bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mild Intraoperative Hypothermia Prolongs Postanesthetic Recovery
Authors: Lenhardt Rainer , Marker Elvine , Goll Veronika , Tschernich Heinz , Kurz Andrea , Sessler Daniel I. , Narzt Edith , Lackner Franz 
Published: November 2003

Background
Intraoperative hypothermia is common and persists for several hours after surgery. Hypothermia may prolong immediate recovery by augmenting anesthetic potency, delaying drug metabolism, producing hemodynamic instability, or depressing cognitive function. Accordingly, the authors tested the hypothesis that intraoperative hypothermia prolongs postoperative recovery.

Methods
Patients undergoing elective major abdominal surgery (n = 150) were anesthetized with isoflurane, nitrous oxide, and fentanyl. They were randomly assigned to routine thermal management (hypothermia) or extra warming (normothermia). Postoperative surgical pain was treated with patient-controlled analgesia. Fitness for discharge from the postanesthesia care unit was evaluated at 20-min intervals by investigators blinded to group assignment and postoperative core temperatures. Scoring was based on a modification of a previously published system that included activity, ventilation, consciousness, and hemodynamic responses. Patients were considered fit for discharge when they sustained a score of 80% (13 points) for at least two consecutive measurement periods.

Results
Morphometric characteristics and anesthetic management were similar in each group. Final intraoperative core temperatures differed by approximately 2 degrees C: 34.8 +/- 0.6 versus 36.7 +/- 0.6 degrees C (mean +/- SD, P < 0.001). Postoperative pain scores and postoperative use of patient-controlled opioid were similar. Hypothermic patients required approximately 40 min longer (94 +/- 65 vs. 53 +/- 36 min) to reach fitness for discharge, even when return to normothermia was not a criterion (P < 0.001). Duration of recovery in the two groups differed by approximately 90 min when a core temperature >36 degrees C was also required (P < 0.001).

Conclusion
Maintaining core normothermia decreases the duration of postanesthetic recovery and may, therefore, reduce costs of care.
Comparison of the Bullard and Macintosh Laryngoscopes for Endotracheal Intubation of Patients with a Potential Cervical Spine Injury
Authors: Watts Andrew D. J. , Gelb Adrian W. , Bach David B. , Pelz David M. 
Published: November 2003

Background
In the emergency trauma situation, in-line stabilization (ILS) of the cervical spine is used to reduce head and neck extension during laryngoscopy. The Bullard laryngoscope may result in less cervical spine movement than the Macintosh laryngoscope. The aim of this study was to compare cervical spine extension (measured radiographically) and time to intubation with the Bullard and Macintosh laryngoscopes during a simulated emergency with cervical spine precautions taken.

Methods
Twenty-nine patients requiring general anesthesia and endotracheal intubation were studied. Patients were placed on a rigid board and anesthesia was induced. Laryngoscopy was performed on four occasions: with the Bullard and Macintosh laryngoscopes both with and without manual ILS. Cricoid pressure was applied with ILS. To determine cervical spine extension, radiographs were exposed before and during laryngoscopy. Times to intubation and grade view of the larynx were also compared.

Results
Cervical spine extension (occiput-C5) was greatest with the Macintosh laryngoscope (25.9 degrees +/- 2.8 degrees). Extension was reduced when using the Macintosh laryngoscope with ILS (12.9 +/- 2.1 degrees) and the Bullard laryngoscope without stabilization (12.6 +/- 1.8 degrees; P < 0.05). Times to intubation were similar for the Macintosh laryngoscope with ILS (20.3 +/- 12.8 s) and for the Bullard without ILS (25.6 +/- 10.4 s). Manual ILS with the Bullard laryngoscope results in further reduction in cervical spine extension (5.6 +/- 1.5 degrees) but prolongs time to intubation (40.3 +/- 19.5 s; P < 0.05).

Conclusions
Cervical spine extension and time to intubation are similar for the Macintosh laryngoscope with ILS and the Bullard laryngoscope without ILS. However, time to intubation is significantly prolonged when the Bullard laryngoscope is used in a simulated emergency with cervical spine precautions taken. This suggests that the Bullard laryngoscope may be a useful adjunct to intubation of patients with potential cervical spine injury when time to intubation is not critical.
Lack of Analgesic Activity of Morphine-6-glucuronide after Short-term Intravenous Administration in Healthy Volunteers
Authors: Lotsch Jorn , Kobal Gerd , Stockmann Anne , Brune Kay , Geisslinger Gerd 
Published: November 2003

Background
The analgesic activity of morphine-6-glucuronide (M-6-G) is well recognized for its contribution to the effects of morphine and its possible use as an opioid analgesic with a wider therapeutic range than morphine. The present study attempted to quantify the relative contribution of M-6-G to analgesia observed after systemic administration of morphine.

Methods
In a placebo-controlled, sixfold crossover study in 20 healthy men, the effects of M-6-G were assessed at steady-state plasma concentrations of M-6-G identical to and two and three times higher than those measured after administration of morphine. Morphine and M-6-G were administered as an intravenous bolus followed by infusion over 4 h. Dosage A was M-6-G-bolus of 0.015 mg/kg plus infusion of 0.0072 mg x kg(-1) x h(-1). Dosage B was M-6-G-bolus of 0.029 mg/kg plus infusion of 0.014 mg x kg(-1) x h(-1). Dosage C was M-6-G-bolus of 0.044 mg/kg plus infusion of 0.022 mg x kg(-1) x h(-1). Dosage D was a morphine bolus of 0.14 mg/kg plus infusion of 0.05 mg x kg(-1) x h(-1) for 4 h. Dosage E was M-6-G combined with morphine (doses A + D). Dosage F was a placebo. The analgesic effects of M-6-G and morphine were measured before administration of the bolus and after 3.5 h using an experimental pain model based on pain-related cortical potentials and pain ratings after specific stimulation of the nasal nociceptor with short pulses of gaseous carbon dioxide.

Results
Morphine significantly reduced subjective and objective pain correlates compared with placebo. In contrast, M-6-G produced no statistically significant effects. The addition of M-6-G to morphine did not increase the effects of morphine. Morphine produced significantly more side effects than M-6-G.

Conclusion
After short-term intravenous administration at doses that produce plasma concentrations of M-6-G similar to those seen after administration of morphine, M-6-G had no analgesic effects in the present placebo-controlled study in healthy volunteers.
Sympathovagal Effects of Spinal Anesthesia Assessed by the Spontaneous Cardiac Baroreflex
Authors: Gratadour P. , Viale J. P. , Parlow J. , Sagnard P. , Counioux H. , Bagou G. , Annat G. , Hughson R. , Quintin L. 
Published: November 2003

Background
The changes in sympathovagal balance induced by spinal anesthesia remain controversial. The spontaneous baroreflex method allows the continuous assessment of the spontaneous engagement of the cardiac baroreflex, giving an index of sympathovagal balance. The purpose of this study was to follow the effects of spinal anesthesia on spontaneous baroreflex sensitivity.

Methods
Continuous electrocardiogram and noninvasive blood pressure were recorded in 24 patients scheduled for elective inguinal hernia repair and randomly assigned to three groups: (1) no volume loading, (2) volume loading of 15 ml/kg lactated Ringer's solution, and (3) continuous infusion of etilefrine (an ephedrine-like drug). Each patient was studied before, during, and after bupivacaine-induced spinal anesthesia (mean sensory block: T4). Spontaneous baroreflex sensitivity and parameters of time-domain analysis of heart rate variability were calculated from 30 min of recording of each period.

Results
No significant change in spontaneous baroreflex slope or parameters of time-domain analysis were observed after regional anesthesia in any group. However, three patients experienced episodes of bradycardia and hypotension in the absence of a high block; these three patients showed an increase in spontaneous baroreflex sensitivity and time-domain parameters.

Conclusions
Using a noninvasive, continuous technique to estimate cardiac sympathovagal balance, no significant variation in autonomic balance induced by spinal anesthesia was observed. However, untoward episodes of bradycardia and hypotension occurred in three patients, who could not be prospectively identified by the parameters studied.
Dose-Response of Rocuronium Bromide in Children Anesthetized with Propofol
Authors: Woolf Rex L. , Crawford Mark W. , Choo Shu May 
Published: November 2003

Background
The aim of this study was to determine the potency of rocuronium during propofol/fentanyl/N2O anesthesia in children and to compare the time course of action of rocuronium at doses of two and three times the ED95 with that of succinylcholine.

Methods
Rocuronium (120, 160, 200, or 240 microg/kg) was administered to 48 children aged 2-10 yr. Neuromuscular block was assessed by monitoring the electromyographic response of the adductor digiti minimi to supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s every 10 s. Potency was determined by log-probit transformation and least-squares linear regression analysis of dose and response. In a second group of 30 children, the onset and recovery profile of rocuronium at doses of two and three times the ED95 was compared with that of succinylcholine (2 mg/kg).

Results
Values for ED50 and ED95 were 210 +/- 24 and 404 +/- 135 microg/kg, respectively. The time to 90% neuromuscular block after 1.2 mg/kg rocuronium (three times the ED95), 33 +/- 5 s (mean +/- SD), did not differ significantly from that after succinylcholine, at 30 +/- 7 s; however, both were significantly less than that after 0.8 mg/kg rocuronium, 46 +/- 8 s (P < 0.05). The time to 25% recovery from 1.2 microg/kg rocuronium, 41 +/- 13 min, was approximately 50% greater than that after 0.8 mg/kg, at 27 +/- 6 min (P < 0.001), and eight times greater than that after succinylcholine, at 5.2 +/- 1.9 min (P < 0.001).

Conclusions
Both 1.2 mg/kg rocuronium (three times the ED95) and 2 mg/kg succinylcholine provide 90% neuromuscular block within 45 s in 95% of children. The present dose-response data support the use of rocuronium at a dose of 1.2 mg/kg when rapid onset and intermediate-duration neuromuscular block are needed in children.
Emulsion Formulation Reduces Propofol's Dose Requirements and Enhances Safety
Authors: Dutta Sandeep , Ebling William F. 
Published: November 2003

Background
Propofol, a highly lipophilic anesthetic, is formulated in a lipid emulsion for intravenous use. Propofol has brisk onset and offset of effect after rapid administration and retains rapid offset characteristics after long-term administration. The authors tried to determine whether the emulsion vehicle is requisite for propofol's evanescent effect-time profile.

Methods
The time course of sedation and electroencephalographic (EEG) effect after propofol administration was measured in three studies in rats instrumented. In study 1, propofol was infused in either emulsion or lipid-free vehicle (n = 12), in a repeated measures cross-over design. In study 2, propofol in lipid-free vehicle was infused with or without simultaneous infusion of drug-free lipid emulsion (n = 6) in a repeated measures cross-over design. In study 3, propofol was infused in either emulsion (n = 5) or lipid-free vehicle (n = 5) to EEG burst suppression.

Results
In study 1, relative to the emulsion formulation, propofol administered at equivalent doses in lipid-free vehicle resulted in a longer time to effect onset (1.4 +/- 0.2 vs. 0.5 +/- 0.1 min, EEG) and a trend for delayed anesthetic recovery (26.8 +/- 9.4 vs. 17 +/- 3.5 min, EEG; 26.1 +/- 8.8 vs. 16.8 +/- 3.3 min, sleep). In study 2, coadministration of drug-free emulsion with propofol did not alter the time course of effect. In study 3, more than twice the dose of propofol was required to achieve EEG burst suppression with the lipid-free formulation. Two animals died after administration of propofol to EEG burst suppression with the lipid-free formulation; no deaths occurred in the emulsion group.

Conclusion
The incorporation of propofol in emulsion reduces dose requirements and produces rapid onset and recovery of anesthetic effect.
Dose-dependent Effects of Halothane on the Phrenic Nerve Responses to Acute Hypoxia in Vagotomized Dogs
Authors: Stuth Eckehard A. E. , Dogas Zoran , Krolo Mirko , Kampine John P. , Hopp Francis A. , Zuperku Edward J. 
Published: November 2003

Background
Previous studies in dogs and humans suggest that the carotid body chemoreceptor response to hypoxia is selectively impaired by halothane. The present studies in an open-loop canine preparation were performed to better delineate the effects of anesthetic concentrations of halothane on the carotid body chemoreceptor-mediated phrenic nerve response to an acute hypoxic stimulus.

Methods
Three protocols were performed to study the effects of halothane anesthesia on the phrenic nerve response to 1 min of isocapnic hypoxia (partial pressure of oxygen [PaO2] at peak hypoxia, 35-38 mmHg) in unpremedicated, anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. In protocol 1, the dose-dependent effects of halothane from 0.5-2.0 minimum alveolar concentration (MAC) on the hypoxic response during moderate hypercapnia (partial pressure of carbon dioxide [PaCO2], 60-65 mmHg) were studied in 10 animals. In protocol 2, the hypoxic responses at 1 MAC halothane near normocapnia (PaCO2, 40-45 mmHg) and during moderate hypercapnia were compared in an additional four animals. In protocol 3, the hypoxic response of 4 of 10 dogs from protocol 1 was also studied under sodium thiopental (STP) anesthesia after they completed protocol 1.

Results
Protocol 1: Peak phrenic nerve activity (PPA) increased significantly during the hypoxic runs compared with the isocapnic hyperoxic controls at all halothane doses. The phrenic nerve response to the hypoxic stimulus was present even at the 2 MAC dose. Protocol 2: The net hypoxic responses for the two carbon dioxide background levels at 1 MAC were not significantly different. Protocol 3: The net hypoxic response of PPA for the STP anesthetic was not significantly different from the 1 MAC halothane dose. Bilateral carotid sinus denervation abolished the PPA response to hypoxia.

Conclusions
The phrenic nerve response to an acute, moderately severe isocapnic hypoxic stimulus is dose-dependently depressed but not abolished by surgical doses of halothane. This analysis does not suggest a selective depression of the carotid body chemoreceptor response by halothane. The observed hypoxic phrenic response was mediated by the carotid body chemoreceptors in vagotomized dogs because bilateral carotid sinus denervation abolished all increases in PPA.
Effects of Halothane on the Phrenic Nerve Responses to Carbon Dioxide Mediated by Carotid Body Chemoreceptors in Vagotomized Dogs
Authors: Stuth Eckehard A. E. , Dogas Zoran , Krolo Mirko , Kampine John P. , Hopp Francis A. , Zuperku Edward J. 
Published: November 2003

Background
Previous studies in dogs showed that the phrenic nerve response to an acute hypoxic stimulus was dose dependently depressed by 0.5-2.0 minimum alveolar concentration (MAC) of halothane but not abolished. Because a carbon dioxide stimulus is transduced by a different mechanism in the carotid body chemoreceptors (CBCRs) than is a hypoxic stimulus, inhalational anesthetics may preferentially depress one of these transduction processes, the central neuronal processing, or both, of the integrated responses to these two types of inputs.

Methods
Carotid body chemoreceptor stimulation was produced by short (1-1.5 s), bilateral, 100% carbon dioxide in saline infusions into the carotid arteries during neural inspiration in unpremedicated, halothane-anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. The phrenic neurogram quantified the neural inspiratory response. Four protocols were performed in the study: (1) the dose-dependent effects of halothane anesthesia (0.5-2.0 MAC) during hyperoxic hypercapnia on phrenic nerve activity, (2) the effects of three background levels of the partial pressure of carbon dioxide (PaCO2) on the magnitude of the carbon dioxide infusion responses at 1 MAC halothane, (3) the effects of anesthetic type on the magnitude of the carbon dioxide infusion response, and (4) the effects of CBCR denervation.

Results
Peak phrenic nerve activity (PPA) increased significantly during the carbon dioxide-stimulated phrenic burst in protocols 1-3; after denervation there was no response (protocol 4). Halothane produced a dose-dependent reduction in the PPA of control and carbon dioxide infusion-stimulated phrenic bursts and in the net carbon dioxide response. The net PPA responses for the different PaCO2 background levels were not different but were somewhat larger for sodium thiopental anesthesia than for 1.0 MAC halothane.

Conclusions
The phrenic nerve response to an acute, severe carbon dioxide stimulus was dose dependently depressed by surgical doses of halothane. The observed responses to carbon dioxide infusion were mediated by the CBCRs because they were eliminated by CBCR denervation. These results suggest that the CBCR transduction and central transmission of the carbon dioxide signal in terms of inspiratory excitatory drive are not abolished at surgical levels of halothane anesthesia.
Involvement of Cerulospinal Glutamatergic Neurotransmission in Fentanyl-induced Muscular Rigidity in the Rat
Authors: Fu Miin-Jiuan , Tsen Le-Yin , Lee Tak-Yu , Lui Ping-Wing , Chan Samuel H. H. 
Published: November 2003

Background
Investigators in the authors' laboratory previously established the critical participation of the cerulospinal noradrenergic pathway in muscular rigidity elicited by fentanyl. The identification of colocalization of glutamate with tyrosine hydroxylase in most locus ceruleus neurons suggests a role for cerulospinal glutamatergic neurotransmission in fentanyl-induced muscular rigidity. This suggestion and the subtype(s) of glutamate receptors involved were investigated here.

Methods
Electromyographic signals activated by bilateral microinjection of 2.5 microg fentanyl into the locus ceruleus were recorded differentially from the left sacrococcygeus dorsi lateralis muscle of adult male Sprague-Dawley rats. The effect of intrathecal administration at the lower lumbar spinal cord of various N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists or agonists on this index of muscular rigidity was studied. Rats were under mechanical ventilation, and intravenous infusion of ketamine (30 mg x kg(-1) x h(-1)) was maintained until 10 min before fentanyl was administered.

Results
Microinjection of fentanyl bilaterally into the locus ceruleus increased the root mean square and decreased the mean power frequency values of electromyographic signals. The efficacy of fentanyl to elicit muscular rigidity in this manner was significantly reduced by previous intrathecal administration of either 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), D-(-)-2-amino-5-phosphonovaleric acid (AP5), or (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP). Intrathecal administration of kainic acid or NMDA also resulted in significant electromyographic activation.

Conclusions
In addition to the cerulospinal noradrenergic mechanism, the cerulospinal glutamatergic pathway and both NMDA and non-NMDA receptors in the spinal cord may mediate fentanyl-induced muscular rigidity in the rat.
Interaction between Anesthetics and the Sodium-Hydrogen Exchange Inhibitor HOE 642 (Cariporide) in Ischemic and Reperfused Rat Hearts
Authors: Mathur Sanjiv , Karmazyn Morris 
Published: November 2003

Background
Sodium (Na+)-hydrogen (H+) exchange (NHE) inhibitors are effective cardioprotective agents. The potent NHE inhibitor HOE 642 (cariporide) is being evaluated clinically in high-risk patients, including those having coronary artery bypass. Volatile anesthetics are also cardioprotective, most likely via different mechanisms. The potential interaction between anesthetics and HOE 642 was investigated.

Methods
Electrically paced isolated rat hearts were perfused at constant flow. Left ventricular developed pressure and end-diastolic pressure were monitored as determinants of function. Hearts were subjected to 60 min each of total ischemia followed by reperfusion. Isoflurane (0.93 minimum alveolar concentration [MAC]), sevoflurane (1.03 MAC), or sufentanil (1.2 nM) was added 15 min before ischemia and throughout reperfusion, either alone or in combination with HOE 642 (5 microM). The effect of HOE 642 alone was also studied. At the end of reperfusion, hearts were freeze-clamped for subsequent determination of tissue metabolites.

Results
In control hearts, left ventricular developed pressure recovered to 40% of preischemia values, whereas left ventricular end-diastolic pressure increased by 650% after reperfusion. Sevoflurane, isoflurane, or HOE 642 alone significantly enhanced left ventricular developed pressure recovery to more than 90%, although recovery with HOE 642 was more rapid and accompanied by significantly reduced left ventricular end-diastolic pressure. HOE 642 plus volatile anesthetics produced additive effects, with left ventricular developed pressure recovering by more that 100%, although left ventricular end-diastolic pressure was not further reduced. Sufentanil had no effect in terms of developed pressure, but protection with HOE 642 was maintained. HOE 642 with or without volatile anesthetics also preserved adenosine triphosphate levels.

Conclusions
Isoflurane, sevoflurane, and HOE 642 enhance ventricular recovery, but the effect of HOE 642 is also associated with reduced contracture and adenosine triphosphate preservation. A combination of the NHE inhibitor and either volatile agent confers additive and superior protection, which could be relevant for the establishment of ideal cardioprotective strategies during surgery.