Tissue Doppler Imaging (TDI) is a new echocardiographic technique employing the Doppler principle to measure the regional left ventricular (LV) myocardial and mitral annular velocities. Pulsed TDI is well-suited for measuring the peak velocity and the timing of LV wall motion along the short- and long-axes. It has introduced new insights into LV physiology and become a useful tool for evaluating LV function overcoming the load-dependence of conventional Doppler techniques. Color TDI has introduced a further development into strain imaging and tissue tracking imaging using velocity information. The modality allows truly quantitative measurement of regional myocardial function without being influenced by whole-heart motion. Intraventricular asynchrony in patients undergoing cardiac resynchronization therapy can be assessed with this technique. This noninvasive method also has potential in diagnosis of tissue characterization in patients with various myocardial diseases.

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  ATP-sensitive potassium (K_ATP) channels are inhibited by intracellular ATP and activated by MgADP and thus provide a link between the cellular metabolic state and excitability. K_ATP (VSM K_ATP channels) are composed of an ATP-binding cassette protein family, sulfonylurea receptor 2B, and an inward rectifying K⁺ channel subunit, Kir6.1. SUR2B that acts as a regulatory subunit while Kir6.1 subunits form the channel pore. Recent molecular biological and molecular genetic studies of VSM K_ATP channels have provided insights into the structure-function relationships, molecular regulation, and pathophysiological roles of K_ATP channels. VSM K_ATP channels respond to changes in cellular metabolism and play important roles in the vascular responses to a variety of pharmacological and endogenous vasodilators. In addition, studies performed in Kir6.1 or SUR2B knockout mice indicate that VSM K_ATP channels are involved in the regulation of vascular tonus, especially in the coronary arteries, and disruption of them may cause Prinzmetal angina. Recent studies also suggest that some anesthetics may influence VSM K_ATP channels activities. The coronary vasodilatory effects of volatile anesthetics are mediated by activation of VSM K_ATP channels. In contrast, most intravenous anesthetics and local anesthetics inhibit VSM K_ATP channels.

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  Popular pulse oximeters are about ± 2.1% accurate without motion, but there is a difference in performance with the noise of motion and low perfusion. This time, we compared the value of the models under the motion and low perfusion with the control model with an SpO₂ of >70% using the three models with new measurement of noise in six healthy adults. As a result, we found that the model with difficulty to showing unmeasurerable values has a high error rate. The models continue to show the previous value during unmeasurerable time from the noise has the advantage of no change in SpO₂. We felt that it was better to select the suitable model after we understood each characteristic although each model was able to take measure during considerable motion and low perfusion.

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  Previous studies showed the frequent abnormal motion of the interventricular septum after uncomplicated cardiac surgery. Septal wall motion must be evaluated cautiously because of the cardiac translation during cardiac surgery and the special anatomic features of the septum. We evaluated the impact of sternal closure on septal wall motion with transesophageal tissue Doppler echocardiography that provides a new objective means to quantify regional ventricular function. In 31 patients undergoing coronary artery bypass grafting, myocardial wall velocity, strain and strain rate were assessed in the basal and mid-septum before and after sternal closure. Peak systolic myocardial wall velocity decreased significantly after sternal closure, while strain and strain rate, which are less affected by cardiac motion, remained unchanged. Regional wall thickening of these segments also remained unchanged. These results suggest that decrease in myocardial systolic velocity after sternal closure reflects a reduction in cardiac translation toward the apex. Accordingly, systolic function assessed by strain and strain rate are not affected by sternal closure. The use of strain and strain rate, rather than myocardial wall velocity, may provide a more accurate quantification of septal wall function.

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  Since the occurence of infections related to the use of propofol has been suggested in previous reports, the growth of different micro-organisms (Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa, Serratia marcescens, Burkholderia cepacia and Candida albicans) in two propofol products in the presence or absence of a bacteriostatic agent, disodium edetate (EDTA) , was investigated at room temperature (20-25°C) . These preparations were inoculated with each micro-organism and samples were plated onto soybean or Sabouraud's agar 0, 6, 12, 24 and 48 hrs or 0 and 12 hrs after inoculation. The number of colony-forming units (CFUs) on the plates was then determined after incubation for 12 hrs. None of the micro-organisms exhibited growth following plating 6 hrs after inoculation in either propofol product, and S. aureus, P. aeruginosa, and C. albicans did not grow for up to 12 hrs. E. coli and B. cepacia grew in propofol without EDTA, and S. marcescens grew in both propofol products. Scrupulous aseptic techniques should be recommended when preparing or administering these anesthetics of propofol products because EDTA was not able to prevent some bacteria from growing.

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  Carbamazepine (CBZ) , using an anticonvulsant or analgesics for neuralgia, occasionally causes severe hematologic disorders. A 72-year-old man with herpes zoster developed severe, isolated thrombocytopenia (1.3 × 10⁴·μl ^-1) due to administration of CBZ (200-400mg·day^-1) for 16 days. After discontinuation of CBZ, his platelet counts returned to the normal range in 6 days. Platelet counts should be monitored more carefully in patients receiving treatment with CBZ.

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  This case report describes the anesthetic management of a case with a giant retropharyngeal abscess that was seen in a one-year-old girl with Kawasaki disease. Marked respiratory distress and cyanosis attributed to airway obstruction required an emergency open-drainage procedure of the lesion under general anesthesia. A difficult airway was expected preoperatively, so awake intubation was performed. As soon as intubation was completed, anesthesia was induced with ketamine and maintained with sevoflurane and nitrous oxide. Surgery was concluded uneventfully and the patient was reawakened promptly. For airway protection from draining pus, the patient was put in the Trendelenburg and lateral decubitus position when an endotracheal tube was extubated. This case made us realized once again the importance of airway management during general anesthesia in a child with a giant retropharyngeal abscess.

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  Patients with advanced esophageal cancer treated by radiotherapy may develop esophagobronchial fistula. We experienced two cases of gastrotracheal (bronchial) fistula as a result of radical surgery (posterior mediastinal reconstruction) for esophageal cancer. In the anesthesia plan, four points require special attention: 1) pneumonia control before anesthesia, 2) ventilation prior to endotracheal intubation, 3) endotracheal intubation (position of double-lumen tube) , and 4) respiratory management during surgery and airway reconstruction. Particularly, for ventilation during anesthesia, precise evaluation of the position of the tracheal fistula is important. The main points of anesthesia management in patients with special complications are described.

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  A 17-year-old boy underwent spinal anesthesia with isobaric 0.5% bupivacaine. Twenty minutes after the injection, systolic blood pressure fell to 60mmHg and SpO₂ decreased to 89%. He complained of dyspnea and had a cough. The erythema appeared over his feet. Symptoms were relieved by the injection of ephedrine, dopamine, methylprednisolone and antihistamine agents. Ten days after the anesthesia, we performed a lidocaine prick test and intradermal test, and confirmed that he had a negative test to lidocaine. Twelve days after the episode, he uneventfully underwent left partial meniscectomy under general anesthesia with 1% lidocaine. The event might have been due to an anaphylactoid reaction to bupivacaine.

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  A 5-year-old girl with severe burns (51% of the body) had been tracheally intubated 4 times without any difficulty during the first 6 weeks. Thereafter, she was scheduled for 3 skin-grafting surgeries within 2-6 months. Physical examination revealed an obvious limitation in mouth opening and a deformity of the neck, which became progressively worse. The anesthetic plan was to attempt intubation using a Macintosh type video-laryngoscope. Tracheal intubation was successfully performed with the assistance of the anesthesia-supervisor, who was watching the TV picture of a wide-angle laryngeal view. We have always preserved all the video records of laryngeal view during tracheal intubation whenever the video-laryngoscope is indicated. We were able to confirm the anatomical abnormality by observing her former records.

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  The concept of ischemic preconditioning refers to protection from myocardial cellular death resulting from ischemic insults by preceding brief ischemic episodes. The phenomenon of ischemic preconditioning has been documented in many animal models, however, investigating ischemic preconditioning in the clinical setting is limited. One of the clinical situations in which we can discuss ischemic preconditioning is repetitive coronary occlusions by balloon inflation during elective percutaneous transluminal coronary angioplasty (PTCA) for stable angina pectoris. The severity of myocardial ischemia assessed by ST-segment elevation or chest pain is less during the second balloon inflation compared with the first, if the duration of the first coronary occlusion is sufficient to precondition the myocardium. Many drugs have been identified producing the reduction of ischemia or induction in indices of ischemic preconditioning during PTCA. Preconditioning-mimetic drugs and substance include adenosine, bradykinin, nitroglycerin and nicorandil. It is of paramount importance that we investigate and develop preconditioning-mimetic drugs which may enable an increased tolerance to exercise-induced angina, limit infarction size of the myocardium, and decrease the incidence of sudden cardiac death as a result of ventricular tachyarrhythmias.

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  Ischemic preconditioning is a phenomenon in which brief intermittent periods of ischemia are paradoxically protective against subsequent ischemic injury. To characterize the memory of ischemic preconditioning, we studied pretreatment effects of 2, 4-dinitrophenol, a protonophore that uncouples mitochondrial respiration from ATP synthesis, on both flavoprotein oxidation, an index of mitochondrial uncoupling, and sarcolemmal K_ATP channel activation in isolated rat ventricular myocytes. Effects of 5-hydroxydecanoic acid, a mitochondrial K_ATP channel inhibitor, on the pretreatment effects were also studied. Major findings of this study were that pretreatment of mitochondrial uncoupler sensitizes flavoprotein oxidation and sarcolemmal K_ATP activation. In the presence of 5-hydroxydecanoic acid, the sensitizing effects were completely abolished. Without metabolic inhibition, sensitized myocardium represents almost normal flavoprotein oxidation and sarcolemmal K_ATP activity. These results suggest that, if we assume a memory molecule, direct effects of the memory molecule on mitochondrial uncoupling and sarcolemmal K_ATP are negligible, but the memory molecule potentiates mitochondrial uncoupling and sarcolemmal K_ATP in the face of metabolic impairment. In addition, the production of the memory molecule is 5-hydroxydecanoic acid-sensitive.

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  A rapidly growing body of evidence indicates that volatile anesthetics protect the myocardium against reversible and irreversible ischemic injury. In 1997, our laboratory demonstrated that isoflurane reduced myocardial infarct size in dogs, and this protective effect persisted despite discontinuation of the agent before coronary occlusion. This phenomenon was termed “anesthetic-induced preconditioning” (APC) , and was characterized by a short-term memory phase similar to that observed during ischemic preconditioning (IPC) . The precise mechanisms responsible for volatile anesthetic-induced protection against ischemic injury remain unclear despite extensive study.
  Our laboratory recently demonstrated that isoflurane directly increases superoxide anion formation in vivo using the fluorescent probe dihydroethidium and laser confocal microscopy independent of an ischemic episode. These data indicated for the first time that volatile anesthetics were capable of producing small amounts of reactive oxygen species (ROS) that were directly correlated with a reduction in myocardial infarct size after prolonged ischemia.
  In this report, we will show our results obtained from the experiments of myocardial infarct size study and in vivo measurements of ROS in rabbits. We also discuss the role of ROS in the mechanisms in APC.

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  The ATP-sensitive K⁺ (mitoK_ATP) channel and large-conductance Ca²⁺-activated K⁺ (mitoK_Ca) channel in the cardiac inner mitochondrial membrane are involved in the cardioprotection afforded by ischemic preconditioning. The K⁺ entry through mitoK_ATP channels depolarizes the mitochondrial membrane potential, which reduces the driving force for Ca²⁺ influx and thus results in the prevention of mitochondrial Ca²⁺ overload. MitoK_Ca channel activation attenuates mitochondrial Ca²⁺ overload in a manner similar to but independent of mitoK_ATP channel activation. Given that cell death results from impairment of mitochondrial homeostasis, such an effect of mitoK_ATP and mitoK_Ca channels can be attributed to the mechanism of cardioprotection. In addition, attenuation of the mitochondrial Ca²⁺ overload inhibits opening of the mitochondrial permeability transition pore, a key event in cell death, and provides powerful antiischemic protection.

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