bluuebunny/crossref_metadata_2025 huggingface dataset:
Patient-controlled Antiemesis
Authors: Gan Tong J. , El-Molem Habib , Ray Jennifer , Glass Peter S. A.
Published: November 2003

Background

The role of propofol for the management of postoperative nausea and vomiting (PONV) is not well established. This study determines the efficacy of small doses of propofol administered by patient-controlled device for the treatment of PONV.

Methods

Patients presenting for ambulatory surgery received a standardized general anesthetic. Those who experienced significant nausea or emesis within 1 h of arrival in the recovery room were randomized to receive repeated doses of propofol 20 mg (P-20), propofol 40 mg (P-40), or intralipid (placebo) on demand. Study medications (in equal volumes) were administered with a patient-controlled delivery device for 2 h. A lockout interval of 5 min between doses was used. The following parameters were assessed: nausea, vomiting, rescue antiemetic use, recovery profile, study drug administration history, and satisfaction with treatment.

Results

Sixty-nine patients participated in the study. Patient demographics were similar. The average nausea score for a patient in the P-20 and P-40 groups was 25% and 29% less, respectively, compared with placebo during the study period (P < 0.05). This difference was apparent 15 min after initiation of therapy. More placebo patients vomited (P-20, 12%; P-40, 23%; placebo, 56%; P = 0.003) and needed rescue antiemetics (P-20, 17%; P-40, 23%; placebo, 70%; P = 0.001) compared with treatment groups. Sedation scores were similar between groups. Propofol-treated patients had shorter stays in the post-anesthesia care unit (PACU; P-20, 131+/-35 min [mean +/- SD]; P-40, 141+/-34 min; placebo, 191+/-92 min; P = 0.005) and higher satisfaction with their control of PONV than placebo (P < 0.01).

Conclusions

Propofol is effective in managing PONV with shorter PACU stay and great degree of patient satisfaction. There were two episodes of oversedation in the P-40 group. Hence, propofol at a demand dose of 20 mg seems more appropriate.
Effect of Combined Mouth Closure and Chin Lift on Upper Airway Dimensions during Routine Magnetic Resonance Imaging in Pediatric Patients Sedated with Propofol
Authors: Reber Adrian , Wetzel Stephan G. , Schnabel Karl , Bongartz Georg , Frei Franz J.
Published: November 2003

Background

In pediatric patients, obstruction of the upper airway is a common problem during general anesthesia. Chin lift is a commonly used technique to improve upper airway patency. However, little is known about the mechanism underlying this technique.

Methods

The authors studied the effect of the chin lift maneuver on airway dimensions in 10 spontaneously breathing children (aged 2-11 yr) sedated with propofol during routine magnetic resonance imaging. The minimal anteroposterior and corresponding transverse diameters of the pharynx were determined at the levels of the soft palate, dorsum of the tongue, and tip of the epiglottis before and during the chin lift maneuver. Additionally, cross-sectional areas were calculated at these sites, including tracheal areas 2 cm below the glottic level.

Results

Minimal anteroposterior diameter of the pharynx increased significantly during chin lift at all three levels in all patients. The diameters of the soft palate, tongue, and epiglottis increased from 6.7+/-2.8 mm (SD) to 9.9+/-3.6 mm, from 9.6+/-3.6 mm to 16.5+/-3.1 mm, and from 4.6+/-2.5 mm to 13.1+/-2.8 mm, respectively. The corresponding transverse diameter of the pharynx also increased significantly at all three levels in all patients but without significant predominance. The diameters at the levels of the soft palate, tongue, and epiglottis increased from 15.8+/-5.1 mm to 22.8+/-4.5 mm, from 13.5+/-4.9 mm to 18.7+/-5.3 mm, and from 17.2+/-3.9 mm to 21.2+/-3.7 mm, respectively. Cross-sectional pharyngeal areas increased significantly at all levels (soft palate, from 0.88+/-0.58 cm2 to 1.79+/-0.82 cm2; tongue, from 1.15+/-0.45 cm2 to 2.99+/-1.30 cm2; epiglottis, from 1.17+/-0.70 cm2 to 3.04+/-0.99 cm2), including the subglottic level (from 0.44+/-0.15 cm2 to 0.50+/-0.14 cm2).

Conclusions

This study shows that all children had a preserved upper airway at all measured sites during propofol sedation. Chin lift caused a widening of the entire pharyngeal airway that was most pronounced between the tip of the epiglottis and the posterior pharyngeal wall. In pediatric patients, chin lift may be used as a standard procedure during propofol sedation.
Halothane Presynaptically Depresses Synaptic Transmission in Wild-type Drosophila Larvae But Not in Halothane-resistant (har) Mutants
Authors: Nishikawa Koh-ichi , Kidokoro Yoshiaki
Published: November 2003

Background

General anesthetics produce important changes in neural function, but the relation between the many individual changes produced by anesthetics in neural components and the responsiveness of the whole organism is uncertain. An analysis of genetically altered animals that have modified responses to volatile anesthetics may help to allay this uncertainty.

Methods

The authors evaluated the effect of halothane on synaptic transmission at the larval neuromuscular junction in wild-type (Ore-R) and halothane-resistant (har) mutants of Drosophila melanogaster. The body wall muscles, which are innervated by glutamatergic nerves, were voltage clamped at -60 mV using the patch-clamp technique in the whole cell configuration. Nerve-evoked excitatory junctional currents and miniature excitatory junctional currents were recorded. The effects of halothane on the amplitude of these currents were compared in Ore-R and two bar mutants derived from the Ore-R strain. The time course and frequency of miniature excitatory junctional currents also were analyzed in the presence of halothane.

Results

In Ore-R, halothane (1.8%; 1.01 mM) significantly reduced the amplitude of nerve-evoked excitatory junctional currents (61.9+/-17% of control, mean +/- SD; n = 7), but not that of miniature excitatory junctional currents. Conversely, in two har mutants, halothane had no effect on the amplitude of either nerve-evoked excitatory junctional currents or miniature excitatory junctional currents. In Ore-R, the frequency of miniature excitatory junctional currents was decreased significantly in the presence of halothane (0.9-2.7%; 0.52-1.46 mM), whereas halothane did not change the frequency in two har mutants. The miniature excitatory junctional current decay time constant, thought to reflect the kinetic properties of junctional glutamate receptor channels, was not changed by halothane in either the Ore-R strain or the har mutants.

Conclusions

Halothane depresses synaptic transmission at the wild-type Drosophila neuromuscular junction, most likely by affecting presynaptic properties. The absence of an effect by halothane in the har mutants provides evidence that the depression of presynaptic function at the glutamate-mediated synapses is an important contributor to the way halothane alters the responsiveness of the whole animal.
The Placental Transfer and Fetal Effects of Levobupivacaine, Racemic Bupivacaine, and Ropivacaine
Authors: Santos Alan C. , Karpel Barry , Noble George
Published: November 2003

Background

The purposes of this study were to assess the effects of levobupivacaine on uterine blood flow and fetal well-being and to compare its placental transfer with that of bupivacaine and ropivacaine.

Methods

After a control period, pregnant ewes that were fitted with instruments for long-term monitoring were randomized to receive a two-step intravenous infusion of levobupivacaine, bupivacaine, or ropivacaine, in a blinded manner, for 1 h. Maternal and fetal hemodynamics were monitored during the study. Arterial blood samples were drawn at 30 and 60 min of infusion from the mother and fetus to determine the acid-base status (60 min only) and serum drug concentrations. The fetal brain, heart, liver, lungs, adrenal glands, and kidneys were obtained to measure tissue drug levels.

Results

Maternal blood pressure, central venous and intraamniotic pressures, acid-base status and uterine blood flow were unaffected by any drug infusion. In contrast to the other two local anesthetics, the infusion of bupivacaine was associated with a small but significant decrease in the ewe's heart rate. At the end of the study, the heart rate in the bupivacaine-treated animals was significantly less than in the animals treated with the other two drugs. All fetuses were in good condition at the start of study, and none of the local anesthetics affected fetal well-being. No significant differences were found among the three drugs in the maternal serum, fetal serum, fetal tissue concentrations, and tissue:serum concentration ratios.

Conclusions

Levobupivacaine was similar to bupivacaine and ropivacaine in causing no important hemodynamic changes in the pregnant ewe and fetus. There were no significant differences in the fetal serum and tissue levels of the drugs.
Comparison of the Effects of Convulsant and Depressant Barbiturate Stereoisomers on AMPA-type Glutamate Receptors
Authors: Kamiya Yoshinori , Andoh Tomio , Furuya Ryosuke , Hattori Satoshi , Watanabe Itaru , Sasaki Tosio , Ito Hideki , Okumura Fukuichiro
Published: November 2003

Background

Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-type glutamate receptors mediate fast excitatory synaptic transmission in the central nervous system. Although barbiturates have been shown to suppress the AMPA receptor-mediated responses, it is unclear whether this effect contributes to the anesthetic action of barbiturates. The authors compared the effects of depressant [R(-)] and convulsant [S(+)] stereoisomers of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) on the AMPA and gamma-aminobutyric acid type A (GABA(A)) receptor-mediated currents to determine if the inhibitory effects on AMPA receptors correlate to the in vivo effects of the isomers.

Method

The authors measured whole-cell currents in the rat cultured cortical neuron at holding potential of -60 mV. Kainate 500 microM was applied as the agonist for AMPA receptors. Thiopental (3-300 microM), R(-)-MPPB or S(+)-MPPB (100-1,000 microM) was coapplied with kainate under the condition in which the GABA(A) receptor-mediated current was blocked. Effects of MPPB isomers on the current elicited by GABA 1 microM were studied in the separate experiments.

Results

Thiopental inhibited the kainate-induced current reversibly and in a dose-dependent manner, with a concentration for 50% inhibition of 49.3 microM. Both R(-)-MPPB and S(+)-MPPB inhibited the kainate-induced current with a little stereoselectivity. R(-)-MPPB was slightly but significantly more potent than S(+)-MPPB. In contrast, R(-)-MPPB enhanced but S(+)-MPPB reduced the GABA-induced current.

Conclusions

Both convulsant and depressant stereoisomers of the barbiturate inhibited the AMPA receptor-mediated current despite of their opposite effects on the central nervous system in vivo. Although thiopental exhibited a considerable inhibition of AMPA receptors, the results suggest that the inhibition of AMPA receptors contributes little to the hypnotic action of the barbiturates.
Signal-averaged P-wave Duration Does Not Predict Atrial Fibrillation after Thoracic Surgery
Authors: Amar David , Roistacher Nancy , Zhang Hao , Baum Michael S. , Ginsburg Ilana , Steinberg Jonathan S.
Published: November 2003

Background

Atrial fibrillation (AF) is the most common dysrhythmia seen early after major thoracic surgery but occurs infrequently after minor thoracic or other operations. A prolonged signal-averaged P-wave duration (SAPWD) has been shown to be an independent predictor of AF after cardiac surgery. The authors sought to determine whether a prolonged SAPWD alone or in combination with clinical or echocardiographic correlates predicts AF after elective noncardiac thoracic surgery.

Methods

Of the 250 patients enrolled, 228 were included in the final analysis. Preoperative SAPWD was obtained in 155 patients who had major thoracic surgery and in 73 patients undergoing minor thoracic or other operations who served as comparison control subjects. The SAPWD was recorded from three orthogonal leads using a sinus P-wave template. The filtered vector composite was used to measure total P-wave duration. Clinical, surgical, and echocardiographic parameters were collected and patients followed for 30 days after surgery for the development of symptomatic AF.

Results

Symptomatic AF developed in 18 of 155 (12%) patients undergoing major thoracic surgery and in 1 of 73 (1%) patients having minor thoracic or abdominal surgery, most commonly 2 or 3 days after surgery. In comparison with similar patients undergoing major thoracic surgery without AF, those who developed AF were older (66+/-8 vs. 62+/-10 yr; P = 0.04) but did not differ in SAPWD (145+/-17 vs. 147+/-16, ms) in standard electrocardiographic P-wave duration (105+/-7 vs. 107+/-10 mns), incidence of left-ventricular hypertrophy on 12-lead electrocardiography, male sex, history of hypertension, diabetes, or coronary heart disease. Thoracic-surgery patients at risk for postoperative AF did not differ from all other patients at low risk for AF in clinical or SAPWD parameters.

Conclusions

Under the conditions of this study, SAPWD did not differentiate patients who did or did not develop AF after noncardiac thoracic surgery, and therefore its measurement cannot be recommended for the routine evaluation of these patients. Older age continues to be a risk factor for AF after thoracic surgery.
Early Reversal of Rapacuronium with Neostigmine
Authors: Purdy Robert , Bevan David R. , Donati Francois , Lichtor Lance J.
Published: November 2003

Background

Rapacuronium is a rapid-onset, short-acting neuromuscular relaxant. This multiple-center study determined neuromuscular recovery when neostigmine was given 2 or 5 min after rapacuronium.

Methods

One hundred seventeen patients were randomized to receive two different doses of rapacuronium and to receive neostigmine in two different doses and at two different times. During propofol anesthesia with nitrous oxide, oxygen, and fentanyl, 1.5 or 2.5 mg/kg rapacuronium was given 1 min before tracheal intubation. Neuromuscular block was measured by train-of-four ulnar nerve stimulation every 12 s: The adductor pollicis force of contraction was recorded mechanomyographically. Two or five minutes after rapacuronium was administered, 0.05 or 0.07 mg/kg neostigmine was administered and recovery was compared with that of control patients who received no neostigmine.

Results

Both doses of rapacuronium produced 100% block in all but one patient, who exhibited 97% block. Neostigmine accelerated recovery in all groups. After 1.5 mg/kg rapacuronium, the time to 25% T1 twitch recovery decreased from a mean of 16 min in control patients to mean values of 8-10 min in the treatment groups: The time to train-of-four ratio of 0.7 decreased from 38 min to 17-19 min. After 2.5 mg/kg rapacuronium, the time to 25% T1 was reduced from 23 min to 11-12 min, and the time to train-of-four ratio of 0.7 decreased from 54 min to 26-32 min. Recovery was not different among the the groups that received different doses and timing of neostigmine.

Conclusions

Recovery of intense rapacuronium block was accelerated by early neostigmine administration. When given 2 min after rapacuronium, neostigmine was as effective as after 5 min, and 0.05 mg/kg neostigmine was comparable to 0.07 mg/kg neostigmine.
The Influence of the Obstetrician in the Relationship between Epidural Analgesia and Cesarean Section for Dystocia
Authors: Segal Scott , Blatman Robert , Doble Melissa , Datta Sanjay
Published: November 2003

Background

The association between epidural analgesia for labor and the risk of cesarean section for dystocia remains controversial The authors hypothesized that if epidural analgesia were an important factor in determining cesarean section rates, then obstetricians with higher rates of utilization of epidural analgesia for labor would have higher rates of cesarean section for dystocia.

Methods

The frequency of use of epidural analgesia and frequency of occurrence of various patient risk factors for cesarean section were calculated for 110 obstetricians caring for > or = 50 low-risk parturients. These frequencies were compared by linear regression to obstetricians' rates of cesarean section for dystocia. Stepwise regression was used to attempt to predict obstetricians' cesarean rates from the incidence of various patient and provider risk factors.

Results

There was no relationship between frequency of epidural analgesia and rate of cesarean section for dystocia across practitioners (R2 = 0.019; P = 0.156). Weighting each obstetrician's data for the number of patients cared for during the study period did not change this result. Stepwise linear regression only modestly predicted obstetricians' cesarean section rates for dystocia, yielding a model containing 12 variables not including epidural analgesia (gestational age, induction of labor, maternal age, provider volume, nulliparity, and seven interactions; adjusted R2 = 0.312; P < 0.0001).

Conclusions

The frequency of use of epidural analgesia does not predict obstetricians' rates of cesarean section for dystocia. After accounting for a number of known patient risk factors, obstetrical practice style appears to be a major determinant of rates of cesarean section.
Optimal Propofol-Alfentanil Combinations for Supplementing Nitrous Oxide for Outpatient Surgery
Authors: Pavlin Janet D. , Arends Rosalin H. , Gunn Holly C. , Van Norman Gail , Koerschgen Meagan E. , Shen Danny D.
Published: November 2003

Background

The combination of propofol and alfentanil with nitrous oxide provides balanced anesthesia with rapid recovery and minimal emetic side effects. The object of this study was to compare recovery parameters at varying proportions of propofol and alfentanil, and to determine the dosing rate and plasma concentration of propofol necessary to supplement nitrous oxide in the presence of varying concentrations of alfentanil

Methods

Forty-eight patients were anesthetized with nitrous oxide, targeted manual infusions of alfentanil (target plasma concentrations of 0, 50, 100, and 150 ng/ml), and propofol at rates that were varied up or down by 25% depending on the response (movement/no movement) of the preceding patient (at the same alfentanil target concentrations) to ulnar-nerve stimulation. The minimum concentrations of propofol and alfentanil required to prevent movement in 50% of patients (EC50) was determined by logistic regression. Speed of emergence and recovery of cognitive function, time to discharge, and incidence of side effects were compared for four different combinations of propofol and alfentanil with nitrous oxide.

Results

The EC50 for propofol alone with nitrous oxide was 6.1 microg/ml. AlfentaniL at concentrations of 41+/-17 (SD), 113+/-54, and 130+/-61 ng/mL reduced the EC50 of propofol to 3.3, 2.3, and 2.2 microg/ml, respectively, and decreased emergence time (eye opening) to 8.1, 4.9, and 3.4 min, compared with 24.3 min for propofol alone. Side effects did not differ between groups.

Conclusions

The authors conclude that there is a synergistic effect between propofol and alfentanil, and that combining alfentanil with propofol is associated with faster early recovery.
Oro- and Nasogastric Tube Passage in Intubated Patients
Authors: Ozer Steven , Benumof Jonathan L.
Published: November 2003

Background

Insertion of a gastric tube (GT) in anesthetized, paralyzed, and intubated patients can be difficult The purpose of this study was to determine fiberoptically why GTs succeed or fail to enter the esophagus and, based on these findings, to determine a mechanism for converting failures into successes.

Methods

Sixty patients under general anesthesia and orotracheally intubated were studied. The larynx and hypopharynx of each patient were viewed via a fiberscope placed through the left naris. GTs were passed orally (OGT) and nasally (NGT) in all patients, and the pathway of passage or site of resistance was visualized. In cases of resistance, medially directed ipsilateral neck pressure was applied over the lateral thyrohyoid membrane (termed lateral neck pressure) to try to allow passage of the GT.

Results

All 60 patients had both an OGT and NGT passed for a total of 120 attempts. The GT passed easily on the first attempt in 92 of 120 insertions (77%) (for OGT 51/60 = 85% and for NGT 41/60 = 68%, P < 0.05). In 92% of these first-pass successes, the GT entered the hypopharynx just lateral to the arytenoid cartilages. The GT met resistance and failed to pass in 28 of 120 insertions (23%) (for OGT 9/60 = 15% and for NGT 19/60 = 32%). The sites of impaction were the piriform sinuses (13/28 = 46%), arytenoid cartilages (7/28 = 25%), and trachea (6/28 = 21%), and two OGTs did not pass the oropharynx (2/28 = 70%). Lateral neck pressure was attempted 20 times (for the piriform sinus and arytenoid cartilage impactions) with 17 successes (85%) and three failures (15%). The average distance to passage of the OGT and NGT by the arytenoid cartilage was 13.2 and 16.2 cm, respectively.

Conclusion

GTs enter the hypopharynx just lateral to the arytenoid cartilages. Consequently, the most common sites of resistance at the laryngeal level are the arytenoid cartilages and piriform sinuses. Lateral neck pressure compresses the piriform sinuses and moves the arytenoid cartilages medially, relieving 85% of these GT impactions.
Fentanyl Pharmacokinetics in Hemorrhagic Shock
Authors: Egan Talmage D. , Kuramkote Suma , Gong Guoqing , Zhang Jie , McJames Scott W. , Bailey Peter L.
Published: November 2003

Background

It is common clinical practice to administer reduced doses of opioid to patients suffering from hemorrhagic shock to minimize adverse hemodynamic consequences and to prevent prolonged opioid effect However, the scientific foundation supporting this practice is not well established. The aim of this study was to test the hypothesis that hemorrhagic shock alters both the distribution and clearance of opioids using fentanyl in a porcine isobaric hemorrhage model.

Methods

Eighteen pigs were randomized to shock or control groups. The animals in the shock group were subjected to hemorrhage using an isobaric method. Pigs in both groups received fentanyl (50 microg/kg) intravenously over 5 min. Frequent arterial blood samples were obtained for radioimmunoassay. Each animal's pharmacokinetic parameters were estimated by fitting a three-compartment model to the concentration versus time data Nonlinear mixed-effects population pharmacokinetic models examining the influence of mean arterial pressure and cardiac index were also constructed. Clinical simulations using the final population model were performed.

Results

The shock cohort reached substantially higher fentanyl concentrations. The shock group's central clearance and central- and second-compartment distribution volumes were significantly reduced. The most useful population model scaled all pharmacokinetic parameters to mean arterial pressure. The simulations illustrated that hemorrhagic shock results in higher fentanyl concentrations for any given dosage scheme.

Conclusion

The essential finding of the study is that fentanyl pharmacokinetics are substantially altered by hemorrhagic shock. The reduced opioid requirement commonly observed during hemorrhagic shock is at least partially attributable to pharmacokinetic mechanisms.
Effect of Isoflurane on In Situ Vascular Smooth Muscle Transmembrane Potential in Spontaneous Hypertension
Authors: Stekiel Thomas A. , Kokita Naohiro , Yamazaki Mitsuaki , Bosnjak Zeljko J. , Kampine John P. , Stekiel William J.
Published: November 2003

Background

Administration of general anesthetics to patients with chronic hypertension often causes hemodynamic instability that has been attributed in part to a poorly understood increased loss of control of peripheral vascular smooth muscle tone. The purpose of the current study was to determine if such an increased loss occurs in the spontaneously hypertensive (SH) rat neurogenic model of chronic hypertension, as reflected by a greater volatile anesthetic-induced in situ vascular smooth muscle hyperpolarization compared with normotensive Wistar-Kyoto (WKY) rat controls.

Methods

Vascular smooth muscle transmembrane potentials (E(m)s) were measured in situ using glass microelectrodes in externalized small mesenteric resistance- and capacitance-regulating blood vessels in 10- to 12-week-old SH and WKY rats before, during and after administration of 1 minimum alveolar concentration levels (1.5%) of inhaled or 0.60 mM superfused isoflurane. Vascular smooth muscle E(m)s were also measured in vessels after local sympathetic denervation with superfused 6-hydroxydopamine.

Results

Local sympathetic denervation caused a significant hyperpolarization of arterial and venous vascular smooth muscle in SH but not WKY rats. Hyperpolarization induced by either inhaled or superfused isoflurane was significantly greater in innervated than in denervated arterial and venous vascular smooth muscle, particularly in SH rats. In addition, for innervated (but not denervated) arterial and venous vascular smooth muscle, hyperpolarization induced by inhaled (but not superfused) isoflurane was significantly greater in SH than in WKY rats.

Conclusions

In the neurogenic SH rat model of human hypertension, a primary mechanism underlying elevated isoflurane-induced vascular smooth muscle hyperpolarization (and reduced vascular smooth muscle tone) in both resistance- and capacitance-regulating blood vessels is a central neural inhibition of excitatory sympathetic input. Peripheral neural and nonneurally mediated hyperpolarization by isoflurane is similar in SH and WKY rat vascular smooth muscles.
Confirmation of Caudal Needle Placement Using Nerve Stimulation
Authors: Tsui Ban C. H. , Tarkkila Pekka , Gupta Sunil , Kearney Ramona
Published: November 2003

Background

The study was designed to examine a new method of confirming proper caudal needle placement using nerve stimulation.

Methods

Thirty-two pediatric patients were studied. A 22-gauge insulated needle was inserted into the caudal canal via the sacral notch until a "pop" was felt. The needle placement was classified as correct or incorrect depending upon the presence or absence of anal sphincter contraction (S2-S4) to electrical simulation (1 to 10 mA).

Results

Three patients were excluded, two because they inadvertently received neuromuscular blockers and one because the patient's anatomy precluded any attempt at a caudal block. The sensitivity and specificity of the test were both 100% in predicting clinical outcomes of the caudal block. Six patients had a negative stimulation test after the first attempt to place the needle. Four of these went on to receive a second attempt of needle insertion after a subcutaneous bulge or resistance to local anesthetic injection were observed. Following needle reinsertion, positive stimulation tests were elicited. These patients received the local anesthetic injection with ease and had good analgesia postoperatively. No attempt was made to reinsert the needle in the remaining two patients with a negative stimulation test, as they did not show subcutaneous bulge or resistance upon injection. These patients had poor analgesia postoperatively. The positive predictive value of the test was greater than the presence of a "pop" alone (P < 0.05) but not significantly different (P = 0.492) over the presence of "pop" and easy injection.

Conclusion

This test may be used as a teaching and adjuvant tool in performing caudal block.
Length-dependent Regulation of Left Ventricular Function in Coronary Surgery Patients
Authors: De Hert Stefan G. , Gillebert Thierry C. , Ten Broecke Pieter W. , Moulijn Adriaan C.
Published: November 2003

Background

Load-dependent impairment of left ventricular (LV) function was observed after leg elevation in a subgroup of coronary surgery patients. The present study investigated underlying mechanisms by comparing hemodynamic effects of an increase in LV systolic pressures with leg elevation to effects of a similar increase in systolic pressures with phenylephrine.

Methods

The study was performed in patients undergoing elective coronary surgery prior to cardiopulmonary bypass. High-fidelity LV pressure tracings (n = 25) and conductance LV volume data (n = 10) were obtained consecutively during leg elevation and after phenylephrine administration (5 microg/kg).

Results

Leg elevation resulted in a homogeneous increase in end-diastolic volume. The change in stroke volume (SV), stroke work (SW) and dP/dtmax was variable, with an increase in some patients but no change or a decrease in other patients. For a matched increase in systolic pressures, phenylephrine increased SW and dP/dtmax in all patients with no change in SV. Load dependence of relaxation (slope R of the tau-end-systolic pressure relation) was inversely related for changes in SV, SW, and dP/dtmax with leg elevation but not with phenylephrine.

Conclusions

The different effects of leg elevation and phenylephrine suggest that the observed decrease in SV, SW, and dP/dtmax with leg elevation in some patients could not be attributed to an impaired contractile response to increased systolic LV pressures. Instead, load-dependent impairment of LV function after leg elevation appeared related to a deficient length-dependent regulation of myocardial function.
Comparative Pharmacodynamic Modeling of the Electroencephalography-slowing Effect of Isoflurane, Sevoflurane, and Desflurane
Authors: Rehberg Benno , Bouillon Thomas , Zinserling Jorg , Hoeft Andreas
Published: November 2003

Background

The most common measure to compare potencies of volatile anesthetics is minimum alveolar concentration (MAC), although this value describes only a single point on a quantal concentration-response curve and most likely reflects more the effects on the spinal cord rather than on the brain. To obtain more complete concentration-response curves for the cerebral effects of isoflurane, sevoflurane, and desflurane, the authors used the spectral edge frequency at the 95th percentile of the power spectrum (SEF95) as a measure of cerebral effect.

Methods

Thirty-nine patients were randomized to isoflurane, sevoflurane, or desflurane groups. After induction with propofol, intubation, and a waiting period, end-tidal anesthetic concentrations were randomly varied between 0.6 and 1.3 MAC, and the EEG was recorded continuously. Population pharmacodynamic modeling was performed using the software package NONMEM.

Results

The population mean EC50 values of the final model for SEF95 suppression were 0.66+/-0.08 (+/- SE of estimate) vol% for isoflurane, 1.18+/-0.10 vol% for sevoflurane, and 3.48+/-0.66 vol% for desflurane. The slopes of the concentration-response curves were not significantly different; the common value was lambda = 0.86+/-0.06. The Ke0 value was significantly higher for desflurane (0.61+/-0.11 min(-1)), whereas separate values for isoflurane and sevoflurane yielded no better fit than the common value of 0.29+/-0.04 min(-1). When concentration data were converted into fractions of the respective MAC values, no significant difference of the C50 values for the three anesthetic agents was found.

Conclusions

This study demonstrated that (1) the concentration-response curves for spectral edge frequency slowing have the same slope, and (2) the ratio C50(SEF95)/MAC is the same for all three anesthetic agents. The authors conclude that MAC and MAC multiples, for the three volatile anesthetics studied, are valid representations of the concentration-response curve for anesthetic suppression of SEF95.
The Role of Tumor Necrosis Factor-α in the Pathogenesis of Aspiration Pneumonitis in Rats
Authors: Davidson Bruce A. , Knight Paul R. , Helinski Jadwiga D. , Nader Nader D. , Shanley Thomas P. , Johnson Kent J.
Published: November 2003

Background

Aspiration pneumonitis is characterized by proteinaceous pulmonary edema and acute infiltration of neutrophils into the alveolar space. This study examined the role of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), on the pathogenesis of the injury produced by the different components that may be present in the aspirate, acid, or gastric particles.

Methods

Rats were injured by intratracheal instillation of a vehicle containing acid or gastric particles. TNF-alpha concentration of bronchoalveolar lavage fluid was determined using a bioassay. upregulation of lung TNF-alpha mRNA was also measured. The effect of intratracheal anti-rat TNF-alpha treatment was assessed by lung protein permeability, blood gases, and lung myeloperoxidase activity.

Results

Injury vehicle alone and acid injury resulted in a small TNF-alpha peak 1-2 h after injury in the lavage fluid. Both particulate and acidic particulate groups produced a much more robust TNF-alpha signal that reached a plateau at 2-4 h after injury and declined at 8 h. Upregulation of TNF-alpha mRNA was only detected in the particulate-containing groups. Acidic particulate exposure yielded a synergistic increase in protein permeability and decrease in blood oxygenation. Anti-TNF-alpha treatment reduced protein permeability and myeloperoxidase activity and increased blood oxygenation in the groups exposed to only acid. Such treatment had no effect on either of the particulate containing injuries.

Conclusions

TNF-alpha is differentially manifested according to the components that make up the aspirate but the levels of TNF-alpha expression do not correlate with the severity of the resultant injury. However, the reduction in acid-induced lung injury by anti-TNF-alpha treatment indicates that TNF-alpha plays a role in the pathogenesis of aspiration pneumonitis.
Thermoregulatory Thresholds for Vasoconstriction in Patients Anesthetized with Various 1-Minimum Alveolar Concentration Combinations of Xenon, Nitrous Oxide, and Isoflurane
Authors: Goto Takahisa , Matsukawa Takashi , Sessler Daniel I. , Uezono Shoichi , Ishiguro Yoshiki , Ozaki Makoto , Morita Shigeho
Published: November 2003

Background

Nitrous oxide limits intraoperative hypothermia because the vasoconstriction threshold with nitrous oxide is higher than with equi-minimum alveolar concentrations of sevoflurane or isoflurane, presumably because of its stimulating actions on the sympathetic nervous system. Xenon, in contrast, does not cause sympathetic activation. Therefore, the authors tested the hypothesis that the vasoconstriction threshold during xenon-isoflurane anesthesia is less than during nitrous oxide-isoflurane anesthesia or isoflurane alone.

Methods

Fifteen patients each were randomly assigned to one of three 1-minimum alveolar concentration anesthetic regimens: (1) xenon, 43% (0.6 minimum alveolar concentration) and isoflurane, 0.5% (0.4 minimum alveolar concentration); (2) nitrous oxide, 63% (0.6 minimum alveolar concentration) and isoflurane 0.5%; or (3) isoflurane, 1.2%. Ambient temperature was maintained near 23 degrees C and the patients were not actively warmed. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients. A gradient exceeding 0 degrees C indicated significant vasoconstriction. The core-temperature threshold that would have been observed if skin had been maintained at 33 degrees C was calculated from mean skin and distal esophageal temperatures at the time of vasoconstriction.

Results

The patients' demographic variables, preinduction core temperatures, ambient operating room temperatures, and fluid balance were comparable among the three groups. Heart rates were significantly less during xenon anesthesia than with nitrous oxide. The calculated vasoconstriction threshold was lowest with xenon (34.6+/-0.8 degrees C, mean +/- SD), intermediate with isoflurane alone (35.1+/-0.6 degrees C), and highest with nitrous oxide (35.7+/-0.6 degrees C). Each of the thresholds differed significantly.

Conclusions

Xenon inhibits thermoregulatory control more than isoflurane, whereas nitrous oxide is the least effective in this respect.
Additive Contribution of Nitrous Oxide to Sevoflurane Minimum Alveolar Concentration for Tracheal Intubation in Children
Authors: Swan Hilton D. , Crawford Mark W. , Pua Hwee Ling , Stephens Derek , Lerman Jerrold
Published: November 2003

Background

To study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MAC(TI)) with and without nitrous oxide in children.

Methods

Seventy-two children aged 1-7 yr were assigned randomly to receive one of three end-tidal concentrations of nitrous oxide and one of four end-tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane: 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end-tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight-blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation.

Results

Logistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P = 0.89) and was removed from the logistic model. The MAC(TI) (+/- SE) of sevoflurane was 2.66+/-0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54+/-0.25%. Thirty-three percent and 66% nitrous oxide decreased the MAC(TI) of sevoflurane by 18% and 40% (P<0.001), respectively.

Conclusions

We conclude that nitrous oxide and sevoflurane suppress the responses to tracheal intubation in a linear and additive fashion in children.
Mechanisms Underlying the Inhibitory Effect of Propofol on the Contraction of Canine Airway Smooth Muscle
Authors: Lin Chih-Chung , Shyr Ming-Hwang , Tan Peter P. C. , Chien Chin-Sung , Pan Shiow-Lin , Wang Chuan-Chwan , Chiu Chi-Tso , Yang Chuen-Mao
Published: November 2003

Background

Propofol has been shown to produce relaxation of preconstricted airway smooth muscle. Although the inhibition of calcium mobilization is supposed to be the major mechanism of action, the whole picture of the mechanisms is not completely clear.

Methods

Contractile response was performed using canine tracheal rings. The effects of propofol on carbachol-induced mobilization of intracellular Ca2+ and phosphoinositide hydrolysis were measured using cultured canine tracheal smooth muscle cells by monitoring fura-2 signal and assessing the accumulation of [3H]-inositol phosphates. To detect the effect of propofol on muscarinic receptor density and affinity, [3H]N-methyl-scopolamine was used as a radioligand for receptor binding assay.

Results

Pretreatment with propofol shifts the concentration-response curves of carbachol-induced smooth muscle contraction to the right in a concentration-dependent manner without changing the maximal response. Propofol not only decreased the release of Ca2+ from internal stores but also inhibited the calcium influx induced by carbachol. In addition, carbachol-induced inositol phosphate accumulation was attenuated by propofol; the inhibitory pattern was similar to the contractile response. Moreover, propofol did not alter the density of muscarinic receptors. The dissociation constant value was not altered by pretreatment with 100 microM propofol but was significantly increased by 300 microM (propofol, 952+/-229 pM; control, 588+/-98 pM; P<0.05).

Conclusions

Propofol attenuates the muscarinic receptor-mediated airway muscle contraction. The mechanism underlying these effects was attenuation of inositol phosphate generation and inhibition of Ca2+ mobilization through the inhibition of the receptor-coupled signal-transduction pathway.
Stereoselectivity of Bupivacaine in Local Anesthetic–sensitive Ion Channels of Peripheral Nerve
Authors: Nau Carla , Vogel Werner , Hempelmann Gunter , Bräu Michael E.
Published: November 2003

Background

The local anesthetic bupivacaine exists in two stereoisomeric forms, R(+)- and S(-)-bupivacaine. Because of its lower cardiac and central nervous system toxicity, attempts were made recently to introduce S(-)-bupivacaine into clinical anesthesia. We investigated stereoselective actions of R(+)-and S(-)-bupivacaine toward two local anesthetic-sensitive ion channels in peripheral nerve, the Na+ and the flicker K+ channel.

Methods

In patch-clamp experiments on enzymatically demyelinated peripheral amphibian nerve fibers, Na+ and flicker K+ channels were investigated in outside-out patches. Half-maximum inhibiting concentrations (IC50) were determined. For the flicker K+ channel, simultaneous block by R(+)-bupivacaine and S(-)-bupivacaine was analyzed for competition and association (k1) and dissociation rate constants (k(-1)) were determined.

Results

Both channels were reversibly blocked by R(+)- and S(-)-bupivacaine. The IC50 values (+/- SEM) for tonic Na+ channel block were 29+/-3 microM and 44+/-3 microM, respectively. IC50 values for flicker K+ channel block were 0.15+/-0.02 microM and 11+/-1 microM, respectively, resulting in a high stereopotency ratio (+/-) of 73. Simultaneously applied enantiomers competed for a single binding site. Rate constants k1 and k(-1) were 0.83+/-0.13x10(6) M(-1) x S(-1) and 0.13+/-0.03 s(-1), respectively, for R(+)-bupivacaine and 1.90+/-0.20x10(6) M(-1) x s(-1) and 8.3+/-1.0 s(-1), respectively, for S(-)-bupivacaine.

Conclusions

Bupivacaine block of Na+ channels shows no salient stereoselectivity. Block of flicker K+ channels has the highest stereoselectivity ratio of bupivacaine action known so far. This stereoselectivity derives predominantly from a difference in k(-1), suggesting a tight fit between R(+)-bupivacaine and the binding site. The flicker K+ channel may play an important role in yet unknown toxic mechanisms of R(+)-bupivacaine.
Effect of Epinephrine on Lidocaine Clearance In Vivo
Authors: Bernards Christopher M. , Kopacz Dan J.
Published: November 2003

Background

Local anesthetic nerve block prolonged by epinephrine is thought to result from local vasoconstriction and consequent decreased local anesthetic clearance from the injection site. However, no study has yet confirmed this directly in humans by measuring tissue concentrations of local anesthetic over time. In addition, recent studies have shown that the alpha2-adrenergic receptor agonist, clonidine, also prolongs nerve block without altering local anesthetic clearance. Because epinephrine is also an alpha2-adrenergic receptor agonist, it is possible that epinephrine prolongs local anesthetic block by a pharmacodynamic mechanism and not a pharmacokinetic one. This study was designed to address this issue.

Methods

Microdialysis probes were placed adjacent to the superficial peroneal nerve in both feet of eight volunteers. Plain lidocaine (1%) was injected along one peroneal nerve and lidocaine with epinephrine (2.5 microg/ml) was injected along the other nerve in a double-blinded, randomized manner. The concentration of lidocaine in tissue was measured at 5-min intervals, and sensory block and cutaneous blood flow were assessed by laser Doppler at 10-min intervals for 5 h. The resulting data for lidocaine concentration versus time were fit to a two-compartment model using modeling software.

Results

Epinephrine prolonged sensory block by decreasing local blood flow and slowing clearance. There was no evidence of a pharmacodynamic effect of epinephrine.

Conclusion

Although epinephrine activates alpha2-adrenergic receptors, its mechanism for prolonging the duration of local anesthetic block rests on its ability to decrease local anesthetic clearance and not on a pharmacodynamically mediated potentiation of local anesthetic effect.
Tooth Pulp– and Facial Hair Mechanoreceptor–evoked Responses of Trigeminal Sensory Neurons Are Attenuated during Ketamine Anesthesia
Authors: Cairns Brian E. , McErlane Shelly A. , Fragoso Miguel C. , Soja Peter J.
Published: November 2003

Background

Evidence exists that ketamine, administered systemically using a dose required for inducing a state of anesthesia, may antagonize nociceptive but not innocuous input to lumbar dorsal horn neurons. However, it is unclear whether ketamine exerts this selective action on sensory inputs to trigeminal sensory neurons. The current study was undertaken to compare the responses evoked in trigeminal sensory neurons by electrical stimuli applied to the tooth pulp versus air-puff stimuli applied to facial hair mechanoreceptors (FHMs) during quiet wakefulness versus ketamine anesthesia.

Methods

Accordingly, responses of rostral trigeminal sensory nuclear complex (TSNC) and trigeminothalamic tract neurons evoked by tooth pulp (a source of small-diameter fiber input) and FHMs (a source of larger-diameter fiber input) were recorded extracellularly from chronically instrumented cats before, during, and after recovery from the anesthetic state induced by a single (2.2 mg/kg) intravenous injection of ketamine.

Results

Overall, tooth pulp-evoked responses of TSNC neurons were maximally suppressed by 50% within 5 min after the intravenous administration of ketamine. Ketamine also suppressed the FHM-evoked responses of TSNC and trigeminothalamic neurons by 45%. The time course of ketamine's suppressive action was equivalent for tooth pulp- and FHM-evoked responses. However, the recovery of tooth pulp-evoked TSNC neuronal responses at suprathreshold intensities was markedly prolonged compared with neuronal responses driven by threshold stimuli or FHM.

Conclusions

These electrophysiologic results in the chronically instrumented cat preparation indicate that a nonselective suppression of orofacial somatosensory information occurs during ketamine anesthesia. The prolonged recovery of suprathreshold responses of TSNC neurons mediated by small-diameter afferent fiber input may partly underlie the analgesic action of ketamine that is clinically relevant at subanesthetic doses.