Most local anesthetics intravenously administered inhibit neuromuscular transmission or enhance the neuromuscular block of both nondepolarizing and depolarizing musde relaxants. Local anesthetics used to treat cardiac arrhythmias intraoperatively or postoperatively may, therefore, greatly augment a residual neuromuscular block. To obtain adequate balanced anesthesia and postoperative analgesia, general anesthesia with epidural anesthesia is frequently selected. In the present study we investigated the effects of lidocaine HC1 administered into epidural space on the neuromuscular blocking action of vecuronium. Eighty adult gynecological patients of ASA class I or II were studied. Patients were divided into four groups as follows ; Group I (n=20); vecuronium 0.1 mg/kg iv administered only Group II(n=20); vecuronium 0.1 mg/kg iv and lidocaine 6 mg/kg administered into epidural space Group III(n=20); vecuronium 0.1 mg/kg iv and lidocaine 8 mg/kg administered into epidural space Group IV(n=20); vecuronium 0.1 mg/kg iv and lidocaine 10 mg/kg administered into epidural space Patients of experimental groups II, III and IV were anesthetized by epidural block with 2 % lidocaine followed by general anesthesia 15 minutes later. Before induction with fentanyl(3 ug/kg), droperidol(0.04 mg/kg), thiopental sodium (5 mg/kg) and vecuronium(0.1 mg/kg) iv, neuromuscular monitoring was set by using ABM(Anesthesia and Brain activity Monitor, Datex Co, Finland) which stimulating ulnar nerve at the wrist with supramaximal stimuli at a frequency of 2 Hz and 20 seconds interval. The electromyographic response of hypothenar muscles was recorded. Following stabilization of the control twitch height, vecuronium(0.1 mg/kg) was intravenously injected, and tracheal intubation was performed when the first twitch height of the train of four twitch response(T1) was 5 % of the controL Anesthesia was maintained with O2 (2 L/min) and N2O (4 L/min). The time of onset of action (time from vecuronium iv to 0 % of T1), time of maximal twitch depression (time from loss of T1 to reappearance of T1), Recovery index (time from recovery of 25 % of T1 to 75 % of T1) and T4 ratios (ratio of the height of the fourth twitch to T1) at 25 %, 50 % and 75% of T1 were measured and compared among the groups. The results were as follows ; 1. The time of onset of action was 3.99+/-0.92 minutes in the control group and 2.94+/-0.89 minutes in the lidocaine 10 mg/kg administered group(P<0.05). 2. The time of maximal twitch depression was 19.055.46 minutes in the control group and 24.02+/-6.94, 25.33+/-5.84, 27.07+/-5.26 minutes in the lidocaine 6 mg/kg, 8 mg/kg, 10 mg/kg administered groups(P<0.05). 3. Recovery index was 14.76+/-5.40 minutes in the control group and 20.39+/-4.56, 22.36+/-7.98 minutes in the lidocaine 8 mg/kg, 10 mg/kg administered groups(P<0.05). 4. The lidocaine administered into epidural space has little effect on the recovery of T4 compared with that of T1(P>0.05). These results suggest that the effect of lidocaine HC1 administered into epidural space on the neuromuscular blocking action of vecuronium showed prolonged depression and recovery time, and reduced time of the onset of action with dose larger than lidocaine 8 mg/kg.
Adult ; Analgesia ; Anesthesia ; Anesthesia, Epidural ; Anesthesia, General ; Anesthetics, Local ; Arrhythmias, Cardiac ; Balanced Anesthesia ; Brain ; Depression ; Epidural Space* ; Humans ; Intubation ; Lidocaine* ; Muscles ; Neuromuscular Blockade* ; Neuromuscular Monitoring ; Thiopental ; Ulnar Nerve ; Vecuronium Bromide* ; Wrist

BACKGROUND: Previous reports have demonstrated the synergistic interaction of midazolam and propofol in the induction of hypnosis. But there haer been some different views expnrsscd as to whether the synergism extended to hemodynamic effects. So we studied the effect of the co-administration of midazolam on induction dose, hemodynamic response, and recovery with the use of continuous infusion of propofol for induction, and the maintenance of anesthesia. METHODS: Thirty-five patients undergoing elective surgery within 2 hours were randomly assigned to one of two groups formed according to the induction agents: Group P (continuous propofol infusion 1,200 mg/h), Group MP (midazolam 2 mg followed by continuous propofol infusion 1,200 mg/h). After induction, anesthesia was maintained with fentanyl (50 microgram), N2O (70%), andpropofol (5 15 mg/kg/h). Outcome measures were propofol doses (induction and maintenance), hemodynamic responses (heart rate, blood pressure) during the induction period, emergence time (eye-opening to command), postoperative nausea and dizziness. RESULTS: The induction dose of propofol was 29% less in Group MP compared to Group P but there was no significant difference in maintenance doses between the two groups. Heart rates showed no differences between the two groups, but the changes of mean arterial pressures from base line at 30 sec, 2 min and 5 min after intubation were greater and the emergence time was delayed in Group MP compared to Group P (P < 0.05). CONCLUSIONS: Midazolam potentiates the hypnotic action of propofol synergistically, but there was no evidence that the synergism extended to the blunting effect of propofol against the hypertensive response to intubation.
Anesthesia ; Arterial Pressure ; Dizziness ; Fentanyl ; Heart Rate ; Hemodynamics ; Humans ; Hypnosis ; Intubation ; Midazolam* ; Outcome Assessment (Health Care) ; Postoperative Nausea and Vomiting ; Propofol*

BACKGROUND: Previous reports have demonstrated the synergistic interaction of midazolam and propofol in the induction of hypnosis. But there haer been some different views expnrsscd as to whether the synergism extended to hemodynamic effects. So we studied the effect of the co-administration of midazolam on induction dose, hemodynamic response, and recovery with the use of continuous infusion of propofol for induction, and the maintenance of anesthesia. METHODS: Thirty-five patients undergoing elective surgery within 2 hours were randomly assigned to one of two groups formed according to the induction agents: Group P (continuous propofol infusion 1,200 mg/h), Group MP (midazolam 2 mg followed by continuous propofol infusion 1,200 mg/h). After induction, anesthesia was maintained with fentanyl (50 microgram), N2O (70%), andpropofol (5 15 mg/kg/h). Outcome measures were propofol doses (induction and maintenance), hemodynamic responses (heart rate, blood pressure) during the induction period, emergence time (eye-opening to command), postoperative nausea and dizziness. RESULTS: The induction dose of propofol was 29% less in Group MP compared to Group P but there was no significant difference in maintenance doses between the two groups. Heart rates showed no differences between the two groups, but the changes of mean arterial pressures from base line at 30 sec, 2 min and 5 min after intubation were greater and the emergence time was delayed in Group MP compared to Group P (P < 0.05). CONCLUSIONS: Midazolam potentiates the hypnotic action of propofol synergistically, but there was no evidence that the synergism extended to the blunting effect of propofol against the hypertensive response to intubation.
Anesthesia ; Arterial Pressure ; Dizziness ; Fentanyl ; Heart Rate ; Hemodynamics ; Humans ; Hypnosis ; Intubation ; Midazolam* ; Outcome Assessment (Health Care) ; Postoperative Nausea and Vomiting ; Propofol*

BACKGROUND: The therapeutic effect of morphine on neuropathic pain states was controversial, but there are some reports that systemic morphine reduced pain. Recently, many investigators have reported that locally administered morphine alleviated pain in local inflammatory pain model. Therefore, we designed this study to evaluate the peripheral effect of morphine and its antagonism by naloxone in rats experiencing neuropathic pain. METHODS: Neuropathic pain was produced by tightly ligating the left 5 th and 6 th lumbar spinal nerves of male Spraw-Dawley rats. To evaluate the systemic effect, morphine 200 microgram was injected into the unaffected right paw. Morphine 50, 100 and, 200 microgram were injected into the affected left paw. Naloxone 5, 10 and 20 microgram were injected into the affected left paw ten minutes before morphine 200 microgram was injected into the affected left paw. Before and after drug injection, mechanical allodynia was quantified by the foot withdrawal frequency to von Frey filaments of 5.50 g or 1.48 g, applied to the affected left paw. RESULTS: Morphine 200 g injected into the unaffected right paw did not affect the foot withdrawal frequency on the affected left paw. Morphine 100 and 200 microgram decreased the foot withdrawal frequency. In rats with morphine 200 microgram injected into the left paw, naloxone 5, 10, and 20 microgram increased foot withdrawal frequency. Conclusion: These data represented that morphine injected into the affected paw dose-relatedly reduced mechanical allodynia via peripheral effect and pretreatment of naloxone significantly antagonized the morphine effect.
Animals ; Foot ; Humans ; Hyperalgesia* ; Male ; Models, Animal* ; Morphine* ; Naloxone ; Neuralgia* ; Rats* ; Research Personnel ; Spinal Nerves

BACKGROUND: The pathophysiologic mechanism of the neuropathic pain is still unclear. We designed this study to evaluate the effect of bilateral cervical sympathectomy on allodynia and the relationship of neuropathic pain with sympathetic nerve system of supraspinal level in rats experiencing neuropathic pain. METHODS: Neuropathic pain was produced by tight ligating the left 5th and 6th lumbar spinal nerves of male Sprague-Dawley rats. Mechanical allodynia was quantified by measuring the foot withdrawal frequency to stimuli with two von Frey filaments of 14.5 mN and 53.9 mN applied to the affected left hind paw, and cold allodynia was quantified with the same manner using 100% acetone. We divided the neuropathic pain models into experimental group (bilateral cervical sympathectomy) and control group (sham operation), and then measured the foot withdrawal frequency 1, 3, 5, 7, 14, 21 and 28 days postoperatively. RESULTS: In experimental group, the foot withdrawal frequency to mechanical stimuli with 14.5 and 53.9 mN of von Frey filament and cold stimuli with 100% acetone was significantly lower than that of control group for all postoperative observation points. Also, the experimental group showed decrease in foot withdrawal frequency compared with preoprative value over the course of the study. CONCLUSIONS: Bilateral cervical sympathectomy reduced mechanical allodynia and cold allodynia in the rat model of neuropathic pain suggesting that neuropathic pain, although the lesions are localized in low extremities, may be correlated with functional disturbance of sympathetic nerve fibers of supraspinal or brain level and help explain the mechanism of neuropathic pain.
Acetone ; Animals ; Brain ; Extremities ; Foot ; Humans ; Hyperalgesia* ; Male ; Models, Animal* ; Nerve Fibers ; Neuralgia* ; Rats* ; Rats, Sprague-Dawley ; Spinal Nerves ; Sympathectomy*

BACKGROUND: Many reports suggest that cervical sympathectomy improves cerebral blood flow. But the basal & medial areas of brain are innervated bilaterally, so unilateral sympathectomy may not improve the outcome of infarction of those areas effectively. Actually it was reported that only bilateral, not unilateral cervical sympathectomy increased the blood flow of thalamus which known to be innervated bilaterally, and also reported that unilateral sympathectomy did not reduce the infarct size of caudate nucleus. So we studied the effect of bilateral superior cervical sympathectomy on focal cerebral infarction. METHODS: Twenty rabbits were divided into two groups. In the sham-operated control group (n=10), focal infarction was achieved by administering an autologous blood clot into the internal carotid artery after exposure of bilateral superior cervical sympathetic ganglia. In the sympathectomy group (n=10), bilateral superior cervical sympathetic ganglia were excised following embolization. Seven hours after embolization, brains were sliced into 2 mm coronal sections, stained with 2,3,5-triphenyltetrazolium chloride, and infarct sizes were determined via image analysis. RESULTS: There were no differences in the physiologic variables between two groups. The percentage of infarct size was significantly greater in the control group as compared to the sympathectomy group in both cortex (23+/-8% vs 12+/-5%, respectively; P<0.05) and subcortical area (35+/-8% vs 17+/-8%, respectively; P<0.05). CONCLUSIONS: These results suggest that bilateral superior cervical sympathectomy may reduce the infarct size of subcortical area as well as of cerebral cortex measured at 7 hours following induction of focal cerebral infarction.
Brain ; Carotid Artery, Internal ; Caudate Nucleus ; Cerebral Cortex ; Cerebral Infarction* ; Ganglia, Sympathetic ; Infarction ; Rabbits* ; Sympathectomy* ; Thalamus

BACKGROUND: The mechanical hyperalgesia that follows peripheral tissue injury results from peripheral and central sensitization. Central sensitization is initiated and maintained by windup that can be prevented by N-methyl-D-aspartate (NMDA) antagonists. NMDA antagonists, therefore, have the potential to prevent and treat pain, although clinical uses are limited because of their side effects. This study was designed to evaluate the analgesic action of intrathecal (IT) magnesium sulphate in a rat model of postoperative pain and investigate the analgesic mechanism of magnesium. METHODS: Forty-two Sprague-Dawley rats (300 +/- 20 g) were prepared with a chronic IT catheter. Under brief enflurane anesthesia, a 1-cm incision including skin, muscle and fascia was made in the plantar aspect of the hind paw and closed. Normal saline, magnesium (30, 100, 300, 600 microgram), NMDA 50 ng or NMDA 50 ng with magnesium 300 microgram was administered via the IT catheter after recovery. Response frequency, using Von Frey filaments, cumulative pain scores and motor deficits were assessed. RESULTS: The mechanical hyperalgesia and nonevoked pain behaviors decreased significantly at 1 h or 1 h and 3 h after IT injection of magnesium 100 microgram or 300 microgram compared to the saline group without profound motor deficits in a rat model of postoperative pain. However, the rats administered with magnesium 600 microgram were lethargic due to severe motor weakness. Effective duration of magnesium decreased significantly in the group of NMDA 50 ng with magnesium 300 microgram compared to that of magnesium 300 microgram administered alone, but the initial effects were similar between the two groups. CONCLUSIONS: We conclude that IT magnesium sulphate can modulate nociceptive processing after tissue injury and the analgesic mechanism of magnesium is involved in NMDA receptors. Magnesium,therefore, may offer a therapeutic agent for postoperative pain and may be an agent that prevents postoperative pain from changing to persistent pathological pain.
Anesthesia ; Animals ; Catheters ; Central Nervous System Sensitization ; Enflurane ; Fascia ; Hyperalgesia ; Magnesium* ; Models, Animal* ; N-Methylaspartate ; Pain, Postoperative* ; Rats* ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; Skin

BACKGROUND: Intra-operative application of continuous hyperthermic peritoneal perfusion (CHPP) in advanced cancer has been introduced as an effective and safe method to lessen the complication and enhance the effectiveness of its treatment. But CHPP induced acute change of body temperature and intra-abdominal pressure would produce various abnormal physiologic response. Now, we investigated to evaluate and understand the trend of changes of cardiac and oxygen parameters during CHPP. METHODS: Closed peritoneal irrigation was done with perfusate at temperature 47oC for 90 min under general anesthesia. Cardiac and oxygen parameters were measured at 10 min before CHPP, 30, 60, 90 min after the initiation of CHPP, 30 min after the end of CHPP with Swan-Ganz catheter application. RESULTS: Hemodynamic parameters; Systemic vascular resistance index and mean arterial pressure were decreased trend during CHPP. Pulmonary capillary wedge pressure and cardiac index were increased during CHPP. Oxygen parameters; AaDO2 and shunt fraction were increased during CHPP and O2 index were decreased during CHPP. Oxygen balance; O2 consumption and delivery increased during CHPP. CONCLUSIONS: We confirmed that systemic oxygen consumption and delivery were increased during CHPP but AaDO2 and shunt fraction were increased which could decrease systemic oxygen delivery. We should need more careful monitoring and proper treatment for maintaining stable hemodynamics and systemic oxygen balance during and after CHPP.
Anesthesia, General ; Arterial Pressure ; Body Temperature ; Catheters ; Hemodynamics ; Oxygen Consumption ; Oxygen* ; Perfusion* ; Peritoneal Lavage ; Pulmonary Wedge Pressure ; Vascular Resistance

BACKGROUND AND OBJECTIVES: The evaluation of subjective outcomes of hearing aid fitting is of paramount importance along with audiometric improvement. The aim of this study was to develop a Korean adaptation of the International Outcome Inventory for Hearing Aids (IOI-HA) and to determine its reliability and validity. SUBJECTS AND METHOD: The translation of IOI-HA into the Korean version (K-IOI-HA) was completed through a process of forward translation, reconciliation, reverse translation and cognitive debriefing. K-IOI-HA was administered to 101 patients using hearing aids and visiting any the 10 referral hospitals. Reliability was evaluated by Cronbach's alpha coefficient and by test-retest analysis. Validity was assessed by confirmatory factor analysis and criterion validity based on the results of pure tone audiometry. RESULTS: K-IOI-HA showed a good internal consistency (Cronbach's alpha=0.83) and a high test-retest reliability (r=0.943, p<0.01). Validity checked by confirmatory factor analysis also showed good construct validity. CONCLUSION: The Korean version of IOI-HA is a reliable and valid tool for evaluating subjective outcomes of hearing aids.
Hearing ; Hearing Aids ; Humans ; Surveys and Questionnaires ; Referral and Consultation ; Reproducibility of Results

Erythema nodosum (EN) is the most common form of panniculitis and may be triggered by a variety of stimuli, including infections, drugs, pregnancy, sarcoidosis, inflammatory bowel disease, and malignancies. Rare cases of vaccination-related EN have been reported, but none due to the coronavirus disease 2019 (COVID-19) vaccine of Pfizer have been documented. We report a case of EN associated with the Pfizer vaccine. A 43-year-old woman presented with acute-onset painful nodular lesions that appeared bilaterally on the extensor surface of the lower legs. These lesions appeared 5 days after the first dose of Pfizer vaccination. The patient reported no recent infectious history other than fever for 3 days after vaccination. Skin biopsy revealed inflammation extending into the subcutaneous fat with a septal distribution. It is important for physicians to be aware of the side effects of the COVID-19 vaccine because more people are bound to be vaccinated.