bluuebunny/crossref_metadata_2025_split huggingface dataset:
Laryngoscopic Intubation
Authors: Mulcaster Julian T. , Mills Joanna , Hung Orlando R. , MacQuarrie Kirk , Law J. Adam , Pytka Saul , Imrie David , Field Chris 
Published: February 2004

Background
Many healthcare professionals are trained in direct laryngoscopic tracheal intubation (LEI), which is a potentially lifesaving procedure. This study attempts to determine the number of successful LEI exposures required during training to assure competent performance, with special emphasis on defining competence itself.

Methods
Analyses were based on a longitudinal study of novices under training conditions in the operating room. The progress of 438 LEIs performed by the 20 nonanesthesia trainees was monitored by observation and videotape analysis. Eighteen additional LEIs were performed by experienced anesthesiologists to define the standard. A generalized linear, mixed-modelling approach was used to identify key aspects of effective training and performance. The number of tracheal intubations that the trainees were required to perform before acquiring expertise in LEI was estimated.

Results
Subjects performed between 18 and 35 laryngoscopic intubations. However, statistical modeling indicates that a 90% probability of a "good intubation" required 47 attempts. Proper insertion and lifting of the laryngoscope were crucial to "good" or "competent" performance of LEI. Traditional features, such as proper head and neck positions, were found to be less important under the study conditions.

Conclusions
This study determined that traditional LEI teaching for nonanesthesia personnel using manikin alone is inadequate. A reevaluation of current standards in LEI teaching for nonanesthesia is required.
Optimal Oxygen Concentration during Induction of General Anesthesia
Authors: Edmark Lennart , Kostova-Aherdan Kamelia , Enlund Mats , Hedenstierna Göran 
Published: February 2004

Background
The use of 100% oxygen during induction of anesthesia may produce atelectasis. The authors investigated how different oxygen concentrations affect the formation of atelectasis and the fall in arterial oxygen saturation during apnea.

Methods
Thirty-six healthy, nonsmoking women were randomized to breathe 100, 80, or 60% oxygen for 5 min during the induction of general anesthesia. Ventilation was then withheld until the oxygen saturation, assessed by pulse oximetry, decreased to 90%. Atelectasis formation was studied with computed tomography.

Results
Atelectasis in a transverse scan near the diaphragm after induction of anesthesia and apnea was 9.8 +/- 5.2 cm2 (5.6 +/- 3.4% of the total lung area; mean +/- SD), 1.3 +/- 1.2 cm2 (0.6 +/- 0.7%), and 0.3 +/- 0.3 cm2 (0.2 +/- 0.2%) in the groups breathing 100, 80, and 60% oxygen, respectively (P < 0.01). The corresponding times to reach 90% oxygen saturation were 411 +/- 84, 303 +/- 59, and 213 +/- 69 s, respectively (P < 0.01).

Conclusion
During routine induction of general anesthesia, 80% oxygen for oxygenation caused minimal atelectasis, but the time margin before unacceptable desaturation occurred was significantly shortened compared with 100% oxygen.
Differential Effects of Propofol and Sevoflurane on Heart Rate Variability
Authors: Kanaya Noriaki , Hirata Naoyuki , Kurosawa Saori , Nakayama Masayasu , Namiki Akiyoshi 
Published: February 2004

Background
Propofol is reported to reduce both sympathetic and parasympathetic tone; however, it is not clear whether the changes in heart rate variability are associated with depth of anesthesia. The purposes of the present study were (1) to evaluate the changes in heart rate variability at different depths of hypnosis and (2) to compare the effects of propofol on heart rate variability with that of sevoflurane.

Methods
Thirty patients were randomly allocated into the propofol or sevoflurane for induction of anesthesia. The depth of hypnosis was monitored by the Bispectral Index (BIS). Spectral analysis of heart rate variability using a maximum-entropy method resulted in a characteristic power spectrum with two main regions, a high frequency (HF) and a low frequency (LF). Hemodynamics, entropy, LF, HF, and LF/HF were monitored when the patients were awake and after induction of anesthesia.

Results
Both propofol and sevoflurane decreased blood pressure in a BIS-dependent manner, whereas heart rate showed no significant changes during the study period. In the propofol group, entropy and HF decreased with a reduction in the BIS value. Although LF decreased after induction of anesthesia, propofol caused no further decrease in LF in spite of a reduction in the BIS value. In the sevoflurane group, LF decreased with a reduction in the BIS value. Entropy and HF decreased after induction of anesthesia (BIS at 80); however, no further decreases were observed in spite of a reduction in the BIS value.

Conclusions
Induction of anesthesia with propofol decreased blood pressure, entropy, and HF in a BIS-dependent manner, indicating that propofol reduces cardiac parasympathetic tone depending on the depth of hypnosis. Conversely, sevoflurane did not show the BIS-dependent decreases in heart rate, blood pressure, HF, and entropy, indicating that sevoflurane has little or no effect on cardiac parasympathetic tone.
Hypothermia and the Approximate Entropy of the Electroencephalogram
Authors: Levy Warren J. , Pantin Enrique , Mehta Sachin , McGarvey Michael 
Published: February 2004

Background
The electroencephalogram is commonly used to monitor the brain during hypothermic cardiopulmonary bypass and circulatory arrest. No quantitative relationship between the electroencephalogram and temperature has been elucidated, even though the qualitative changes are well known. This study was undertaken to define a dose-response relationship for hypothermia and the approximate entropy of the electroencephalogram.

Methods
The electroencephalogram was recorded during cooling and rewarming in 14 patients undergoing hypothermic cardiopulmonary bypass and circulatory arrest. Data were digitized at 128 Hz, and approximate entropy was calculated from 8-s intervals. The dose-response relationship was derived using sigmoidal curve-fitting techniques, and statistical analysis was performed using analysis of variance techniques.

Results
The approximate entropy of the electroencephalogram changed in a sigmoidal fashion during cooling and rewarming. The midpoint of the curve averaged 24.7 degrees C during cooling and 28 degrees C (not significant) during rewarming. The temperature corresponding to 5% entropy (T 0.05 ) was 18.7 degrees C. The temperature corresponding to 95% entropy (T 0.95 ) was 31.3 degrees C during cooling and 38.2 degrees C during rewarming ( P < 0.02).

Conclusions
Approximate entropy is a suitable analysis technique to quantify the electroencephalographic changes that occur with cooling and rewarming. It demonstrates a delay in recovery that is of the same magnitude as that seen with conventional interpretation of the analog electroencephalogram and extends these observations over a greater range of temperatures.
Isoflurane Pretreatment Inhibits Lipopolysaccharide-induced Inflammation in Rats
Authors: Plachinta Roman V. , Hayes John K. , Cerilli Lisa A. , Rich George F. 
Published: February 2004

Background
Previous studies have indicated that volatile anesthetic pretreatment protects cells from inflammation; therefore, the authors hypothesized that pretreatment with isoflurane may attenuate the hemodynamic and pathologic changes to the vasculature that are associated with inflammation.

Methods
Rats received intravenous lipopolysaccharide or saline placebo with and without pretreatment with isoflurane (1.4% for 30 min immediately before lipopolysaccharide). Mean arterial pressure (MAP) and response to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) vasodilators were assessed hourly for 6 h. Tumor necrosis factor-alpha concentrations, arterial blood gases, and vascular histology were also determined.

Results
Lipopolysaccharide decreased MAP and vasodilation to acetylcholine and sodium nitroprusside. Lipopolysaccharide also caused acidosis, endothelial swelling, and endothelial detachment from the smooth muscle. Isoflurane pretreatment prevented the decrease in MAP for 5 h and attenuated the decrease at 6 h. Pretreatment increased the vasodilation to acetylcholine in lipopolysaccharide rats to control concentrations but had no effect on sodium nitroprusside. In control rats, isoflurane pretreatment increased the response to acetylcholine and sodium nitroprusside but had no effect on MAP. Isoflurane pretreatment prevented the acidosis and endothelial damage to mesenteric and aortic vessels, and attenuated the increase in tumor necrosis factor-alpha associated with lipopolysaccharide-induced inflammation.

Conclusion
Pretreatment with 30 min of isoflurane attenuated the decrease in MAP and endothelium-dependent vasodilation, the acidosis, the increase in tumor necrosis factor-alpha, and the damage to the vascular endothelium associated with lipopolysaccharide-induced inflammation in rats. This study suggests that isoflurane pretreatment may protect the vasculature during inflammation.
Ketamine Differentially Blocks Sensory Afferent Synaptic Transmission in Medial Nucleus Tractus Solitarius (mNTS)
Authors: Jin Young-Ho , Bailey Timothy W. , Doyle Mark W. , Li Bai-yan , Chang Kyoung S. K. , Schild John H. , Mendelowitz David , Andresen Michael C. 
Published: February 2004

Background
Ketamine increases blood pressure and heart rate by unknown mechanisms, but studies suggest that an intact central nervous system and arterial baroreceptors are required. In the brain stem, medial nucleus tractus solitarius receives afferents from nodose neurons that initiate cardiovascular autonomic reflexes. Here, the authors assessed ketamine actions on afferent medial nucleus tractus solitarius synaptic transmission.

Methods
Ketamine was applied to horizontally sliced brain stems. Solitary tract (ST) stimulation evoked excitatory postsynaptic currents (eEPSCs) in medial nucleus tractus solitarius neurons. Capsaicin (200 nm) block of ST eEPSCs sorted neurons into sensitive (n = 19) and resistant (n = 23). In nodose ganglion slices, shocks to the peripheral vagal trunk activated afferent action potentials in sensory neurons classified by conduction velocities and capsaicin.

Results
Ketamine potently (10-100 mciro m) blocked small, ST-evoked -methyl-d-aspartate synaptic currents found only in a subset of capsaicin-resistant neurons (6 of 12). Surprisingly, ketamine reversibly inhibited ST eEPSC amplitudes and induced synaptic failure at lower concentrations in capsaicin-sensitive than in capsaicin-resistant neurons (P < 0.005; n = 11 and 11). Spontaneous EPSCs using non- -methyl-d-aspartate receptors were insensitive even to 1-3 mm ketamine, suggesting that ST responses were blocked presynaptically. Similarly, ketamine blocked C-type action potential conduction at lower concentrations than A-type nodose sensory neurons.

Conclusion
The authors conclude that ketamine inhibits postsynaptic -methyl-d-aspartate receptors and presynaptic afferent processes in medial nucleus tractus solitarius. Unexpectedly, capsaicin-sensitive (C-type), unmyelinated afferents are significantly more susceptible to block than capsaicin-resistant (A-type), myelinated afferents. This differentiation may be related to tetrodotoxin-resistant sodium currents. Since C-type afferents mediate powerful arterial baroreflexes effects, these differential actions may contribute to ketamine-induced cardiovascular dysfunction.
Pharmacokinetic–Pharmacodynamic Modeling of Rocuronium in Case of a Decreased Number of Acetylcholine Receptors
Authors: De Haes Ann , Proost Johannes H. , De Baets Mark H. , Stassen Maurice H. W. , Houwertjes Martin C. , Wierda J. Mark K. H. 
Published: February 2004

Background
In myasthenic patients, the sensitivity for nondepolarizing relaxants is increased and the time course of effect is prolonged due to a reduced number of functional acetylcholine receptors at the neuromuscular junction. The authors investigated both the performance of the link model proposed by Sheiner and a pharmacodynamic-pharmacokinetic model taking into account the number of unbound acetylcholine receptors in myasthenic pigs.

Methods
After obtaining the approval of the Animal Experiments Committee of their institution, the authors studied eight myasthenic pigs and eight control pigs. Myasthenia gravis was induced by injecting Torpedo acetylcholine receptors in weeks 1 and 4. On the day of the experiments, the pigs were anesthetized and intubated, and the appropriate muscles and nerves were prepared for the measurements. Rocuronium was administered by infusion to reach 90% twitch height block. Arterial blood was sampled during onset and offset of effect, and the plasma concentration of rocuronium was measured with high-performance liquid chromatography. Plasma concentration-time effect data were analyzed using two different pharmacokinetic-pharmacodynamic models, the link model according to Sheiner and a pharmacokinetic-pharmacodynamic model taking into account the unbound receptor concentration. Muscles were removed after the experiment for laboratory analysis of the acetylcholine receptor concentration.

Results
All eight pigs of the myasthenic group developed clinical signs of myasthenia gravis (muscle weakness) and showed increased sensitivity toward rocuronium. Pharmacokinetic modeling revealed no significant differences between myasthenic and control pigs. In pharmacokinetic-pharmacodynamic analysis, visual inspection as well as the Akaike Information Criterion (3,605 3,769) and the residual SD (3.2 3.6%) revealed a better fit for the unbound receptor model in myasthenic animals compared to the Sheiner model. Pharmacokinetic-pharmacodynamic analysis with the unbound receptor model demonstrated a decreased EC50 of 0.27 micro m (ranging from 0.17 to 0.59 micro m) compared to 2.71 micro m (ranging from 2.42 to 4.43 micro m) in control animals. The results of the Sheiner pharmacokinetic-pharmacodynamic analysis were in the same range. Both the laboratory analysis and pharmacokinetic-pharmacodynamic modeling showed a decrease in receptor concentration of more than 75%.

Conclusion
Both the Sheiner model and the unbound receptor model may be used to fit plasma concentration-effect data of rocuronium in pigs. The unbound receptor concentration model, however, can explain the observed differences in the time course of effect, based on receptor concentration.
Effects of Preemptive Analgesia on Pain and Cytokine Production in the Postoperative Period
Authors: Beilin Benzion , Bessler Hanna , Mayburd Eduard , Smirnov Genady , Dekel Arie , Yardeni Israel , Shavit Yehuda 
Published: February 2004

Background
The postoperative period is associated with increased production of proinflammatory cytokines, which are known to augment pain sensitivity, among other effects. In a previous study, the authors found that patients treated with patient-controlled epidural analgesia (PCEA) exhibited attenuated proinflammatory cytokine response in the postoperative period. In the present study, the authors examined whether preemptive analgesia continued with PCEA may further attenuate the proinflammatory cytokine response and reduce pain sensitivity in the postoperative period. They compared cytokine production in two groups of patients, one receiving PCEA, the other receiving preemptive epidural analgesia continued by PCEA.

Methods
Female patients hospitalized for transabdominal hysterectomy were randomly assigned to one of two pain management techniques: PCEA or preemptive epidural analgesia followed by PCEA (PA + PCEA). Postoperative pain was assessed using the visual analog scale. Blood samples were collected before, 24, 48, and 72 h following surgery. Production of the following cytokines was assessed in stimulated peripheral blood mononuclear cells: interleukin (IL)-1beta, tumor necrosis factor alpha, IL-6, IL-1ra, IL-10, and IL-2.

Results
Patients of the PA + PCEA group exhibited lower pain scores throughout the 72 h postoperatively, compared with patients of the PCEA group. In patients of the PA + PCEA group in the postoperative period, production of IL-1beta, IL-6, IL-1ra, and IL-10 was significantly less elevated, while IL-2 production was significantly less suppressed.

Conclusions
Proinflammatory cytokines are key mediators of illness symptoms, including hyperalgesia. The present results suggest that preemptive epidural analgesia is associated with reduced postoperative pain and attenuated production of proinflammatory cytokines.
Preoperative Cardiac Events in Elderly Patients with Hip Fracture Randomized to Epidural or Conventional Analgesia
Authors: Matot Idit , Oppenheim-Eden Arieh , Ratrot Ruand , Baranova Julia , Davidson Elyad , Eylon Sharon , Peyser Amos , Liebergall Meir 
Published: February 2004

Background
Perioperative myocardial ischemia occurs in 35% of unselected elderly patients undergoing hip fracture surgery. Perioperative epidural analgesia may reduce the incidence of adverse cardiac events.

Methods
The effect of early administration of epidural analgesia during the stressful period, on cardiac events was evaluated in a prospective randomized study in 68 patients with hip fractures who either had known coronary artery disease or were at high risk for coronary artery disease. On admission to the emergency room, patients were assigned to receive a usual care analgesic regimen (intramuscular meperidine, control group, n = 34) or continuous epidural infusion of local anesthetic and opioid (epidural group, n = 34). Monitoring in the preoperative period included a preoperative history and physical examination, daily assessment of cardiac adverse events, serial electrocardiograms, cardiac enzymes, and pain scores.

Results
Preoperative adverse cardiac events were significantly more prevalent in the control group compared with the epidural group (7 of 34 0 of 34; = 0.01). Adverse cardiac events included fatal myocardial infarction in three, fatal congestive heart failure in one, nonfatal congestive heart failure in one, and new onset atrial fibrillation in two. The incidence of intraoperative and postoperative adverse cardiac events was similar for the two groups. The significant difference between groups in the incidence of preoperative cardiac events prompted interruption of the study after the planned interim analysis.

Conclusions
The authors' data indicate that compared with conventional analgesia, early administration of continuous epidural analgesia is associated with a lower incidence of preoperative adverse cardiac events in elderly patients with hip fracture who have or are at risk for coronary artery disease. Preoperative epidural analgesia may be advantageous for this surgical population.
Transient Up-regulation of Spinal Cyclooxygenase-2 and Neuronal Nitric Oxide Synthase following Surgical Inflammation
Authors: Dolan Sharron , Kelly James G. , Huan Marie , Nolan Andrea M. 
Published: February 2004

Background
Surgery induces pain and hyperalgesia postoperatively. The products of cyclooxygenases and nitric oxide synthase (NOS) have been implicated in the development of inflammatory pain and hyperalgesia experimentally, and the use of drugs clinically that modify cyclooxygenase activity has been advocated in the management of perioperative pain. However, regulation of these enzymes following surgery has not been studied.

Methods
Adult female sheep (n = 12) undergoing a midline laparotomy for collection of ova were used in this study. Lumbar and cervical spinal cord tissue was collected from animals euthanized 1 day and 6 or 7 days after surgery and processed for cyclooxygenase (cyclooxygenase-1 and cyclooxygenase-2), neuronal NOS mRNA expression using reverse-transcription polymerase chain reaction and hybridization. Tissues were also processed for NADPH-diaphorase staining and cyclooxygenase-1 and cyclooxygenase-2 protein expression by immunohistochemistry and Western blotting.

Results
No alteration in cyclooxygenase-1 or cyclooxygenase-2 mRNA or protein concentrations were detected in spinal cord by reverse-transcription polymerase chain reaction and Western blotting, respectively, at 1 day or 6 or 7 days after surgery. However, using techniques that localize mRNA and protein expression ( hybridization and immunohistochemistry, respectively), increases in cyclooxygenase-2 were identified in lamina V dorsal horn neurons in lumbar spinal cord 1 day after surgery. A significant increase in neuronal NOS mRNA was observed in lumbar spinal cord 1 day after surgery, localized to laminae I-II and lamina V neurons, which returned to baseline concentrations by 6 to 7 days. NADPH-diaphorase staining was significantly increased in laminae I-II in lumbar spinal cord 1 day after surgery but not after 6 to 7 days.

Conclusions
Spinal cyclooxygenase and neuronal NOS pathways are differentially altered following surgical inflammation. The early and transient nature of these changes suggests that these enzymes are implicated in postoperative pain and hypersensitivity.
On the Mechanism by Which Epinephrine Potentiates Lidocaine's Peripheral Nerve Block
Authors: Sinnott Catherine J. , Cogswell Lawrence P. , Johnson Anthony , Strichartz Gary R. 
Published: February 2004

Background
Adding epinephrine to lidocaine solutions for peripheral nerve block potentiates and prolongs the action, but by incompletely understood mechanisms. In an effort to discriminate the pharmacokinetic from the pharmacodynamic effects of epinephrine, the authors measured the lidocaine content of peripheral nerve over the course of block produced by 0.5% lidocaine, with and without epinephrine, and correlated it with the degree of analgesia.

Methods
Percutaneous sciatic nerve blocks were performed in 18 groups of rats (10 in each) with 0.1 ml of either 0.5% lidocaine or 0.5% lidocaine with epinephrine (1:100,000). Over the full course of nerve block, the authors regularly measured analgesia to toe pinch and then rapidly removed nerves to assay intraneural lidocaine content at 2-120 min after injection.

Results
The kinetics of lidocaine's clearance from nerve was composed of a fast-decaying transient superimposed on a very slowly decaying component. The effect of epinephrine on the intraneural lidocaine content was to increase the amount of lidocaine in the slow-decaying component by threefold to fourfold, although the total neural content was not altered by epinephrine for the first 10 min after injection. Epinephrine prolonged blockade by almost fourfold and enhanced the intensity of peak analgesia, as well as the fraction of rats with complete block, almost throughout the 2-120-min period of behavioral observation.

Conclusions
Adding epinephrine to lidocaine solutions increases the intensity and duration of sciatic nerve block in the rat. The early increase in intensity is not matched with an increase in intraneural lidocaine content at these early times, although the prolonged duration of block by epinephrine appears to correspond to an enlarged lidocaine content in nerve at later times, as if a very slowly emptying "effector compartment" received a larger share of the dose. The increase in early analgesia without increased lidocaine content may be explained by a pharmacodynamic action of epinephrine that transiently enhances lidocaine's potency, but also by a pharmacokinetic effect that alters the distribution of the same net content of lidocaine within the nerve.