used to quantitatively determine the amount of carbon monoxide to which a patient is exposed. If any warning of anesthetic breakdown results from this technique then remedial steps should be taken immediately to stop patient exposure to carbon monoxide. No warning can be provided for the breakdown of enflurane by this technique.
Vomiting and Recovery after Outpatient Tonsillectomy and Adenoidectomy in Children
Authors: Ved Sudha A. , Walden Tom L. , Montana JoAnne , Lea Dawn E. , Tefft Mariella C. , Kataria Bideshwar K. , Pudimat Mary Ann , Nicodemus Honorato F. , Milmoe Gregory J. 
Published: November 2003

Background
The authors' purpose in this study was to compare prospectively four different anesthetic induction and maintenance techniques using nitrous oxide with halothane and/or propofol for vomiting and recovery after outpatient tonsillectomy and adenoidectomy procedures in children.

Methods
Eighty unpremedicated children, aged 3-10 yr, were assigned randomly to four groups: group H/H, 0.5-2% halothane induction/halothane maintenance; group P/P, 3-5 mg.kg-1 propofol induction and 0.1-0.3 mg.kg-1.min-1 propofol maintenance; group H/P, 0.1-0.3 mg.kg-1.min-1 halothane induction/propofol maintenance; and group P/H, 3-5 mg.kg-1 propofol induction and 0.5-2% halothane maintenance. Nitrous oxide (67%) and oxygen (33%) were administered in all the groups. Other treatments and procedures were standardized intra- and postoperatively. Results of postoperative vomiting and recovery were analyzed in the first 6 h and beyond 6 h.

Results
Logistic regression showed that vomiting occurred 3.5 times as often when halothane was used for maintenance of anesthesia (groups H/H and P/H) compared with the use of propofol (groups P/P and H/P; Odds Ratio 3.5; 95% confidence interval 1.3 and 9.4, respectively; P = 0.012). A significant association between vomiting ( < 6 h: yes/no) and discharge times ( > 6 h: yes/no) (Odd's Ratio = 3.6; 95% confidence interval: 1.02, 12.4, respectively) (P = 0.046) was shown. However, no significant differences among the groups in the incidence of vomiting beyond 6 h, recurrent vomiting, or hospital discharge times were shown.

Conclusions
After tonsillectomy and adenoidectomy procedures, despite reduced postoperative vomiting with use of propofol rather than halothane, along with nitrous oxide for anesthetic maintenance, the authors found no differences in "true" endpoints such as unplanned admissions or discharge times. Among the groups, the main factor that delayed hospital discharge beyond 6 h was vomiting within the first 6 h.
Cervical Spine Motion with Direct Laryngoscopy and Orotracheal Intubation
Authors: Sawin Paul D. , Todd Michael M. , Traynelis Vincent C. , Farrell Stella B. , Nader Antoine , Sato Yutaka , Clausen John D. , Goel Vijay K. 
Published: November 2003

Background
Cervical spine kinetics during airway manipulation are poorly understood. This study was undertaken to quantify the extent and distribution of segmental cervical motion produced by direct laryngoscopy and orotracheal intubation in human subjects without cervical abnormality.

Methods
Ten patients without clinical or radiographic evidence of cervical spine abnormality underwent laryngoscopy using a #3 Macintosh blade while under general anesthesia and neuromuscular blockade. Cervical motion was recorded with continuous lateral fluoroscopy. The intubation sequence was divided into distinct stages and the corresponding fluoroscopic images were digitized. Segmental motion, occiput through C5, was calculated for each stage using the digitized data.

Results
During exposure and laryngoscope blade insertion, minimal displacement of the skull base and rostral cervical vertebral bodies was observed. Visualization of the larynx created superior rotation of the occiput and C1 in the sagittal plane, and mild inferior rotation of C3-C5. C2 maintained nearneutral posture. This pattern of displacement resulted in extension at each motion segment, with the most significant motion produced at the occipitoatlantal and atlantoaxial joints (mean = 6.8 degrees and 4.7 degrees, respectively). Intubation created slight additional superior rotation at the occiput and C1, without substantial alteration in the posture of C2-C5. After laryngoscope removal, position trended toward baseline at all levels, although exact neutral posture was not regained.

Conclusions
This investigation quantifies the behavior of the normal cervical spine during direct laryngoscopy with a Macintosh blade. With this maneuver, the vast majority of cervical motion is produced at the occipitoatlantal and atlantoaxial joints. The subaxial cervical segments (C2-C5) are displaced only minimally. This study establishes a highly reliable and reproducible method for analyzing cervical motion in real time.
Size of Human Lower Thoracic and Lumbosacral Nerve Roots
Authors: Hogan Quinn 
Published: November 2003

Background
Nerve root size may determine degree of blockade after epidural or spinal anesthesia, but good measures of this fundamental anatomic parameter have not been published. Models of subarachnoid anesthetic distribution have lacked valid cauda equina dimensions. In this study, the author sought to measure cross-section areas of anterior and posterior roots at different levels for basic anthropomorphic analysis.

Methods
Samples from 12 adult autopsy subjects were obtained from roots at levels T6 through S5. Cross-section area was determined by dividing the root sample weight by length and correcting for tissue density.

Results
Roots were variably composed of as many as five easily separable independent strands. Areas of anterior roots are approximately half the area of posterior roots. On average, the largest anterior and posterior root is at S1, but this may occur at L3 through S2. There is a large degree of interindividual variability (e.g., range of posterior L5 root is 2.33-7.71 mm2).

Conclusions
The large size of low lumbar and high sacral roots may cause resistance to anesthetic effects, whereas the smaller dimensions of the thoracic roots may facilitate neural blockade. The small size of the low sacral roots may, in part, explain selective neurotoxic damage of these fibers after subarachnoid injections. Interindividual variability in root sizes may contribute to lack of predictability in anesthetic response.
Ventilatory Response to Hypoxia in Humans
Authors: Dahan Albert , Sarton Elise , van den Elsen Maarten , van Kleef Jack , Teppema Luc , Berkenbosch Aad 
Published: November 2003

Background
At low dose, the halogenated anesthetic agents halothane, isoflurane, and enflurane depress the ventilatory response to isocapnic hypoxia in humans. In the current study, the influence of subanesthetic desflurane (0.1 minimum alveolar concentration [MAC]) on the isocapnic hypoxic ventilatory response was assessed in healthy volunteers during normocapnia and hypercapnia.

Methods
A single hypoxic ventilatory response was obtained at each of 4 target end-tidal partial pressure of oxygen concentrations: 75, 53, 44, and 38 mmHg, before and during 0.1 MAC desflurane administration. Fourteen subjects were tested at a normal end-tidal partial pressure of carbon dioxide (43 mmHg), with 9 subjects tested at an end-tidal carbon dioxide concentration of 49 mmHg (hypercapnia). The hypoxic sensitivity (S) was computed as the slope of the linear regression of inspired minute ventilation (V1) on (100-SPO2). Values are mean +/- SE.

Results
Sensitivity was unaffected by desflurane during normocapnia (control: S = 0.45 +/- 0.07 l.min-1.%-1 vs. 0.1 MAC desflurane: S = 0.43 +/- 0.09 l.min-1.%-1). With hypercapnia S decreased by 30% during desflurane inhalation (control: S = 0.74 +/- 0.09 l.min-1.%-1 vs. 0.1 MAC desflurane: S = 0.53 +/- 0.06 l.min-1.%-1; P < 0.05).

Conclusions
On the basis of the data, subanesthetic desflurane has no detectable effect on the normocapnic hypoxic ventilatory response sensitivity. However, the carbon dioxideinduced augmentation of the hypoxic response was reduced. This indicates that subanesthetic desflurane effects the chemoreceptors at the carotid bodies.
Mivacurium Neuromuscular Block at the Adductor Muscles of the Larynx and Adductor Pollicis in Humans
Authors: Plaud Benoit , Debaene Bertrand , Lequeau Frank , Meistelman Claude , Donati Francois 
Published: November 2003

Background
Laryngeal muscles must be paralyzed for tracheal intubation. Time to peak effect (onset time) is shorter and intensity of blockade is less at laryngeal muscles compared with the adductor pollicis. The authors' aim in this study was to determine the neuromuscular effects of mivacurium at the laryngeal adductor muscles and the adductor pollicis.

Methods
In 22 adults, anesthesia was induced and maintained with propofol and alfentanil. The force of contraction of the adductor pollicis was recorded, and the laryngeal response was evaluated by measuring the pressure change in the cuff of a tracheal tube positioned between the vocal cords after train-of-four stimulation. Mivacurium (0.07 mg.kg-1 or 0.14 mg.kg-1) was given intravenously (10s).

Results
With 0.07 mg.kg-1 mivacurium, onset time was 151 +/- 40 s(mean +/- SD) at the larynx and 241 +/- 79 s at the adductor pollicis, respectively (P < 0.005). Maximum block was 78 +/- 18% and 95 +/- 8%, respectively (P < 0.002), and time to 90% recovery was 11.1 +/- 2.9 min and 23.3 +/- 7.6 min, respectively (P < 0.001). With 0.14 mg.kg-1 mivacurium, onset time also was more rapid at the vocal cords (137 +/- 20 s) than at the adductor pollicis (201 +/- 59 s, P < 0.01). Maximum block was 90 +/- 7% and 99 +/- 1% (P < 0.005), and time to 90% recovery was 16.4 +/- 4.9 min and 27.4 +/- 7.8 min, respectively (P < 0.01).

Conclusions
With mivacurium, onset and recovery are faster at the laryngeal muscles, but block is less intense than at the adductor pollicis. A dose greater than 0.14 mg.kg-1 mivacurium is necessary to ensure complete relaxation at the vocal cords.