Uno Imaizumi

Comparative effects of verapamil, nicardipine, and nitroglycerin on myocardial ischemia/reperfusion injury.

The aim of this experiment was to establish whether verapamil, nicardipine, and nitroglycerin have (1) infarct size-limiting effects and (2) antiarrhythmic effects in in vivo rabbit hearts during ischemia/reperfusion. Rabbits received regional ischemia by 30 min of left anterior descending coronary artery occlusion followed by 3 hours of reperfusion under ketamine and xylazine anesthesia. The animals were randomly assigned to the following 4 treatment groups: a control group, a verapamil group, a nicardipine group, and a nitroglycerin group. A continuous infusion of verapamil, nicardipine, or nitroglycerin was initiated 5 min prior to ischemia. Infarct size/area at risk decreased in verapamil, and nitroglycerin. The incidence of ischemia-induced arrhythmia decreased in nicardipine, verapamil and nitroglycerin. The incidence of reperfusion-induced arrhythmias decreased in verapamil and nitroglycerin. From the present experimental results, verapamil and nitroglycerin rather than nicardipine did afford significant protection to the heart subjected to ischemia and reperfusion in a rabbit model.

Effects of Lidocaine on Ischemia/Reperfusion Injury in In vivo Rabbit Hearts

Objective: The aim of this study was to investigate the cardioprotective effects of lidocaine administered at three different timings, as indexes of hemodynamics, infarct size, antiarrhythmic action, and changing activation time by electrocardiogram in in vivo rabbit hearts. Methods: Thirty two rabbits received regional ischemia by 30 min of left anterior descending coronary artery occlusion followed 3 hours of reperfusion under ketamine and xylazine anesthesia. The animals were randomly assigned to the following 4 treatment groups: a control group, a lidocaine-preconditioned group, a lidocainepostconditioned group, and a lidocaine-continuous administration group. Results: The ratio of areas at risk revealed no significant difference among all groups. Mean infarct size of the area at risk was significantly less in a lidocaine-continuous administration group than other 3 groups. The incidence of arrhythmias during myocardial ischemia was no significant difference between a control group and other 3 groups. The incidence of arrhythmias during reperfusion was no significant difference among all groups. However, lidocaine depressed the activation time which was prolonged by ischemia.

Airway management for glossopexy in infants with micrognathia and obstructive breathing

STUDY OBJECTIVES To identify airway management and tracheal intubation techniques for glossopexy in infants with preexisting airway obstruction under general anesthesia. DESIGN Retrospective, observational study. SETTINGS Operating room of a university hospital between January 2003 and March 2015. All operations were performed by oral and maxillofacial surgeons. PATIENTS Thirteen patients who received general anesthesia for glossopexy and reversal after 7 months. MEASUREMENTS The medical records of these infants were retrospectively examined to evaluate the following: age, sex, height and weight at surgery, preoperative airway status, tracheal intubation route (oral or nasal), method for inducing general anesthesia, method for establishing the airway during mask ventilation, apparatus used for tracheal intubation, Cormack-Lehane classification when using a Macintosh laryngoscope and video laryngoscope, and the need for airway placement after extubation. RESULTS Prone positioning and/or an airway of some kind before surgery were required in 38.5% of infants needing glossopexy. Difficult mask ventilation was common, occurring in 50% of the patients, and the incidence of airway placement during mask ventilation was significantly higher in infants with preoperative complete or incomplete obstruction (100%) than in infants with snoring (25%). Of these high-risk infants, 25% could not be intubated with a direct laryngoscope or Glidescope Cobalt and required fiberoptic intubation. CONCLUSION There are severe cases of infants with difficult mask ventilation and difficult tracheal intubation in which a fiberscope is required because video laryngoscopy fails to improve the view of the larynx.

Effects of Ischemic and Sevoflurane-induced Preconditioning on Myocardial Infarction and Arrhythmias in Rabbits In Vivo

Objectives: The present study aimed to investigate whether ischemic or sevoflurane-induced preconditioning exerts infarct size limiting effects and depresses ischemia-reperfusion arrhythmias through opening of mitochondrial KATP channels in rabbits in vivo. Methods: Rabbits anesthetized with ketamine and xylazine given intramuscularly underwent 30 min of left anterior descending coronary artery (LAD) occlusion followed by 3 hrs of reperfusion. Before this, rabbits were randomized into one of five groups. Control rabbits received no intervention before 30 min LAD occlusion and 3 h reperfusion (Group-C). The ischemia-preconditioned (IP) rabbits underwent 5 min LAD occlusion followed by 10 min of reperfusion before prolonged ischemia-reperfusion (Group-IP). In the sevoflurane (S)–preconditioned group, 30 min of sevoflurane exposure at a 1.5% end-tidal concentration was followed by 15 min of washout before prolonged ischemia-reperfusion (Group-S). The selective mitochondrial KATP channel blocker, 5-hydroxy-decanoate (5-HD, 5 mg/kg) was given intravenously 10 min before ischemic preconditioning and sevoflurane exposure, respectively (Group-5-HD-IP, Group-5-HD-S). An electrocardiogram was recorded throughout the experiment via lead 2 of the standard electrocardiogram. At the end of the 3 hrs reperfusion period, area at risk (R) and infarct size (I) were measured. Results: RPP decreased in Group-5-HD-IP and Group-5-HD-S compared with Group-S at 30 min after ischemia. The ratio of R to left ventricular mass showed no significant difference among all groups. I/R values of each group were 51.6 ± 3.0% in Group-C, 33.3 ± 4.7% in Group-IP, 36.6 ± 4.8% in Group-S, 48.9 ± 5.2% in Group-5-HD-IP, 54.8 ± 4.2% in Group-Group-5-HD-S. There was no significant difference in duration of arrhythmias during myocardial ischemia and reperfusion among 5 groups. Conclusion: Ischemic preconditioning and sevoflurane-induced preconditioning exert infarct size limiting effects through opening of mitochondrial KATP channels. However, ischemic preconditioning and sevoflurane-induced preconditioning do not have antiarrhythmic effects. This suggests that the opening of mitochondrial KATP channels does not cause antiarrhythmic effects.