Okayama University Medical SchoolActa Medica Okayama0386-300X7062016Isoflurane Induces Transient Impairment of Retention of Spatial Working Memory in Rats455460ENMasaakiTaninoDepartment of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesMotomuKobayashiDepartment of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesToshihiroSasakiDepartment of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesKenTakataDepartment of Anesthesiology and Intensive Care Medicine, Kawasaki Medical SchoolYoshimasaTakedaDepartment of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesSatoshiMizobuchiDivision of Anesthesiology, Department of Surgery Related, Kobe University Graduate School of MedicineKiyoshiMoritaOkayama UniversityTakuNagaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of MedicineHiroshiMorimatsuDepartment of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOriginal Article10.18926/AMO/54808Postoperative cognitive dysfunction (POCD) occurs in nearly one-third of patients after non-cardiac surgery. Many animal behavior studies have investigated the effect of general anesthesia on cognitive function. However, there have been no studies examining the effects on working memory specifically, with a focus on the retention of working memory. We demonstrate here that isoflurane anesthesia induces deficits in the retention of spatial working memory in rats, as revealed by an increase in isoflurane-induced across-phase errors in the delayed spatial win-shift (SWSh) task with a 30-min delay in an 8-arm radial arm maze on post-anesthesia days (PADs) 1,2,4, and 10. A post-hoc analysis revealed a significant increase in across-phase errors on PAD 1 and recovery on PAD 10 in the isoflurane group. In contrast, within-phase errors independent of the retention of working memory were unaffected by isoflurane. These results demonstrate that isoflurane anesthesia transiently impairs the retention of spatial working memory in rats.No potential conflict of interest relevant to this article was reported.Elsevier Ireland Ltd.Acta Medica Okayama0300-957285122014Feasibility study of immediate pharyngeal cooling initiation in cardiac arrest patients after arrival at the emergency room16471653ENYoshimasaTakedaTakahisaKawashimaKazuyaKiyotaShigetoOdaNaokiMorimotoHitoshiKobataHisashiIsobeMitsuruHondaSatoshiFujimiJunOndaSeishiITetsuyaSakamotoMasamiIshikawaHiroshiNakanoDaikaiSadamitsuMasanobuKishikawaKosakuKinoshitaTomoharuYokoyamaMasahiroHaradaMichioKitauraKiyoshiIchiharaHiroshiHashimotoHidekazuTsujiTakashiYorifujiOsamuNaganoHiroshiKatayamaYoshihitoUjikeKiyoshiMoritaAIM:
Cooling the pharynx and upper oesophagus would be more advantageous for rapid induction of therapeutic hypothermia since the carotid arteries run in their vicinity. The aim of this study was to determine the effects of pharyngeal cooling on brain temperature and the safety and feasibility for patients under resuscitation.
METHODS:
Witnessed non-traumatic cardiac arrest patients (n=108) were randomized to receive standard care with (n=53) or without pharyngeal cooling (n=55). In the emergency room, pharyngeal cooling was initiated before or shortly after return of spontaneous circulation by perfusing physiological saline (5 ‹C) into a pharyngeal cuff for 120 min.
RESULTS:
There was a significant decrease in tympanic temperature at 40 min after arrival (P=0.02) with a maximum difference between the groups at 120 min (32.9 } 1.2‹C, pharyngeal cooling group vs. 34.1 } 1.3‹C, control group; P<0.001). The return of spontaneous circulation (70% vs. 65%, P=0.63) and rearrest (38% vs. 47%, P=0.45) rates were not significantly different based on the initiation of pharyngeal cooling. No post-treatment mechanical or cold-related injury was observed on the pharyngeal epithelium by macroscopic observation. The thrombocytopaenia incidence was lower in the pharyngeal cooling group (P=0.001) during the 3-day period after arrival. The cumulative survival rate at 1 month was not significantly different between the two groups.
CONCLUSIONS:
Initiation of pharyngeal cooling before or immediately after the return of spontaneous circulation is safe and feasible. Pharyngeal cooling can rapidly decrease tympanic temperature without adverse effects on circulation or the pharyngeal epithelium.No potential conflict of interest relevant to this article was reported.Okayama UniversityActa Medica Okayama22014Ensuring a cool recovery from cardiac arrestENYoshimasaTakedaNo potential conflict of interest relevant to this article was reported.Acta Medica Okayama0306-45222352013EFFECT OF LIDOCAINE ON DYNAMIC CHANGES IN CORTICAL REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE FLUORESCENCE DURING TRANSIENT FOCAL CEREBRAL ISCHEMIA IN RATS5969ENH.NaitoY.TakedaT.DanuraI. S.KassK.MoritaRats were subjected to 90 min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n = 10), 30 min before ischemia, an intravenous bolus (1.5 mg/kg) of lidocaine was administered, followed by a continuous infusion (2 mg/kg/h) for 150 min. In the control group (n = 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P = 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of pen-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P = 0.046) and 24 h later (P = 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.No potential conflict of interest relevant to this article was reported.Acta Medica Okayama0898-49212532013Quantitative evaluation of the neuroprotective effects of a short-acting ƒÀ-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils: effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1.292298ENTetsuyaDanuraYoshimasaTakedaKensukeShiraishiHiromichiNaitoRyoichiMizoueSachikoSatoKiyoshiMoritaBACKGROUND:
Neuroprotective effects of esmolol in laboratory and clinical settings have been reported. The present study was designed to quantitatively evaluate the neuroprotective effects of esmolol using logistic regression curves and extracellular potentials.
MATERIALS AND METHODS:
In 42 gerbils, bilateral occlusion of common carotid arteries was performed for 3, 5, or 7 minutes (n=7 in each group). In treated animals, esmolol (200 µg/kg/min) was administered for 90 minutes, 30 minutes before the onset of ischemia. Direct current potentials were measured in the bilateral CA1 regions, in which histologic evaluation was performed 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined using logistic regression curves.
RESULTS:
There was no significant difference in onset time between the 2 groups (the control group vs. the esmolol group: 1.65}0.46 vs. 1.68}0.45 min, P=0.76), and significant differences in durations of ischemic depolarization were not observed with any ischemic duration. However, logistic regression curves indicated that esmolol has a neuroprotective effect from 2.95 to 7.66 minutes of ischemic depolarization (P<0.05), and esmolol prolonged the duration of ischemic depolarization causing 50% neuronal damage from 4.97 to 6.34 minutes (P<0.05). Logistic regression curves also indicated that esmolol has a neuroprotective effect from 3.77 to 7.74 minutes of ischemic duration (P<0.05), and esmolol prolonged the ischemic duration causing 50% neuronal damage from 4.26 to 4.91 minutes (P<0.05).No potential conflict of interest relevant to this article was reported.Okayama University Medical SchoolActa Medica Okayama0386-300X6722013Stereoscopic Three-Dimensional Images of an Anatomical Dissection of the Eyeball and Orbit for Educational Purposes8791ENToshihikoMatsuoYoshimasaTakedaAijiOhtsukaOriginal Article10.18926/AMO/49666The purpose of this study was to develop a series of stereoscopic anatomical images of the eye and orbit for use in the curricula of medical schools and residency programs in ophthalmology and other specialties. Layer-by-layer dissection of the eyelid, eyeball, and orbit of a cadaver was performed by an ophthalmologist. A stereoscopic camera system was used to capture a series of anatomical views that were scanned in a panoramic three-dimensional manner around the center of the lid fissure. The images could be rotated 360 degrees in the frontal plane and the angle of views could be tilted up to 90 degrees along the anteroposterior axis perpendicular to the frontal plane around the 360 degrees. The skin, orbicularis oculi muscle, and upper and lower tarsus were sequentially observed. The upper and lower eyelids were removed to expose the bulbar conjunctiva and to insert three 25-gauge trocars for vitrectomy at the location of the pars plana. The cornea was cut at the limbus, and the lens with mature cataract was dislocated. The sclera was cut to observe the trocars from inside the eyeball. The sclera was further cut to visualize the superior oblique muscle with the trochlea and the inferior oblique muscle. The eyeball was dissected completely to observe the optic nerve and the ophthalmic artery. The thin bones of the medial and inferior orbital wall were cracked with a forceps to expose the ethmoid and maxillary sinus, respectively. In conclusion, the serial dissection images visualized aspects of the local anatomy specific to various procedures, including the levator muscle and tarsus for blepharoptosis surgery, 25-gauge trocars as viewed from inside the eye globe for vitrectomy, the oblique muscles for strabismus surgery, and the thin medial and inferior orbital bony walls for orbital bone fractures.No potential conflict of interest relevant to this article was reported.Okayama University Medical SchoolActa Medica Okayama0386-300X6532011The Excitement of Multiple Noradrenergic Cell Groups in the Rat Brain Related to Hyperbaric Oxygen Seizure163168ENMinakoAraiKenTakataYoshimasaTakedaSatoshiMizobuchiKiyoshiMoritaOriginal Article10.18926/AMO/46627The mechanism of oxygen toxicity for central nervous system and hyperbaric oxygen (HBO) seizure has not been clarified. Noradrenergic cells in the brain may contribute to HBO seizure. In this study, we defined the activation of noradrenergic cells during HBO exposure by c-fos immunohistochemistry. Electroencephalogram electrodes were pre-implanted in all animals under general anesthesia. In HBO seizure animals, HBO was induced with 5 atm of 100% oxygen until manifestation of general tonic convulsion. HBO non-seizure animals were exposed to 25 min of HBO. Control animals were put in the chamber for 120 min without pressurization. All animals were processed for c-fos immunohistochemical staining. All animals in the HBO seizure group showed electrical discharge on EEG. In the immunohistochemistry, c-fos was increased in the A1, A2 and A6 cells of the HBO seizure group, and in the A2 and A6 cells of the HBO non-seizure group, yet was extremely low in all three cell types in the control group. These results suggest the participation of noradrenaline in HBO seizure, which can be explained by the early excitement of A1 cells due to their higher sensitivity to high blood pressure, hyperoxia, or by the post-seizure activation of all noradrenergic cells.No potential conflict of interest relevant to this article was reported.Okayama University Medical SchoolActa Medica Okayama0386-300X5822004The close relationship between decreases in extracellular GABA concentrations and increases in the incidence of hyperbaric oxygen-induced electrical discharge.9195ENShanZhangYoshimasaTakedaShingoHagiokaKeijiGotoKiyoshiMoritaArticle10.18926/AMO/32101<p>To elucidate the mechanism by which hyperbaric oxygen (HBO2) induces electrical discharge, changes in the extracellular concentrations of GABA and glutamate were measured every 5 min using a microdialysis technique in rats during a period of exposure to HBO2 (5 atm abs). Electrical discharge was observed at 28 +/- 4 min after the onset of exposure. Though the extracellular concentrations of glutamate remained unchanged, the extracellular GABA concentrations (pre-exposure level, 0.026 +/- 0.005 microM in dialysate) began to decrease 15 min after the onset of exposure and reached their lowest level (74 +/- 14%, 0.019 +/- 0.004 microM) at the time of appearance of the discharge. There was a close logistic relationship between extracellular GABA concentrations and the discharge incidence, and the extracellular concentrations of GABA causing electrical discharge in 50% of the animals were estimated to be 80% of the pre-exposure level. These results suggest a possible mechanism that HBO2 exposure-induced discharge is caused by the decrease in extracellular concentration of GABA.</p>
No potential conflict of interest relevant to this article was reported.‰ªŽRˆãŠw‰ïActa Medica Okayama0030-155810341991ƒCƒk‚ÌŠ®‘S‘S”]‹•ŒŒŒã‚Ì”]áŠQ‚É‹y‚Ú‚·SMA-SOD ‚ÌŒø‰Ê‚ÉŠÖ‚·‚éŽÀŒ±“IŒ¤‹†257266ENYoshimasaTakedaThe effects of stylene maleinic acid butyl ester superoxide dismutase (SMA-SOD) on the brain damage induced by ischemia were studied in dogs. Eighteen minutes of cerebral ischemia was produced by clamping the ascending aorta with aorta-atrial and aorta-femoral vein bypass circuit. SMA-SOD(10mg/kg) was administered just after the initiation of recirculation. Dogs were divided into, control group and SMA-SOD group. In each group, cerebral blood flow (CBF) and intracranial pressure (ICP) were measured for 7 hours after ischemia, and neurologic outcome was evaluated up to 7 days after ischemia. Furthermore, extravasation of evans blue dye (EB, 100mg/kg) were observed 30 minutes after ischemia. SMA-SOD increased CBF during the hyperemia, and improved both delayed post-ischemic hypoperfusion (DHP) and neurologic outcomes. Extravasation of EB were recognized in the control group, but not in the SMA-SOD group.
In conclusion, vasogenic edema might play a role in the elevation of ICP besides the hyperemia, and SMA-SOD improved neurologic outcome by prevention of edema, and improvement of DHP. Furthermore, free radicals might play a role in the appearance of ischemic brain damage.No potential conflict of interest relevant to this article was reported.Acta Medica Okayama1991ƒCƒk‚ÌŠ®‘S‘S”]‹•ŒŒŒã‚Ì”]áŠQ‚É‹y‚Ú‚·SMA-SOD‚ÌŒø‰Ê‚ÉŠÖ‚·‚éŽÀŒ±“IŒ¤‹†ENNo potential conflict of interest relevant to this article was reported.