bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Role of Transcranial Motor Evoked Potentials in Predicting Neurologic and Histopathologic Outcome after Experimental Spinal Cord Ischemia
Authors: Lips Jeroen , de Haan Peter , de Jager Steven W. , Vanicky Ivo , Jacobs Michael J. , Kalkman Cor J. 
Published: November 2003

Background
Monitoring of myogenic motor evoked potentials to transcranial stimulation (tcMEPs) is clinically used to assess motor pathway function during aortic and spinal procedures that carry a risk of spinal cord ischemia (SCI). Although tcMEPs presumably detect SCI before irreversible neuronal deficit occurs, and prolonged reduction of tcMEP signals is thought to be associated with impending spinal cord damage, experimental evidence to support this concept has not been provided. In this study, histopathologic and neurologic outcome was examined in a porcine model of SCI after different durations of intraoperative loss of tcMEP signals.

Methods
In 15 ketamine-sufentanil-anesthetized pigs (weight, 35-45 kg) the spinal cord feeding lumbar arteries were exposed. tcMEP were recorded from the upper and lower limbs. Under normothermic conditions, animals were randomly allocated to undergo short-term tcMEP reduction (group A, < 10 min, n = 5) or prolonged tcMEP reduction (group B, 60 min, n = 10), resulting from temporary or permanent clamping of lumbar segmental arteries. Neurologic function was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated 72 h after induction of SCI.

Results
In all animals except one, segmental artery clamping reduced tcMEP to below 25% of baseline. All but one animal in group A had reduced tcMEP for less than 10 min and had normal motor function and no infarction at 72 h after the initial tcMEP reduction. Seven animals in group B (70%) had reduced tcMEP signals for more than 60 min and were paraplegic with massive spinal cord infarction at 72 h. Two animals (one in both groups) had tcMEP loss for 40 min, with moderate infarction and normal function. In general, histopathologic damage and neurologic dysfunction did not occur when tcMEP amplitude recovered within 10 and 40 min after the initial decline, respectively.

Conclusion
Prolonged reduction of intraoperative tcMEP amplitude is predictive for postoperative neurologic dysfunction, while recovery of the tcMEP signal within 10 min after the initial decline corresponds with normal histopathology and motor function in this experimental model. This finding confirms that intraoperative tcMEPs have a good prognostic value for neurologic outcome during procedures in which the spinal cord is at risk for ischemia.
Isoflurane Hyperalgesia Is Modulated by Nicotinic Inhibition
Authors: Flood Pamela , Sonner James M. , Gong Diane , Coates Kristen M. 
Published: November 2003

Background
The inhaled anesthetic isoflurane inhibits neuronal nicotinic acetylcholine receptors (nAChRs) at concentrations lower than those used for anesthesia. Isoflurane produces biphasic nociceptive responses, with both hyperalgesia and analgesia within this concentration range. Because nicotinic agonists act as analgesics, the authors hypothesized that inhibition of nicotinic transmission by isoflurane causes hyperalgesia.

Methods
The authors studied female mice at 6-8 weeks of age. They measured hind paw withdrawal latency at isoflurane concentrations from 0 to 0.98 vol% after the animals had received a nicotinic agonist (nicotine), a nicotinic antagonist (mecamylamine or chlorisondamine), or saline intraperitoneally. In addition, the authors tested the interactions between mecamylamine and isoflurane and nicotine and isoflurane in heterologously expressed alpha(4)beta(2) nAChRs.

Results
Female mice had significant hyperalgesia from isoflurane. Nicotine administration prevented isoflurane-induced hyperalgesia without altering the antinociception produced by higher isoflurane concentrations. Mecamylamine treatment caused a biphasic nociceptive response similar to that caused by isoflurane. Mecamylamine and isoflurane had an additive effect, both at heterologously expressed alpha(4)beta(2) nAChRs and on the production of hyperalgesia in vivo. Mecamylamine thus potentiated hyperalgesia but did not affect analgesia.

Conclusions
Since hyperalgesia occurs in vivo at isoflurane doses that antagonize nAChRs in vitro, is prevented by a nicotinic agonist, and is mimicked and potentiated by nicotinic antagonists, the authors conclude that isoflurane inhibition of nAChRs activation is involved in the pathway that causes hyperalgesia. At subanesthetic doses, isoflurane can either enhance pain responses (produce hyperalgesia) or be analgesic (antinociceptive). In rats, low volatile anesthetic concentrations (0.1-0.2 minimum alveolar concentration [MAC]) elicit hyperalgesia, while 0.4-0.6 MAC elicits antinociception.
Ca2+-Calmodulin-dependent Protein Kinase II Plays a Major Role in Halothane-induced Dose-dependent Relaxation in the Skinned Pulmonary Artery
Authors: Su Judy Y. , Vo Anhkiet C. 
Published: November 2003

Background
Previously, the authors have shown in Ca(2+)-clamped skinned arterial strips that protein kinase C (PKC) plays a role in 3% halothane- or isoflurane-increased force. PKC in the pulmonary artery and Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) in the femoral artery have been implicated in isoflurane-induced relaxation. For this study, the authors used clinical concentrations of halothane to examine the role of PKC and CaMKII in the halothane-induced biphasic effect on contraction in skinned pulmonary arterial strips.

Methods
Rabbit pulmonary arterial strips were mounted on force transducers and treated with saponin to make the sarcolemma permeable ("skinning"). Skinned strips were activated by low Ca(2+) (pCa 6.3) buffered with 7 mm EGTA, or the PKC activator phorbol-12,13-dibutyrate (PDBu, 1 microm) until force reached a steady state (control). Halothane (1, 2, and 3%) was administered, and the force was observed at peak and 15 min (test results). Ca(2+) ionophore (A23187, 10 microm) and inhibitors were preincubated in a relaxing solution and present in subsequent contracting solutions. Inhibitors were bisindolylmaleimide and Gö6976 for PKC, and KN-93 and the inhibitor protein (CKIINtide) for CaMKII.

Results
Halothane (1-3%) dose-dependently caused an initial increase (18-35%) and a subsequent decrease (48-68%) in pCa 6.3-induced force. Bisindolylmaleimide, 3 and 10 microm, completely blocked the increase in force at 2% and 3% halothane, respectively. CKIINtide, 0.1 microm, reduced the force at 3% halothane. The decrease in force at 1% and 2% halothane was partially prevented by 0.01 microm bisindolylmaleimide, and at 1, 2, and 3% halothane by 0.01, 0.1, and 1 microm CKIINtide, respectively. At 3% halothane, the increased force was abolished by A23187. In PDBu-induced force, 3% halothane-induced relaxation was also partially prevented by lower concentrations of KN-93 and CKIINtide.

Conclusions
In skinned pulmonary arterial strips, the dose-dependent increase in force by halothane is associated with PKC activation, and that of decrease is associated with CaMKII activation.
Ambulatory Surgery Patients May Be Discharged before Voiding after Short-acting Spinal and Epidural Anesthesia
Authors: Mulroy Michael F. , Salinas Francis V. , Larkin Kathleen L. , Polissar Nayak L. 
Published: November 2003

Background
Voiding before discharge is usually required after outpatient epidural or spinal anesthesia because of concern about bladder overdistention and dysfunction. Shorter duration spinal and epidural anesthesia may allow return of bladder function before overdistention occurs in low-risk patients (those younger than age 70, not having hernia, rectal, or urologic surgery, and without a history of voiding difficulty), and predischarge voiding may not be necessary.

Methods
After institutional review board approval and informed consent, 201 low-risk ambulatory patients were prospectively studied in either a standard or accelerated pathway after undergoing spinal or epidural anesthesia with procaine, lidocaine, 2-chloroprocaine, or less than 7 mg bupivacaine; epinephrine was not used in any anesthetic. Standard pathway patients (n = 70) were required to void before discharge. Accelerated pathway (n = 131) patients were not required to void. (After randomization of an initial 163 patients to one of the two tracks, 38 additional patients were assigned to the accelerated pathway.) If accelerated pathway patients voided, they were discharged when all other discharge criteria were met. If they did not spontaneously void after block resolution, a bladder ultrasound (BUS) was performed. If the BUS indicated a urine volume of less than 400 ml, the patients were discharged and instructed to return to the emergency department if they were unable to void within 8 h of discharge. If the BUS indicated a urine volume of greater than 400 ml, the patients were reassessed in 1 h and were discharged if they could void spontaneously. If they could not void spontaneously, they were catheterized to facilitate discharge. All patients were contacted the next day to assess the return of normal bladder function.

Results
All standard pathway patients voided without difficulty, and were discharged in 153 +/- 49 (SD) min. 62 patients in the accelerated pathway voided spontaneously after resolution of their block and were discharged in 127 +/- 41 min. 46 patients were discharged with a BUS less than 400 ml in 120 +/- 42 min. 23 patients had a BUS greater than 400 ml: of these, 20 patients voided within an hour and were discharged in 162 +/- 45 min. Three were catheterized after 1 h, and were discharged in 186 +/- 61 min. Mean discharge time for all patients in the accelerated pathway was 22 min shorter than the standard pathway (P = 0.002). No patients had difficulty voiding or returned to the hospital for urinary problems. None reported new urologic symptoms.

Conclusions
Delay of discharge after outpatient spinal or epidural anesthesia with short-duration drugs for low-risk procedures is not necessary, and may result in prolonged discharge times.
Levobupivacaine 0.125% and Lidocaine 0.5% for Intravenous Regional Anesthesia in Volunteers
Authors: Atanassoff Peter G. , Aouad Rima , Hartmannsgruber Maximilian W.B. , Halaszynski Thomas 
Published: November 2003

Background
Levobupivacaine, a long acting, amino-amide, local anesthetic, may offer advantages over lidocaine for intravenous regional anesthesia (IVRA). The objective of this investigation was to compare levobupivacaine to lidocaine for IVRA.

Methods
After institutional review board approval and informed consent, eight unpremedicated male American Society of Anesthesiologists (ASA) I-II volunteers received 40 ml of levobupivacaine 0.125% or lidocaine 0.5% for IVRA on separate days. Onset and regression of sensory anesthesia by pinprick, transcutaneous electrical stimulation (TES), and of motor function were tested before, during, and after release of the tourniquet. Central nervous system and cardiac side effects were evaluated after local anesthetic administration and tourniquet release. The tourniquet remained inflated for 30-45 min.

Results
Intravenous regional anesthesia with either agent provided surgical anesthesia. Sensory anesthesia to pinprick (lateral antebrachial cutaneous nerve) was faster with lidocaine at median 1.5 min. versus 12.5 min with levobupivacaine. Loss of sensation to TES occurred at median 22.5 and 27.5 min for lidocaine and levobupivacaine, respectively. Loss of motor function occurred earlier after lidocaine administration. After release of the tourniquet, return of sensation to TES, pinprick (ulnar nerve), and return of motor function occurred later with levobupivacaine at median 25, 15, and 21.25 versus 10, 4.5, and 10 min with lidocaine. Central nervous system side effects were absent in volunteers given levobupivacaine, but five of eight volunteers given lidocaine experienced mild side effects. No cardiac events were noted.

Conclusions
Levobupivacaine 0.125% may be an alternative to lidocaine 0.5% for IVRA. Longer lasting analgesia after release of the tourniquet may be caused by a more profound and prolonged tissue binding effect of levobupivacaine.
A Neuroanatomical Construct for the Amnesic Effects of Propofol
Authors: Veselis Robert A. , Reinsel Ruth A. , Feshchenko Vladimir A. , Dnistrian Ann M. 
Published: November 2003

Background
This study was designed to identify neuroanatomical locations of propofol's effects on episodic memory by producing minimal and maximal memory impairment during conscious sedation. Drug-related changes in regional cerebral blood flow (rCBF) were located in comparison with rCBF increases during a simple word memory task.

Methods
Regional cerebral blood flow changes were assessed in 11 healthy volunteers using H215O positron emission tomography (PET) and statistical parametric mapping (SPM99) at 600 and 1,000 ng/ml propofol target concentrations. Study groups were based on final recognition scores of auditory words memorized during PET scanning. rCBF changes during propofol administration were compared with those during the word memory task at baseline.

Results
Nonoverlapping memory effects were evident: low (n = 4; propofol concentration 523 +/- 138 ng/ml; 44 +/- 13% decrement from baseline memory) and high (n = 7; 829 +/- 246 ng/ml; 87 +/- 6% decrement from baseline) groups differed in rCBF reductions primarily in right-sided prefrontal and parietal regions, close to areas activated in the baseline memory task, particularly R dorsolateral prefrontal cortex (Brodmann area 46; x, y, z = 51, 38, 22). The medial temporal lobe region exhibited relative rCBF increases.

Conclusions
As amnesia becomes maximal, rCBF reductions induced by propofol occur in brain regions identified with working memory processes. In contrast, medial temporal lobe structures were resistant to the global CBF decrease associated with propofol sedation. The authors postulate that the episodic memory effect of propofol is produced by interference with distributed cortical processes necessary for normal memory function rather than specific effects on medial temporal lobe structures.
Randomized Prospective Comparison of Forced Air Warming Using Hospital Blankets versus Commercial Blankets in Surgical Patients
Authors: Kabbara Abdallah , Goldlust Samuel A. , Smith Charles E. , Hagen Joan F. , Pinchak Alfred C. 
Published: November 2003

Background
The purpose of this study was to evaluate the efficacy of an experimental approach to forced air warming using hospital blankets or a Bair Hugger warming unit (Augustine Medical Inc., Eden Prairie, MN) to create a tent of warm air.

Methods
Adult patients undergoing major surgery were studied. Patients were randomized to receive forced air warming using either a commercial Bair Hugger blanket (control group, n = 44; set point, 43 degrees C) or standard hospital blankets (experimental group, n = 39; set point, 38 degrees C). Distal esophageal temperatures were monitored. Patients were contacted the following day regarding any problems with the assigned warming technique.

Results
Surface area covered was 36 +/- 12% (mean +/- SD) in the experimental group and 40 +/- 10% in the control group. Final temperatures at the end of surgery were similar between groups: experimental, 36.2 +/- 0.6 degrees C; control, 36.4 +/- 0.7 degrees C. A similar number of patients had esophageal temperature less than 36 degrees C at the end of surgery in both groups (experimental, 12 of 39 [31%]; control, 12 of 44 [27%]). The majority of patients were satisfied with their anesthetic and warming technique: experimental, 38 of 39 patients; control, 44 of 44 patients. There were no thermal injuries.

Conclusions
Standard hospital blankets heated to 38 degrees C forced air were equally as effective as commercial blankets heated with forced air at 43 degrees C. However, based on concerns expressed by the manufacturer, this experimental technique should not be used until further safety evaluation has been undertaken.
P6 Acupoint Injections Are as Effective as Droperidol in Controlling Early Postoperative Nausea and Vomiting in Children
Authors: Wang Shu-Ming , Kain Zeev N. 
Published: November 2003

Background
P6 acupuncture in adults is reported to be an effective preventive treatment for postoperative nausea and vomiting (PONV). It is not clear, however, whether this technique is effective as a preventive treatment for PONV in children.

Methods
Children undergoing anesthesia and surgery were randomized to four groups: (a) intravenous saline + bilateral P6 acupoint injections (n = 50); (b) intravenous droperidol + bilateral P6 sham acupuncture (n = 49); (c) intravenous saline + bilateral sham point injections (n = 43); (d) intravenous saline +bilateral P6 sham acupuncture (n = 45). The perioperative anesthetic technique was standardized in all subjects. The incidence of postoperative nausea and vomiting (PONV) was evaluated in postanesthesia care unit (PACU) and 24 h after surgery.

Results
Incidence of nausea in the PACU was significantly lower in the acupoint group as compared with the sham point group (32% vs. 56%, P = 0.029) and P6 sham group (32% vs. 64%, P = 0.002) but not as compared with the droperidol group (32% vs. 46%, P = ns). Similarly, subjects in the acupoint group had a significantly lower incidence of vomiting in the PACU as compared with the sham point group (12% vs. 33%, P = 0.026) and P6 sham group (12% vs. 31%, P = 0.029) but not as compared with the droperidol group (12% vs. 18%, P = ns). The combined incidence of early PONV was also lower in the acupoint group as compared with the sham point group (P = 0.045) and P6 sham group (P = 0.004) but not as compared with the droperidol group (42% vs. 51%, P = ns). Finally, significantly fewer subjects in the acupoint group required intravenous ondansetron as an initial rescue therapy (P = 0.024). At 24 h after surgery, however, the incidence of late PONV was similar among the four study groups (P = ns).

Conclusion
In children, P6 acupoint injections are as effective as droperidol in controlling early postoperative nausea and vomiting.
Pharmacokinetics of Tranexamic Acid during Cardiopulmonary Bypass
Authors: Dowd Noreen P. , Karski Jacek M. , Cheng Davy C. , Carroll Jo A. , Lin Yonggu , James Robert L. , Butterworth John 
Published: November 2003

Background
Tranexamic acid (TA) reduces blood loss and blood transfusion during heart surgery with cardiopulmonary bypass (CPB). TA dosing has been empiric because only limited pharmacokinetic studies have been reported, and CPB effects have not been characterized. We hypothesized that many of the published TA dosing techniques would prove, with pharmacokinetic modeling and simulation, to yield unstable TA concentrations.

Methods
Thirty adult patients undergoing elective coronary artery bypass grafting, valve surgery, or repair of atrial septal defect received after induction of anesthesia: TA 50 mg/kg (n = 11), TA 100 mg/kg (n = 10), or TA 10 mg/kg (n = 10) over 15 min, with 1 mg x kg(-1) x hr(-1) maintenance infusion for 10 h. TA was measured in plasma using high performance liquid chromatography. Pharmacokinetic modeling was accomplished using a mixed effects technique. Models of increasing complexity were compared using Schwarz-Bayesian Criterion (SBC).

Results
Tranexamic acid concentrations rapidly fell in all three groups. Data were well fit to a 2-compartment model, and adjustments for CPB were supported by SBC. Assuming a body weight of 80 kg, our model estimates V1 = 10.3 l before CPB and 11.9 l during and after CPB; V2 = 8.5 l before CPB and 9.8 l during and after CPB; Cl1 = 0.15 l/s before CPB, 0.11 l/s during CPB, and 0.17 l/s after CPB; and Cl2 = 0.18 l/s before CPB and 0.21 l/s during and after CPB. Based on simulation of previous studies of TA efficacy, we estimate that a 30-min loading dose of 12.5 mg/kg with a maintenance infusion of 6.5 mg x kg(-1) x hr(-1) and 1 mg/kg added to the pump prime will maintain TA concentration greater than 334 microm, and a higher dose based on 30 mg/kg loading dose plus 16 mg x kg(-1) x h(-1) continuous infusion and 2 mg/kg added to the pump prime would maintain TA concentrations greater than 800 microm.

Conclusions
Tranexamic acid pharmacokinetics are influenced by CPB. Our TA pharmacokinetic model does not provide support for the wide range of TA dosing techniques that have been reported. Variation in TA efficacy from study to study and confusion about the optimal duration of TA treatment may be the result of dosing techniques that do not maintain stable, therapeutic TA concentrations.
Halothane Suppression of Spinal Sensory Neuronal Responses to Noxious Peripheral Stimuli Is Mediated, in Part, by Both GABAAand Glycine Receptor Systems
Authors: Yamauchi Masanori , Sekiyama Hiroshi , Shimada Steven G. , Collins J. G. 
Published: November 2003

Background
A major effect of general anesthesia is lack of response in the presence of a noxious stimulus. Anesthetic depression of spinal sensory neuronal responses to noxious stimuli is likely to contribute to that essential general anesthetic action. The authors tested the hypothesis that gamma-aminobutyric acid receptor type A (GABA(A)) and strychnine-sensitive glycine receptor systems mediate halothane depression of spinal sensory neuronal responses to noxious stimuli.

Methods
Extracellular activity of single spinal dorsal horn wide dynamic range (WDR) neurons was recorded in decerebrate, spinal cord transected rats. Neuronal responses to noxious (thermal and mechanical) and nonnoxious stimuli were examined in the drug-free state. Subsequently, cumulative doses (0.1-2.0 mg/kg) of bicuculline (GABA(A) antagonist) or strychnine (glycine antagonist) were administered intravenously in the absence or presence of 1 minimum alveolar concentration (MAC) of halothane.

Results
Halothane, 1.1%, depressed the response of WDR neurons to both forms of noxious stimuli. Antagonists, by themselves, had no effect on noxiously evoked activity. However, bicuculline and strychnine (maximum cumulative dose, 2.0 mg/kg) partially but significantly reversed the halothane depression of noxiously evoked activity. Similar results were seen with most, but not all, forms of nonnoxiously evoked activity. In the absence of halothane, strychnine significantly increased neuronal responses to low threshold receptive field brushing.

Conclusion
Halothane depression of spinal WDR neuronal responses to noxious and most nonnoxious stimuli is mediated, in part, by GABA(A) and strychnine-sensitive glycine systems. A spinal source of glycine tonically inhibits some forms of low threshold input to WDR neurons.