bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preoperative Intradermal Acupuncture Reduces Postoperative Pain, Nausea and Vomiting, Analgesic Requirement, and Sympathoadrenal Responses
Authors: Kotani Naoki , Hashimoto Hiroshi , Sato Yutaka , Sessler Daniel I. , Yoshioka Hideki , Kitayama Masatou , Yasuda Tadanobu , Matsuki Akitomo 
Published: November 2003

Background
In a controlled and double-blind study, the authors tested the hypothesis that preoperative insertion of intradermal needles at acupoints 2.5 cm from the spinal vertebrae (bladder meridian) provide satisfactory postoperative analgesia.

Methods
The authors enrolled patients scheduled for elective upper and lower abdominal surgery. Before anesthesia, patients undergoing each type of surgery were randomly assigned to one of two groups: acupuncture (n = 50 and n = 39 for upper and lower abdominal surgery, respectively) or control (n = 48 and n = 38 for upper and lower abdominal surgery, respectively). In the acupuncture group, intradermal needles were inserted to the left and right of bladder meridian 18-24 and 20-26 in upper and lower abdominal surgery before induction of anesthesia, respectively. Postoperative analgesia was maintained with epidural morphine and bolus doses of intravenous morphine. Consumption of intravenous morphine was recorded. Incisional pain at rest and during coughing and deep visceral pain were recorded during recovery and for 4 days thereafter on a four-point verbal rating scale. We also evaluated time-dependent changes in plasma concentrations of cortisol and catecholamines.

Results
Starting from the recovery room, intradermal acupuncture increased the fraction of patients with good pain relief as compared with the control (P < 0.05). Consumption of supplemental intravenous morphine was reduced 50%, and the incidence of postoperative nausea was reduced 20-30% in the acupuncture patients who had undergone either upper or lower abdominal surgery (P < 0.01). Plasma cortisol and epinephrine concentrations were reduced 30-50% in the acupuncture group during recovery and on the first postoperative day (P < 0.01).

Conclusion
Preoperative insertion of intradermal needles reduces postoperative pain, the analgesic requirement, and opioid-related side effects after both upper and lower abdominal surgery. Acupuncture analgesia also reduces the activation of the sympathoadrenal system that normally accompanies surgery.
Role of the Atrial Natriuretic Factor in Obstetric Spinal Hypotension
Authors: Frölich Michael A. 
Published: November 2003

Background
In recent years, the concept of prophylactic volume expansion to prevent hypotension caused by spinal anesthesia has been challenged. Investigators have reevaluated the concept of prehydration in the obstetric patient and the physiologic mechanisms involved. This article addresses whether the hypotensive effects attributed to the atrial natriuretic factor are the reason for the apparent failure of prehydration.

Methods
Atrial natriuretic factor was measured before (baseline) and 10 min after spinal anesthetic drug injection (control) in 48 healthy pregnant patients scheduled for elective cesarean section. Sixteen patients received hydration with 15 ml/kg crystalloid immediately before spinal anesthesia, 16 patients received the same volume starting with the spinal anesthetic injection, and the remaining 16 patients received no prehydration (control). Blood pressure, heart rate, ephedrine requirements, infused fluids, and urine output were measured.

Results
Atrial natriuretic factor concentrations increased significantly in prehydrated patients but not in the control group. There was a significant correlation in the change in atrial natriuretic factor concentrations and urine output but no correlation in the control atrial natriuretic factor concentrations and blood pressure or ephedrine requirements. Ephedrine requirements and blood pressure did not differ significantly among study groups.

Conclusions
Atrial natriuretic factor is a potent endogenous diuretic in the pregnant patient but does not appear to be involved in short-term cardiovascular homeostasis after spinal anesthesia. Prehydration appears to be an ineffective measure to prevent post spinal hypotension in the obstetric patient [corrected].
Allosteric Adenosine Modulation to Reduce Allodynia
Authors: Pan Hui-Lin , Xu Zemin , Leung Edward , Eisenach James C. 
Published: November 2003

Background
Adenosine and adenosine agonists reduce hypersensitivity following inflammation and peripheral nerve injury models of chronic pain. Because inhibitors of adenosine reuptake or metabolism are also effective at reducing hypersensitivity, it is likely that there is a tonic release of spinal adenosine in these models. One approach to avoid adverse effects from direct agonists is to enhance the effect of the endogenous ligand by administering a positive allosteric modulator of its receptor.

Methods
Rats with mechanical hypersensitivity after spinal nerve ligation received intrathecal injections of adenosine, the allosteric adenosine receptor modulator T62, or their combination, or received systemic T62 alone or with intrathecal injection of a specific A1 adenosine antagonist.

Results
Both adenosine and T62 reduced hypersensitivity alone, with 50% maximal doses (ED50) of 14+/-5.9 and 3.7+/-0.8 microg, respectively. They interacted in an additive manner as determined by isobolography. T62 also reduced mechanical hypersensitivity after systemic administration (15 mg/kg), and this effect was blocked by intrathecal injection of 9 microg of the A1-specific adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine.

Conclusions
These results add to previous studies that suggest ongoing spinal release of adenosine, which is antiallodynic, in this animal model of neuropathic pain. Positive allosteric modulation of the adenosine receptor reduces hypersensitivity by a spinal mechanism involving A1 adenosine receptor stimulation. Although obvious adverse effects were not observed in this investigation, further study is required to determine the feasibility of the use of such modulators in the treatment of chronic pain associated with hyperalgesia and allodynia.
Neuroprotective Effect of Low-dose Lidocaine in a Rat Model of Transient Focal Cerebral Ischemia
Authors: Lei Baiping , Cottrell James E. , Kass Ira S. 
Published: November 2003

Background
A low concentration of lidocaine (10 microM) has been shown to reduce anoxic damage in vitro. The current study examined the effect of low-dose lidocaine on infarct size in rats when administered before transient focal cerebral isehemia.

Methods
Male Wistar rats (weight, 280-340 g) were anesthetized with isoflurane, intubated, and mechanically ventilated. After surgical preparation, animals were assigned to lidocaine 2-day (n = 10), vehicle 2-day (n 12), lidocaine 7-day (n = 13), and vehicle 7-day (n = 14) groups. A 1.5-mg/kg bolus dose of ildocaine was injected intravenously 30 mm before isehemia in the lidocaine 2-day and 7-day groups. Thereafter, an infusion was initiated at a rate of 2 mg x kg(-1) x h(-1) until 60 min of reperfusion after isehemia. Rats were subjected to 90 min of focal cerebral isehemia using the intraluminal suture method. Infarct size was determined by image analysis of 2,3,5-triphenyltetrazolium chloride-stained sections at 48 h or hematoxylin and eosin-stained sections 7 days after reperfusion. Neurologic outcome and body weight loss were also evaluated.

Results
The infarct size was significantly smaller in the lidocaine 2-day group (185.0+/-43.7 mm3) than in the vehicle 2-day group (261.3+/-45.8 mm3, P < 0.01). The reduction in the size of the infarct in the lidocaine 7-day group (130.4+/-62.9 mm3) was also significant compared with the vehicle 7-day group (216.6+/-73.6 mm3, P < 0.01). After 7 days of reperfusion, the rats in the lidocaine group demonstrated better neurologic outcomes and less weight loss.

Conclusions
The current study demonstrated that a clinical anriarrhythmic dose of lidocaine, when given before and during transient focal cerebral isehemia, significantly reduced infaret size, improved neurologic outcome, and inhibited postisehemic weight loss.
Mechanisms of Direct Inhibitory Action of Ketamine on Vascular Smooth Muscle in Mesenteric Resistance Arteries
Authors: Akata Takashi , Izumi Kaoru , Nakashima Mikio 
Published: November 2003

Background
Ketamine was previously suggested to relax vascular smooth muscle by reducing the intracellular Ca2+ concentration ([Ca2+]i). However, no direct evidence is available to indicate that ketamine reduces the [Ca2+]i in vascular smooth muscle of systemic resistance arteries.

Methods
Endothelium-intact or -denuded smooth muscle strips were prepared from rat small mesenteric arteries. Isometric force and [Ca2+]i were measured simultaneously in the fura-2-loaded, endothelium-denuded strips. In some experiments, only isometric force was measured in either the endothelium-intact or beta-escin-treated, endothelium-denuded strips.

Results
In the endothelium-intact strips, lower concentrations (< or = 30 microm) of ketamine slightly enhanced norepinephrine-induced contraction, whereas higher concentrations (> or = 100 microM) of ketamine inhibited both norepinephrine- and KCl-induced contractions. In the fura-2-loaded strips, ketamine (> or = 100 microM) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine or KCl. Ketamine also inhibited the norepinephrine-induced increase in [Ca2+]i after treatment with ryanodine. In the absence of extracellular Ca2+, ketamine notably inhibited the norepinephrine-induced increase in [Ca2+]i, whereas it only minimally inhibited caffeine-induced increase in [Ca2+]i. Ketamine had little influence on the [Ca2+]i-force relation during force development to stepwise increment of extracellular Ca2+ concentration during either KCl depolarization or norepinephrine stimulation. Ketamine did not affect Ca2+-activated contractions in the beta-escin membrane-permeabilized strips.

Conclusions
The action of ketamine on contractile response to norepinephrine consists of endothelium-dependent vasoconstricting and endothelium-independent vasodilating components. The direct vasorelaxation is largely a result of reduction of[Ca2+]i in vascular smooth muscle cells. The [Ca2+]i-reducing effects are caused by inhibitions of both voltage-gated Ca2+ influx and norepinephrine-induced Ca2+ release from the intracellular stores.
Acute Pain Induces Insulin Resistance in Humans
Authors: Greisen Jacob , Juhl Claus B. , Grøfte Thorbjørn , Vilstrup Hendrik , Jensen Troels S. , Schmitz Ole 
Published: November 2003

Background
Painful trauma results in a disturbed metabolic state with impaired insulin sensitivity, which is related to the magnitude of the trauma. The authors explored whether pain per se influences hepatic and extrahepatic actions of insulin.

Methods
Ten healthy male volunteers underwent two randomly sequenced hyperinsulinemic-euglycemic (insulin infusion rate, 0.6 mU x kg(-1) x min(-1) for 180 min) clamp studies 4 weeks apart. Self-controlled painful electrical stimulation was applied to the abdominal skin for 30 min, to a pain intensity of 8 on a visual analog scale of 0-10, just before the clamp procedure (study P). In the other study, no pain was inflicted (study C).

Results
Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Differences in glucose oxidation rates were not statistically significant. The suppression of isotopically determined endogenous glucose output during hyperinsulinemia tended to be decreased after pain (1.67+/-0.48 mg x kg(-1) x min(-1) in study P vs. 2.04+/-0.45 mg x kg(-1) x min(-1) in study C; P = 0.06). Pain elicited a twofold to threefold increase in serum cortisol (P < 0.01), plasma epinephrine (P < 0.05), and serum free fatty acids (P < 0.05). Similarly, circulating concentrations of glucagon and growth hormone tended to increase during pain.

Conclusions
Acute severe pain decreases insulin sensitivity, primarily by affecting nonoxidative glucose metabolism. It is conceivable that the counterregulatory hormonal response plays an important role. This may indicate that pain relief in stress states is important for maintenance of normal glucose metabolism.
North American Malignant Hyperthermia Population
Authors: Sambuughin Nyamkhishig , Sei Yoshitatsu , Gallagher Kathleen L. , Wyre Hadley W. , Madsen Daniel , Nelson Thomas E. , Fletcher Jeffrey E. , Rosenberg Henry , Muldoon Sheila M. 
Published: November 2003

Background
Malignant hyperthermia (MH) is a disorder of skeletal muscle manifested as a life-threatening hypermetabolic crisis in susceptible individuals after exposure to inhalational anesthetics and depolarizing muscle relaxants. Mutations in the gene encoding the skeletal muscle ryanodine receptor (RYR1) are considered a common cause of the disorder, and, to date, more than 20 RYR1 mutations have been reported in European and Canadian families. Some studies suggest that differences may exist in the frequencies and distribution of mutations in the RYR1 gene between European and North American MH families the frequency and distribution of mutations in the RYR1 gene.

Methods
Skeletal muscle samples from 73 unrelated individuals diagnosed as MH susceptible according to the North American MH caffeine-halothane contracture test were studied. Genomic DNA of MH-susceptible patients was investigated by polymerase chain reaction-based restriction fragment length polymorphism, single-strand conformation polymorphism, and sequencing analysis. The majority of known RYR1 mutations were analyzed using the restriction fragment length polymorphism method, whereas new mutations were searched by single-strand conformation polymorphism in exons 12, 15, 39, 40, 44, 45, and 46 of the gene.

Results
Seven known RYR1 mutations (Arg163Cys, Gly248Arg, Arg614Cys, Val2168Met, Thr2206Met, Gly2434Arg, and Arg2454His) were detected at frequencies of 2.7, 1.4, 1.4, 1.4, 1.4, 5.5, and 4.1%, respectively. In addition, three novel amino acid substitutions (Val2214Ile, Ala2367Thr, and Asp2431Asn) were detected at frequency of 1.4% each. These 10 mutations account for 21.9% of the North American MH-susceptible population.

Conclusion
Three novel candidate mutations in the RYR1 gene were identified in these MH patients. The frequency and distribution of RYR1 mutations observed in this North American MH population was markedly different from that previously identified in Europe. Larger-scale studies are necessary to clarify the type and frequency of mutations in RYR1 associated with MH in North American families.
Response to Mivacurium in a Patient Compound Heterozygous for a Novel and a Known Silent Mutation in the Butyrylcholinesterase Gene
Authors: Gätke Mona R. , Østergaard Doris , Bundgaard Jens R. , Varin France , Viby-Mogensen Jørgen 
Published: November 2003

Background
Patients who are homozygous for the atypical mutation, compound heterozygous for atypical and silent mutations, or homozygous for silent mutations (SS) respond to mivacurium with extensively prolonged neuromuscular block. Although important, exact phenotyping of these patients is difficult. This article presents the pharmacodynamics and pharmacokinetics of a normal dose of mivacurium in a patient with phenotype SS, including a pedigree analysis and delineation of the molecular genetic method used to identify the genotype.

Methods
The neuromuscular block following administration of mivacurium, at a dose of 0.14 mg/kg, was monitored in a 30-yr-old healthy man with use of a mechanosensor and mechanomyography, and times to different levels of recovery were measured. Venous samples for determination of the mivacurium isomers were collected during the interval 134-494 min after administration of mivacurium, and the terminal half-lives were calculated. Butyrylcholinesterase activity, phenotype, and genotype were determined for both the patient and the family. Complete nucleotide sequencing was used to identify the genotype.

Results
A train-of-four ratio of 0.75 was reached 469 min after the injection of mivacurium. The terminal elimination half-lives of the mivacurium isomers, cis-trans and trans-trans, were 90 min. Complete nucleotide sequencing revealed two point mutations, the known silent variant S7 and a previously undescribed mutation of amino acid residue 170 introducing a stop codon.

Conclusions
The patient was compound heterozygous for silent mutations in the butyrylcholinesterase gene. The response to mivacurium was an extensively prolonged duration of action. Identification of the rare silent mutations presupposes access to modern molecular genetic methods such as complete nucleotide sequencing.
Clinical Experience of Percutaneous Femoral Venous Catheterization in Critically Ill Preterm Infants Less Than 1,000 Grams
Authors: Chen Kuen-Bao 
Published: November 2003

Background
Venous access is relatively difficult in preterm infants. Central venous catheterization is indicated for pressure monitoring, drug therapy, and nutrition supplementation, which are often critical in the anesthetic management of infants undergoing major surgery.

Methods
In 49 critically ill preterm infants weighing less than 1,000 g, the femoral vein was cannulated using a 22-gauge Angiocath (25 mm; Beckton Dickinson, Sandy, UT). A 2.5-ml syringe was attached to the Angiocath, and the Angiocath was advanced with constant negative pressure over the syringe. When blood return was observed, the cannula was advanced. When free blood reflux was achieved, a J wire was inserted, followed by a 24-gauge central venous catheter.

Results
The overall catheterization success rate was 79.6% (39 of 49 attempts). The time required for successful catheterization was less than 10 min in 18 cases (46.2%), 10-20 min in 17 cases (43.6%), and 20-30 min in 4 cases (10.3%). In the successful group, 1 catheter tip was positioned in the vein of the liver (2.6%), 2 were in the common iliac vein (5.1%), 6 were in the right atrium (15.4%), and 30 were in the infracardiac inferior vena cava (76.9%). Complications included hematoma in six cases (12.2%), arterial puncture in five cases (10.2%), bleeding in two cases (4.1%), and transient bradycardia in two cases (4.1%).

Conclusions
The results indicate that percutaneous femoral venous catheterization is a reliable and valuable technique for critically ill preterm infants weighing less than 1,000 g.
Hemodynamic and Catecholamine Responses to Laryngoscopy and Tracheal Intubation in Patients with Complete Spinal Cord Injuries
Authors: Yoo Kyung Y. , Lee JongUn , Kim Hak S. , Im Woong M. 
Published: November 2003

Background
Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia, which may be altered when the efferent sympathetic fiber to the cardiovascular system is interrupted. The aim of the current study was to investigate the effects of different levels of spinal cord injury on the cardiovascular responses to intubation.

Methods
Fifty-four patients with traumatic complete cord injuries requiring tracheal intubation were grouped into quadriplegics (above C7; n = 22), high paraplegics (T1-T4, n = 8), and low paraplegics (below T5, n = 24) according to the level of injury. Twenty patients without spinal injury served as controls. Arterial pressure, heart rate, and rhythm were recorded at intervals for up to 5 min after intubation. Plasma concentrations of catecholamines were also measured.

Results
The intubation increased the systolic blood pressure similarly in control, high-paraplegic, and low-paraplegic groups (P < 0.05), whereas it did not alter the blood pressure in the quadriplegic group. Heart rate was significantly increased in all groups; however, the magnitude was more pronounced in the high-paraplegic group (67%) than in the control (38%) and quadriplegic (33%) groups. Plasma concentrations of norepinephrine were significantly increased after intubation in all groups; however, values were lower in the quadriplegic group and higher in the low-paraplegic group compared with those in the control group. Incidence of arrhythmias did not differ among groups.

Conclusions
The cardiovascular and plasma catecholamine changes associated with endotracheal intubation may differ according to the affected level in patients with complete spinal cord injuries.
Direct Neurotoxicity of Tetracaine on Growth Cones and Neurites of Growing Neurons In Vitro
Authors: Saito Shigeru , Radwan Inas , Obata Hideaki , Takahashi Kenichiro , Goto Fumio 
Published: November 2003

Background
Local anesthetics have direct neurotoxicity on neurons. However, precise morphologic changes induced by the direct application of local anesthetics to neurons have not yet been fully understood. Also, despite the fact that local anesthetics are sometimes applied to the sites where peripheral nerves may be regenerating after injury, the effects of local anesthetics on growing or regenerating neurons have never been studied.

Methods
Three different neuronal tissues (dorsal root ganglion, retinal ganglion cell layer, and sympathetic ganglion chain) were isolated from an age-matched chick embryo and cultured for 20 h. Effects of tetracaine were examined microscopically and by a quantitative morphologic assay, growth cone collapse assay.

Results
Tetracaine induced growth cone collapse and neurite destruction. Three neuronal tissues showed significantly different dose-response, both at 60 min and at 24 h after the application of tetracaine (P < 0.01). The ED50 values (mean +/- SD) at 60 min were 1.53+/-1.05 mM in dorsal root ganglion, 0.15+/-0.05 mM in retinal, and 0.06+/-0.02 mM in sympathetic ganglion chain cultures. The ED50 values at 24 h were 0.43+/-0.15 mM in dorsal root ganglion, 0.07+/-0.03 mM in retinal, and 0.02+/-0.01 mM in sympathetic ganglion chain cultures. Concentration of nerve growth factor in the culture media did not influence the ED50 values. The growth cone collapsing effect was partially reversible in dorsal root ganglion and retinal neurons. However, in the sympathetic ganglion culture, no reversibility was observed after exposure to 1 mM tetracaine for 10 or for 60 min. Bupivacaine had similar neurotoxicity to the three types of growing neurons. (The ED50 values at 60 min were 2.32+/-0.50 mM in dorsal root ganglion, 0.96+/-0.16 mM in retinal, and 0.18+/-0.05 mM in sympathetic ganglion chain cultures. The ED50 values at 24 h were 0.34+/-0.09 mM in dorsal root ganglion, 0.21+/-0.06 mM in retinal, and 0.45+/-0.10 mM in sympathetic ganglion chain cultures.)

Conclusions
Short-term exposure to tetracaine produced irreversible changes in growing neurons. Growth cones were quickly affected, and neurites degenerated subsequently. Sensitivity varied with neuronal type and was not influenced by the concentration of nerve growth factor. Because a similar phenomenon was observed after exposure to bupivacaine, the toxicity to growing neurons may not be unique to tetracaine.