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Background A brief episode of cerebral ischemia confers transient ischemic tolerance to a subsequent ischemic challenge that is otherwise lethal to them. This study was purposed to evaluate the effect of mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat. Methods Seven-day old Sprague-Dawley rat pups were used. The rats were divided into five groups; control group (n = 91), pretreatment hypoxic preconditioning group (n = 43), pretreatment ischemic preconditioning group (n = 52), hypoxic preconditioning group (n = 39), and ischemic preconditioning group (n = 51). Rats in the pretreatment hypoxic preconditioning group and pretreatment ischemic preconditioning group were treated by an intraperitoneal injection with 5-hydroxydecanoate (60 mg/kg). Thirty minutes after injection, right common carotid artery was temporarily occluded for ten minutes in pretreatment ischemic preconditioning group. Rats in the pretreatment hypoxic preconditioning group and hypoxic preconditioning group underwent hypoxia (8% oxygen/92% nitrogen) for four hours. Twenty-four hours after the preconditioning, rats from all groups were exposed to right common carotid artery ligation followed by 2.5 hour hypoxia. On the 1st day after hypoxic-ischemic brain injury, terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) reaction was evaluate as apoptotic markers and triphenyl tetrazolium chloride (TTC) was done to measure necrotic tissue. All rats were sacrificed 2 weeks after hypoxic-ischemia brain injury and the brains were examined for morphologic study. Results There were no differenced in survival rate, infarct area, number of TUNEL positive cells and morphologic score either between hypoxic preconditioning group and pretreatment hypoxic preconditioning group or between ischemic preconditioning group and pretreatment ischemic preconditioning group. Conclusions The results suggests that mitochondrial K(ATP) channel blocker, 5-hydroxydecanoate, does not change hypoxic-ischemic preconditioning in the neonatal rat.

Compression of the airway is relatively common in pediatric patients, although it is often an unrecognized complication of congenital cardiac and aortic arch anomalies. Aortopexy has been established as a surgical treatment for tracheobronchial obstruction associated with vascular anomaly, aortic arch anomaly, esophageal atresia, and tracheoesophageal fistula. The tissue-to-tissue arch repair technique could result in severe airway complication such as compression of the left main bronchus which was not a problem before the correction. We report three cases of corrective open heart surgery monitored by intraoperative bronchoscopy performed during prebypass, and performed immediately before weaning from bypass, to evaluate tracheobronchial obstruction caused by congenital, complex cardiac anomalies in the operating room.

Ethanol sclerotherapy for the treatment of low-flow vascular malformations can cause catastrophic cardiopulmonary complications, including pulmonary embolism and pulmonary hypertension, that can result in right heart failure and fatal arrhythmias, leading to death. We here report a case of abrupt cardiovascular collapse that developed immediately following ethanol sclerotherapy in 31-year-old female patient who had a large arteriovenous malformation in her leg. An esthesiologists should be aware of the fatal cardiopulmonary complications that are associated with ethanol sclerotherapy and consider the use of invasive hemodynamic monitoring, such as pulmonary artery pressure monitoring, when large doses of ethanol are required. (Korean J Anesthesiol 2014; 66: 388-391)

Lumbar spinal stenosis is a commonly treated with epidural injections of local anesthetics and corticosteroids, however, these therapies may relieve leg pain for weeks to months but do not influence functional status. Furthermore, the majority of patients report no substantial symptom change over the repeated treatment. Utilizing balloon catheters, we successfully treated with three patients who complained persistent symptoms despite repeated conventional steroid injections. Our results suggest that transforaminal decompression using a balloon catheter may have potential in the nonsurgical treatment of spinal stenosis by modifying the underlying pathophysiology.

Torsade de pointes (TdP) is a devastating form of polymorphic ventricular arrhythmia associated with corrected QT (QTc) interval prolongation. TdP usually terminates spontaneously but frequently recurs and may degenerate to ventricular fibrillation. The present report describes a case of TdP in a patient being transferred to the postanesthetic care unit following an emergency laparoscopic appendectomy. The patient had undergone open heart surgery 1 week before. Retrospective electrocardiogram analysis revealed the patient had QTc and Tpeak-Tend interval prolongation that had gone unrecognized. We believe TdP may have been induced by accentuation of sympathetic nervous system during emergence from general anesthesia.

Background Propofol and remifentanil are used for tracheal intubation in the absence of neuromuscular blocking agents. We hypothesized that the addition of sevoflurane to propofol and remifentanil would improve intubation conditions and provide hemodynamic stability. Methods Seventy-six patients scheduled for elective surgery were randomly allocated to be ventilated with either 4% (group I) or 7% sevoflurane (group II) after propofol injection (2 mg/kg). All patients received remifentanil (1 µg/kg) 30 seconds after administration of propofol. Ninety seconds after remifentanil was given, laryngoscopy and tracheal intubation were performed. Intubation conditions and hemodynamic changes were evaluated. Results The overall incidence of clinically acceptable intubation conditions was significantly higher in group II (92%) than group I (58%) (P = 0.001). Scores for vocal cord position, coughing, and limb movement were significantly better in group II (P < 0.05). Mean blood pressure remained significantly lower than the pre-induction level throughout the investigation in both groups (P < 0.001), but there was no incidence of bradycardia or hypotension requiring treatment. Conclusions Tracheal intubation without neuromuscular blocking agents can be achieved safely and reliably by adding 7% sevoflurane to propofol (2 mg/kg) and remifentanil (1 µg/kg).

Background: Stellate ganglion block (SGB) is performed for the diagnosis and treatment of sympathetic dependent pain in the head, neck and upper limbs. However, the effects of bilateral SGB on cardiovascular and autonomic regulation remain unknown. The aim of this study was to assess the effects of bilateral SGB on cardiovascular and autonomic function by measuring heart rate variability (HRV), systolic blood pressure variability (SBPV) and spontaneous baroreflex sensitivity (SBRS). Methods and Results: Twenty healthy volunteers were randomly allocated to receive right or left SGB with 8 ml 1% lidocaine solution; after 20 min, the contralateral side SGB was performed. Changes in the RR interval (RRI), systolic blood pressure (SBP), HRV, SBPV and SBRS were assessed before and after bilateral SGB. The low-frequency (LF, 0.04-0.15 Hz) and high-frequency (HF, 0.15-0.4 Hz) components of HRV and SBRS decreased significantly; however, no significant changes were found in RRI, SBP and the LF and HF components of SBPV after bilateral SGB. In subjects with symptoms of vagal blockade, HRV, SBP and SBRS were significantly affected by bilateral SGB. Conclusions: Bilateral SGB should be performed cautiously because it can reduce cardiac vagal modulation and BRS, especially for those with symptoms of vagal blockade after bilateral SGB. (Circ J 2009; 73: 1909-1913)

Transposition of the great arteries (TGA) requires early surgical repair during the neonatal period. Several preoperative factors have been identified for the postoperative poor outcome after arterial switch operation (ASO). However, the data remain uncertain an association. Therefore, we investigated the preoperative factors which affect the early postoperative outcomes. Between March 2005 and May 2012, a retrospective study was performed which included 126 infants with an ASO for TGA. Preoperative data included the vasoactive inotropic score (VIS) and baseline hemodynamics. Early postoperative outcomes included the duration of mechanical ventilation, the length of stay in the intensive care unit and hospital, and early mortality. Multivariate linear regression and receiver operating characteristics analysis were performed. The duration of mechanical ventilation was significantly correlated with the preoperative mechanical ventilator support and VIS, and CPB time. On multivariate linear regression analysis, a higher preoperative VIS, preoperative B-type natriuretic peptide (BNP) level, and the CPB time were identified as independent risk factors for delayed mechanical ventilation. Preoperative VIS (OR 1.154, 95 % CI 1.024–1.300) and the CPB time (OR 1.034, 95 % CI 1.009–1.060) were independent parameters predicting early mortality. A preoperative VIS of 12.5 had the best combined sensitivity (83.3 %) and specificity (85.3 %) and an AUC of 0.852 (95 % CI 0.642–1.061) predicted early mortality. Our results suggest that preoperative VIS and BNP can predict the need for prolonged postoperative mechanical ventilation. Moreover, preoperative VIS may be used as a simple and feasible indicator for predicting early mortality.

UNLABELLED Intrathecal neostigmine reverses mechanical allodynia in humans and animals. The efficacy of morphine in a neuropathic pain state is still controversial. This study examines the antiallodynic interaction between morphine and neostigmine in a rat model of neuropathic pain. Rats were prepared with tight ligation of left L5-6 (fifth and sixth lumbar) spinal nerves and chronic intrathecal catheter implantation. Mechanical allodynia was measured by using application of von Frey hairs to the left hindpaw. Morphine (1, 3, 10, and 30 microg) and neostigmine (0.3, 1, 3, and 10 microg) were administered intrathecally to obtain the dose-response curves and the 50% effective dose (ED(50)) for each drug. ED(50) values and fractions of the ED(50) values (1/2, 1/4, and 1/8) were administered intrathecally in an equal dose ratio to establish the ED(50). Isobolographic and fractional analyses for the drug interaction were performed. Intrathecal morphine produced a moderate antagonism of the tactile allodynia. A morphine-neostigmine combination produced a dose-dependent increase in withdrawal threshold of the lesioned hind paw with reduced side effects. Both analyses revealed a synergistic interaction after the coadministration of morphine and neostigmine. These experiments suggest that the antiallodynic action of a morphine-neostigmine combination is synergistic at the spinal level. IMPLICATIONS This study indicates that, by using both isobolographic and fractional analyses, the antiallodynic effect of intrathecal morphine and neostigmine is synergistic when coadministered intrathecally. In a rat model of neuropathic pain, the intrathecal morphine produced a moderate antagonism on touch-evoked allodynia at the spinal level.

Background This study determined the effect of intrathecally administered cholinesterase inhibitors, edrophonium and neostigmine, on nerve injury-induced, touch-evoked allodynia and identified the pharmacologic characteristics of this action. Methods Rats were prepared with tight ligation of the left L5 and L6 spinal nerves and with lumbar intrathecal catheters fitted for long-term monitoring. Edrophonium (3, 10, 30, or 100 microg) or neostigmine (0.3, 1, 3, or 10 microg) was administered intrathecally. Tactile allodynia and motor weakness were assessed. To evaluate the pharmacologic characteristics of the activity, a muscarinic receptor antagonist or a nicotinic receptor antagonist was administered intrathecally before edrophonium or neostigmine was injected. To compare the action of subtype antagonists, the M1 muscarinic receptor antagonist pirenzepine, the M2 antagonist methoctramine, the M3 antagonist 4-DAMP (diphenylacetoxy-N-methypiperidine), and the M4 antagonist tropicamide were administered intrathecally before cholinesterase inhibitors were injected. Results Intrathecal edrophonium or neostigmine produced a dose-dependent antagonism of the touch-evoked allodynia. Neostigmine resulted in a moderate effect on motor weakness at doses of 3 and 10 microg. Pretreatment with intrathecal atropine but not mecamylamine yielded a complete antagonism of the effects of the cholinesterase inhibitors. In addition, antiallodynia produced by edrophonium (100 microg) was reversed by pretreatment with methoctramine, 4-DAMP, tropicamide, and pirenzepine. In the neostigmine (10 microg) group, only the M1 antagonist pirenzepine had a moderate effect on reversal of increased allodynic threshold. Conclusions These experiments suggest that intrathecal edrophonium or neostigmine produces an antagonism on touch-evoked allodynia at the spinal level in a rat model of neuropathic pain and that the antiallodynic action of cholinesterase inhibitors is probably mediated by a spinal muscarinic system, especially at the M1 receptor subtype.

BACKGROUND: Nerve injury can generate neuropathic pain. The accompanying mechanical allodynia may be reduced by the intrathecal administration of adenosine. The neuroprotective effects of adenosine are mediated by the adenosine triphosphate (ATP)-sensitive potassium (K ATP ) channel. We assessed the relationship between the adenosine A1 receptor agonist, N 6 -(R)-phenylisopropyl adenosine (R-PIA), and K ATP channels to determine whether the antiallodynic effects of R-PIA are also mediated through K ATP channels in a rat nerve ligation injury model of neuropathic pain. METHODS: Mechanical allodynia was induced by tight ligation of the left lumbar fifth and sixth spinal nerves. Mechanical allodynia in the left hindpaw was evaluated using von Frey filaments to measure withdrawal thresholds. R-PIA (0.5, 1, or 2 μg) was administered intrathecally to induce antiallodynia. We assessed whether pretreatment with the K ATP channel blockers glibenclamide or 5-hydroxydecanoate reversed the antiallodynic effect of R-PIA. Also, we evaluated whether diazoxide, a K ATP channel opener, had an antiallodynic effect and promoted the antiallodynic effect of R-PIA. Lastly, we investigated whether the voltage-activated K channel blocker 4-aminopyridine attenuated the effect of R-PIA. RESULTS: Intrathecal R-PIA produced maximal antiallodynia at 2 μg (P < 0.05). Intrathecal pretreatment with glibenclamide and intraperitoneal pretreatment 5-hydroxydecanoate significantly reduced the antiallodynic effect of R-PIA. Diazoxide produced an antiallodynic effect and also enhanced the antiallodynic action of R-PIA. 4-Aminopyridine had no effect on the antiallodynic action of R-PIA. CONCLUSIONS: The antiallodynic effects of adenosine A1 receptor stimulation may be related to K ATP channel activity in a rat model of nerve ligation injury.

To assess the capability of gadolinium polylysine-enhanced cardiac magnetic resonance (MR) imaging in depicting normal and ischemic myocardium during occlusion and reperfusion of the left anterior descending artery.Contrast-enhanced MR images were obtained in 18 cats during 90 minutes each of occlusion and reperfusion. The change in signal intensity (SI) was compared among normal myocardium and central and peripheral ischemic zones. Results were compared with those of 2,3,5-triphenyltetrazolium chloride staining.During occlusion, the ischemic zone lacked enhancement while normal myocardium had gradual enhancement. During reperfusion, the ischemic zone had strong enhancement. In cats with large infarction, the central and peripheral ischemic zones had intermediate and high SI, respectively; in cats with focal or no infarction, the entire ischemic zone had high SI.Occlusive and reperfused myocardial infarction can be detected at gadolinium polylysine-enhanced MR imaging by means of differential SI changes in normal myocardium and central and peripheral ischemic zones.

Increasing evidence indicates that lithium is a neuroprotective agent against transient focal and global ischemic injury in the adult animal. In the developing brain, lithium has shown protective effects against neuroapoptosis induced by drugs. This study was designed to investigate the neuroprotective effects of lithium on hypoxic-ischemic brain injury in the neonatal rat.Seven-day-old Sprague-Dawley rats underwent hypoxic-ischemic injury (HII) induced by ligation of the common carotid artery followed by exposure to ~2.5 h of hypoxia (~7% oxygen). After HII, rat pups were randomly assigned into two groups: a control group (n = 21), which received a daily subcutaneous injection of 0.9% normal saline for 14 days following HII; and a lithium group (n = 32), treated with daily injection of lithium chloride. N-acetylaspartate/creatinine, choline/creatinine, lipid/creatinine ratios at 1.3 ppm (Lip(1.3)/Cr) and 0.9 ppm (Lip(0.9)/Cr) lipid peaks were evaluated by proton magnetic resonance spectroscopy on the day of HII and on days 7 and 14 after HII. Infarct ratios based on magnetic resonance images were also determined at the same time points.Seven days after HII, the Lip(1.3)/Cr and Lip(0.9)/Cr ratios as well as the infarct ratio were significantly lower in the lithium group than in the control group. The Lip(1.3)/Cr and Lip(0.9)/Cr ratios were significantly correlated with infarct ratio.This study showed that post-HII treatment with lithium may have a neuroprotective effect in the immature brain. Further studies are needed to elucidate the mechanism of neuroprotective properties of lithium against HII-induced neonatal brain damage.

We have described herein a 39-year-old male patient with hepatitis B virus-related cirrhosis (Child class C), showing a prolonged corrected QT interval, who developed torsades de pointes (TdP) in the neohepatic stage of liver transplantation (LT). There was no arrhythmia in the pre-anhepatic and anhepatic stages. Multiple premature ventricular complexes, ventricular tachycardia, and TdP suddenly developed at 16 minutes after graft reperfusion without any prodromal arrhythmia; they persisted for 118 seconds. Laboratory tests showed that serum potassium, calcium, and magnesium concentrations of 4.7 mmol/L, 1.05 mmol/L, and 1.85 mg/dL, respectively were within normal ranges. Likely causative factors for TdP in this patient included a prolonged corrected QT interval (553 msec), a low hematocrit (21%), and a low arterial blood pressure (systolic blood pressure, 80-90 mm Hg; diastolic blood pressure; 20-26 mm Hg) in the neohepatic stage. This case demonstrated the importance of optimal maintenance of coronary perfusion, with an adequate hematocrit level and electrolyte concentrations, to prevent the development of TdP in cirrhotic patients with a prolonged corrected QT interval during LT.

Editor’s key points † This study assessed the effects of pre-exposure to sevoflurane on the bispectral index (BIS) during induction of anaesthesia for Caesarean section. † Pre-exposure to subanaesthetic concentrations of sevoflurane reduced BIS values in the period before neonatal delivery, and maintained the BIS below 60 in the interval before delivery. † Neither maternal nor Background. Patients undergoing Caesarean delivery under inhalation anaesthesia are at a high risk of awareness, especially in the period before delivery. We assessed the effects of pre-exposure to sevoflurane on the bispectral index (BIS) in the interval before delivery. Methods. Sixty-four patients undergoing elective Caesarean delivery were randomly assigned to receive 1.0‐1.1 vol% (control 1) or 1.2‐1.3 vol% (control 2) end-tidal sevoflurane, or the same concentrations of end-tidal sevoflurane combined with preexposure to 1 vol% sevoflurane for the last 1 min of the preoxygenation period (the preSevo 1 and preSevo 2 groups, respectively). We assessed BIS values, arterial pressure, and heart rate at the time of induction; before intubation; and upon skin incision, uterine incision, and delivery. We also determined the maternal incidence of intraoperative awareness and the neonatal Apgar scores, and conducted umbilical blood gas analysis. Results. At skin incision, BIS values were significantly lower in the preSevo 1 group than in the control 1 group [50 (13) vs 72 (8), P,0.001] and in the preSevo 2 group than in the control 2 group [44 (11) vs 67 (10), P,0.001]. The mean BIS values in the preSevo 1 and 2 groups were maintained below 60 in the period before delivery. No other parameter differed among groups, and no patient exhibited intraoperative awareness.

Antiallodynic effects have been demonstrated after intrathecal administration of alpha-2 adrenoceptor agonists and cholinesterase inhibitors in rats. Intrathecal carbachol also increases the activity of cholinergic receptor system at the spinal level. However, there is no study regarding the antagonism of carbachol on touch-evoked allodynia and the interaction with clonidine. This study examines the intrathecal interaction between two drugs in a rat model of nerve ligation injury.Rats were prepared with tight ligation of the left L5-6 spinal nerves and chronic intrathecal catheter implantation. Tactile allodynia was measured by using application of von Frey filaments to the lesioned hindpaw. Carbachol (0.3-10 microg) and clonidine (1-30 microg) were administered to obtain the dose-response curves and the 50% effective dose (ED(50)) for each drug. Fractions of ED(50) values (1/2, 1/4, 1/8, and 1/16) were administered intrathecally to establish the ED(50) of the carbachol-clonidine combination. Isobolographic and fractional analyses of drug interaction were performed.Intrathecal carbachol and clonidine alone produced a dose-dependent reduction of tactile allodynia without severe motor weakness or sedation. A carbachol-clonidine combination produced a dose-dependent increase in withdrawal threshold of the lesioned hindpaw with a reduced incidence and magnitude of side effects. Both analyses revealed a synergistic interaction after the coadministration of carbachol and clonidine.This study indicates that carbachol, like clonidine, provides a moderate antagonism on touch-evoked allodynia at the spinal level. The results suggest that intrathecally administered carbachol is synergistic when combined with clonidine.

UNLABELLED Nerve ligation injury may produce a pain syndrome that includes tactile allodynia. Reversal effects on tactile allodynia have been demonstrated after the intrathecal administration of gamma-aminobutyric acid (GABA) receptor agonists or cholinesterase inhibitors in rats. We examined the drug interactions between neostigmine and muscimol or baclofen in a rat model of nerve ligation injury. Rats were prepared with tight ligation of the left L5-6 spinal nerves and chronic intrathecal catheter implantation. Tactile allodynia was measured by applying von Frey filaments ipsilateral to the lesioned hindpaw. Thresholds for paw withdrawal were assessed. Neostigmine (0.3-10 microg), muscimol (0.1-10 microg), and baclofen (0.1-3.0 microg) were administered to obtain the dose-response curve and the 50% effective dose (ED(50)). Fractions of ED(50) values were administered intrathecally to establish the ED(50)s of drug combinations (neostigmine-muscimol and neostigmine-baclofen). The drug interactions were performed. Intrathecal neostigmine, muscimol, baclofen, and their combinations produced a dose-dependent increase in withdrawal threshold of the lesioned hindpaw. Both analyses revealed a synergistic interaction for the neostigmine-muscimol combination, whereas the effect of the neostigmine-baclofen combination was additive. These results suggest that the activation of both muscarinic and GABA(A) receptors is required for synergistic interaction. IMPLICATIONS This study indicates that drug interaction is synergistic for the neostigmine-muscimol combination, whereas the effect of the neostigmine-baclofen combination is additive. In a rat model of nerve ligation injury, neostigmine, muscimol, baclofen, and their combinations provide an antagonism on touch-evoked allodynia at the spinal level.

Cyanosis in children is most often caused by pulmonary disease, or cyanotic heart disease but is rarely caused by hematological problems such as methemoglobinemia and sulfhemoglobinemia. Abnormal hemoglobins with a reduced oxygen affinity are an exceptionally uncommon cause of cyanosis in children. Hemoglobin-M (Hb-M) is rapidly auto-oxidized into the met-form resulting in the loss of its -binding ability. This hemoglobinopathy is inherited in an autosomal dominant pattern and is characterized by marked cyanosis. Hb-M affects the anesthetic management because of the anomalous absorption spectrum of Hb-M in standard pulse oximetry. Sufficient delivery should be maintained by keeping a high and intermittently checking the delivery state using arterial blood gas analysis. We reported our experience of the anesthetic management of a patient with hemoglobin M.

Background: The heme oxygenase system catalyzes the conversion of heme to free iron, carbon monoxide and bilirubin. This study was purposed to evaluate the effect of the heme oxygenase inhibitor, Tin protoporphyrin IX (SnPPIX) on the hypoxic ischemic brain injury in a neonatal rat. Methods: Seven-day old Sprague-Dawley rat pups were used. The rats were divided into two groups; control group (n = 9) and SnPPIX group (n = 6). SnPPIX 50/kg and the dissolvent were administered respectively intraperitoneally. For hypoxic ischemic brain injury, the right common carotid artery was ligated with 5-0 silk and the rats were put in the moisturized hypoxic gas chamber for 150 minutes. Lipid/N-acetyl aspartate and Lipid/Creatine ratio of magnetic resonance spectroscopy were evaluated on the 1st day and the 7th day after hypoxic ischemic brain injury. All rats were sacrificed 2 weeks after hypoxic ischemic brain injury for morphological study. Results: There were no statistically significant differences between two groups in the result of MRS and Lip/Cr and Lip/NAA ratio on 1th day and 7th day after hypoxic ischemic brain injury. In addition, there was no significant difference in the gross morphological evaluation on the 14th day. Conclusions: Our results suggest that the pretreatment of the Tin protoporphyrin IX does not affect the degree of brain damage which is caused by apoptosis in the model of hypoxic ischemic brain injury in a neonatal rat.

Background: A brief episode of cerebral ischemia confers transient ischemic tolerance to a subsequent ischemic challenge. We examined the effect of ischemic and hypoxic preconditioning in the neonatal rat. Methods: Seven-day old Sprague-Dawley rat pups were divided into three groups:control (n = 53), ischemic preconditioning (n = 51), and hypoxic preconditioning (n = 48). For ischemic preconditioning, the right common carotid artery was occluded for 10 min. Rats in the hypoxic preconditioning group were kept under hypoxic (8% oxygen/92% nitrogen) conditions for 4h. Twenty-four hours after the preconditioning, rats from all groups were exposed to the right common carotid artery ligature, followed by 2.5 h of hypoxia. Lipid/N-acetyl aspartate (Lip/NAA) and lipid/creatine (Lip/Cr) ratios from 1H MR spectroscopy and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) were evaluated as measures of apoptosis 1 and 7 days after hypoxic-ischemic injury. Results: In the ischemic and hypoxic preconditioning groups, the Lip/NAA and Lip/Cr ratios and the numbers of TUNEL- positive cells were significantly lower than those in the control group (P

Brugada syndrome is characterized by an ECG pattern of right bundle branch block and ST segment elevation in right precordial leads ( to ), without structural heart disease. However, these ECG manifestations transiently normalize in up to 40% of cases. Brugada syndrome is responsible for up to one half of all sudden cardiac deaths in young adults and they may be worsened by beta blockers. We present the anesthetic management of a patient with Brugada syndrome without the characteristic ECG pattern.

Background: Laryngoscopy, tracheal intubation and the suspension laryngoscopy often provoke an undesirable increase in blood pressure and/or heart rate during laryngeal microscopic surgery. Thus, the anesthesiologist's objectives are to maintain sufficient anesthetic depth and to promote rapid awakening. Nicardipine, a direct arterial dilator, can be used to attenuate increasing blood pressure. We investigated the effects of nicardipine on changes of blood pressure and heart rate during laryngeal microscopic surgery. Methods: Eighty patients of ASA class 1 or 2 scheduled for laryngeal microscopic surgery were randomly allocated into 4 groups. For anesthetic induction, IV propofol 1.5 mg/kg, rocuronium 0.4 mg/kg, and glycopyrrolate 0.2 mg were administered followed by mask ventilation for 5 minutes with isoflurane. One minute before tracheal intubation and suspension laryngoscopy saline, nicardipine 10, 20, or 30/kg was injected in each group. Thereafter we measured blood pressure and heart rate one minute after each procedure. Results: Increases in blood pressure were blunted in the nicardipine 20 and 30/kg group. In the nicardipine 30/kg group, heart rates were significantly increased and facial flushing was observed in two patients. Conclusions: We suggest that nicardipine 20/kg can alleviate blood pressure increases with little effect on heart rate during laryngeal microscopic surgery. However, although nicardipine 30/kg could blunt blood pressure increases, it produces tachycardia and perhaps overdose.

Background: Perfluorocarbon (PFC) liquids have high oxygen carrying capacity and relatively low surface tension allowing them to spread evenly through the diseased lung, especially in the case of adult respiratory distress syndrome. But few studies have demonstrated the effects of PFC on a bronchoconstriction model. The aim of this study was to investigate the effects of PFC on pulmonary mechanics and gas exchange in methacholine-induced bronchoconstricted cats using a flow interruption technique. Methods: Twenty male cats were divided into four groups; control group(group C, n = 5), PFC group (group P, PFC 5 ml/kg, n = 5), methacholine group (group M, 25g/kg/min, n = 5), PFC and methacholine group (group MP, n = 5). Respiratory pressure using a flow interruption technique was measured immediately after stabilizing the heart rate and blood pressure 0, ad 15, 30 and 60 min after the start of the intratracheal administration of PFC and/or methacholine infusion, depending on the group. Arterial blood gas analysis was done to compare arterial partial oxygen pressure among the groups at the time of measuring the pressure values. The pressure data was transferred to a personal computer and analyzed using ANADAT software program. Respiratory, airway and tissue viscoelastic pressure were calculated, Statistical analysis was done by ANOVA and statistical significance was defined as P

Background: The Freund's complete adjuvant (FCA)-induced inflammation may produce allodynia against a touch stimulus. The antiallodynic effects of brimonidine, a new selective 2 receptor agonist, and of rilmenidine, a new more selective imidazoline receptor agonist, have not been evaluated in rats with FCA induced inflammation. Therefore, we investigated the sympathetic component of mechanical allodynia after the development of allodynia secondary to FCA-induced inflammation in rats. Methods: A lumbar intrathecal catheter was implantated in male Sprague Dawley rats. Inflammation was induced by the intradermal injection of 0.15 ml FCA under enflurane anesthesia. Using Von Frey filaments, the antiallodynic effects of intrathecal (I.T.) brimonidine (1, 3), rilmenidine (30, 100) and saline were examined. In antagonistic study intrathecal yohimbine 30 and rauwolscine 30 were administered to investigate the reversal of the antiallodynic effect by each agonist. We also examined the effects of intradermal norepinephrine followed by I.T. brimonidin, rilmenidine or saline on the withdrawal threshold of rats secondary to allodynia induced by FCA. Results: I.T. brimonidine or rilmenidine produced dose-dependent antiallodynic effect and which were moderately antagonized by I.T. yohimbine or rauwolscine. Intradermal norepinephrine produced a reduction in the withdrawal threshold in rats. Conclusions: Our results suggest that a sympathetic component is likely to be involved in the mechanism of allodynia secondary to FCA-induced inflammation.

Background: Inducible nitric oxide synthase (iNOS) is expressed during the late stage of ischemia and may play an important role in the delayed progression of ischemic brain injury. This study was conducted to investigate the effect of N-(3-[aminomethyl] benzyl] acetamidine (1,400 W), a selective inhibitor of iNOS on hypoxic ischemic injury in a neonatal rat model. Methods: Seven-day old Sprague-Dawley rats were used. The right common carotid artery was ligated under halothane anesthesia. Three 3 hours after recovery, animals were exposed to 8% oxygen in 92% nitrogen. The treatment group (n = 14) received 7 intraperitoneal injection of 20 mg/kg of 1,400 W. The first dose was given 18 hours after the injury and interval between injections was 8 hours. The control group (n = 13) did not receive 1,400 W. The degree of ischemic damage and apoptosis were evaluated 3 days after injury by H magnetic resonance spectroscopy (MRS) and terminal deoxynucletidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining. The authors obtained Lipid/N-acetyl aspartate (Lip/NAA) and lipid/ creatine (Lip/Cr) ratios as apoptotic markers via H MRS, and counted the apoptotic cell number by TUNEL staining in the right hemisphere. Data were analyzed using the unpaired t-test. Results: There were no significant differences in the Lip/NAA or Lip/Cr ratios of the 2 groups, and no significant differences were found in terms of the number of TUNEL positive cells between 2 groups, either. Conclusions: The iNOS inhibitor investigated did not show protective effects against delayed neuronal damage and apoptosis after the hypoxic-ischemic injury in newborn rats, at least during the 3 days following injury. Our results suggest that NO has different roles in cerebral hypoxia-ischemia according to the stage of neonatal cerebral development.

Background: Poly (ADP-ribose) polymerase (PARP) has been described as an important candidate for mediation of neurotoxicity after brain ischemia. This study was purposed to evaluate the effects of a PARP inhibitor on hypoxic-ischemic injury in the neonatal rat brain. In this study, a highly potent inhibitor of PARP, 3, 4-Dihydro-5-[4-(I-piperidinyl) butoxy]-1 (2H)-isoquinolinone (DPQ) was investigated. Methods: Seven-day old Sprague-Dawley rat pups were used. The right common carotid artery was ligated under halothane anesthesia. After a recovery period of 3 hours, they were exposed to 8% oxygen at 37 for about 120 minutes. The animals were divided into four groups: the pre-treatment group (n = 13) and post-treatment group (n = 21) were given DPQ 10 mg/kg and the pre-control group (n = 7) and post-control group (n = 14) were given a vehicle for controls. Pre-treatment and pre-control groups were injected 30 minutes prior to the hypoxic injury while post-treatment and post-control groups were injected 30 minutes after the hypoxic period intraperitoneally. The right cerebral hemisphere of the rats were examined with localized magnetic resonance spectroscopy on day 1 and 7 after the hypoxic insult. Lipid/N-acetyl aspartate (Lip/NAA) and lipidjcreatine (Lip/Cr) ratios were used as apoptotic markers. On day 14, the degree of brain injury was scored by morphological changes. Results: In the DPQ treated groups, the Lip/NAA and Lip/Cr ratios were lower than those of the control groups on day 1 after the hypoxic-ischemic injury (P

Background : The effect of arterial carbon dioxide tension(PaCO2) during ischemia and reperfusion has been a controversial issue. In this study, the effect of PaCO2 during ischemia and reperfusion was evaluated by 31P magnetic resonance spectroscopy(MRS). Methods : Incomplete global cerebral ischemia was induced by ligation of carotid artery under lowered mean blood pressure(mean blood pressure= 40 mmHg) for 30 minutes followed by 2 hours of reperfusion. Eighteen cats were divided into 3 groups: For group 1(n=6)(control group), animals were subjected to normocarbia(PaCO2=28∼33 mmHg) during ischemia and reperfusion, for group 2(n=6), animals were subjected to hypocarbia(PaCO2=18∼23 mmHg) during ischemia and reperfusion, and for group 3(n=6), animals were subjected to normocarbia during ischemia and hypocarbia during reperfusion. Results : For group 1, the energy metabolism measured by [PCr/Pi] was recovered about 74.7 6.4%. For group 2, the energy metabolism failed to be completely recovered by 120 minutes of reperfusion(69.3 7.3%), whereas for group 3, the energy matabolism was completely recovered by 120 minutes of reperfusion(97.6 2.4%). There were statistically significant differences between group 1 and group 3(p ＜0.05). The changes in pH were not significantly different among the groups Conclusion: In this study, a condition of hypocarbia during reperfusion seems better for the energy metabolism after incomplete global ischemia of cats. (Korean J Anesthesiol 1997; 33: 610∼616)

연구배경: 기존의 양압환기법은 기관내관이나 기관절개술을 통해서만 시행되어 왔으나 최근 이러한 인공기도에 의한 기도합병증을 피하기 위한 방법으로 안연 또는 코마스크를 환자~인공환기기 사이의 매체로 이용하는 비침습적 환기법 (noninvasive positive pressure ventilation, 이하 NIV라 함)이 시도되고 있다. 이에 저자 등응 급성호흡부전 환자들에서 NIV의 적용 가능성, 치료성공율 및 치료성공과 연관된 지표를 알아보고자 본 연구를 시행하였다. 방법: 대상응 급성 환기부전 (acute vemilarory failure, 이하 VF : $PaCO_2$ > 43 mrn Hg & pH $PaO_2/FIO_2$ $pH{\geq}7.35$ )으로 기계호흡이 필요했던 환자 106 예 중 NIV 시도가 가능한 환자 26명이었으며, 총 VF 19예 중 11 예 (57.9%) (남 : 여 =7 : 4, $55.4{\pm}14.6$ 세), 총 OF 87예 중 15 예 (17.2%) (남 : 여 =12 : 3, $50.6{\pm}15.6$ 세)에서 NIV 시도가 가능하였다. 결과: 1. 기관내삽관 없이 NIV로 기계호흡 이탈까지 성공한 환자는 VF에서 81.8% (9/11), OF에서 40%(6/15)였다. NIV 의 합병증은 코부위 피부괴사와 가스성 위장 팽대 각 1예씩 이었다. 2. 환기부전 환자의 NIV 성공 예 에서 분당호흡 수는 기저치에 비해 NIV 시작 12시간 후(각각 $34{\pm}9$ 회, $26{\pm}6$ 회, p=0.045)에 유의한 감소를 보였다. $PaCO_2$ 와 pH는 모두 기저치에 비해 NIV 시작 24시간 후( $PaCO_2$ 각각 $87.3{\pm}20.6$ , $81.2{\pm}9.1$ mm Hg, p $7.26{\pm}0.04$ , $7.32{\pm}0.02$ , p $PaCO_2$ 는 NIV 시작전 (각각 $59.8{\pm}9.2$ , $76.0{\pm}22.8$ mm Hg), NIV 시작 후 30분 (각각 $121.5{\pm}20.2$ , $99.6{\pm}35.8$ mm Hg,), 6시간 (각각 $100.0{\pm}26.4$ , $76.2{\pm}22.3$ mm Hg) 및 12시간 ( $88.7{\pm}28.7$ , $74.3{\pm}16.7$ mm Hg)에 서로 유의한 차이가 없었으나 (모두 p > 0.05), $PaO_2/FIO_2$ 비는 NIV 성공 예에서는 각각 $120.0{\pm}19.6$ , $218.9{\pm}98.3$ , $191.3{\pm}55.2$ 및 $232.8{\pm}17.6$ mm Hg (p=0.0211)로 상승한 반면, 실패 예에서는 $127.9{\pm}63.0$ , $116.8{\pm}24.4$ , $100.6{\pm}34.6$ 및 $129.8{\pm}50.3$ mm Hg (p=0.5319)로 유의한 상승이 관찰되지 않았다. 결론: 비침습적 환기법은 급성 환기부전군에서 급성 산소화부전에 비해 적용성과 성공율이 높으며, 환기부전의 NIV 성공 예에서는 분당호흡수의 감소가 선행하고 $PaO_2$ 와 pH의 호전이 뒤따랐고 산소화부전에서는 NIV 시작 30분 후의 $PaO_2/FIO_2$ 비가 성공적 NIV 적용 여부의 한 예측 지표가 될 수 있을 것으로 사료되었다. 【Background : We prospectively evaluated the applicability and effect of noninvasive ventilation (NIV) in acute respiratory failure and tried to find out the parameters that could predict successful application of NIV. Methods : Twenty-six out of 106 patients with either acute ventilatory failure (VF: $PaCO_2$ > 43 mm Hg with pH $PaO_2/AO_2$ $pH{\geq}7.35$ ) requiring mechanical ventilation were managed by NIV (CPAP + pressure suppon, or BiPAP) with face mask. Eleven out of 19 cases with VF (57.9%) (M : F=7 : $55.4{\pm}14.6$ yrs) and 15 out of 87 cases with OF (17.2%) (M : F=12 : 3, $50.6{\pm}15.6$ yrs) were s uilable for NIY. Respiratory rates, arterial blood gases and success rate of NIV were analyzed in each group. Results: 81.8% (9/11) of YF and 40% (6/15) of OF were successfully managed on NIV and were weruled from mechanical ventilator without resorting to endotracheal intubation. Complications were noted in 2 cases (nasal skin necrosis 1, gaseous gastric distension 1). In NIV for ventilatory failure, the respiration rate was significantly decreased at 12 hour of NIV ( $34{\pm}9$ /min pre-NIV, $26{\pm}6$ /min at 12 hour of NIV, p=0.045), while $PaCO_2$ ( $87.3{\pm}20.6$ mm Hg pre-NIV, $81.2{\pm}9.1$ mm Hg at 24 hour of NIV) and pH ( $7.26{\pm}0.04$ , $7.32{\pm}0.02$ , respectively, p $PaCO_2$ were not different between the successful and the failed cases at pre-NIV and till 12 hours after NIV. The $PaO_2/FIO_2$ ratio, however, significantly improved at 0.5 hour of NIV in successful cases and were maintained at around 200 mm Hg (n=6 : at baseline, 0.5h, 6h, 12h : $120.0{\pm}19.6$ , $218.9{\pm}98.3$ , $191.3{\pm}55.2$ , $232.8{\pm}17.6$ mm Hg, respectively, p=0.0211), but it did not rise in the failed cases (n=9 : $127.9{\pm}63.0$ , $116.8{\pm}24.4$ , $100.6{\pm}34.6$ , $129.8{\pm}50.3$ mm Hg, respectively, p=0.5319). Conclusion : From the above results we conclude that NIV is effective for hypercapnic respiratory failure and its success was heralded by reduction of respiration rale before the reduction in $PaCO_2$ level. In hypoxic respiratory failure, NIV is much less effective, and the immediate improvement of $PaO_2/FIO_2$ ratio at 0.5h after application is thought to be a predictor of successful NIV.】