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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.

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)