[show abstract][hide abstract] ABSTRACT: Remifentanil enhances intraoperative hemodynamic stability, suggesting that it may decrease intraoperative blood loss when included as an adjuvant to general anesthesia. This retrospective study compared intraoperative blood loss during spinal surgery in patients administered either remifentanil or fentanyl as an opioid adjuvant.
We reviewed clinical and surgical data from 64 consecutive laminoplasty or laminectomy patients treated at National Hospital Organization Zentsuji Hospital between April 2010 and March 2011. Patients received either remifentanil (n = 35) or fentanyl (n = 29) as an opioid analgesic during general anesthesia. In addition to intraoperative blood loss, indices of hemodynamic stability, including heart rate as well as systolic, mean, and diastolic blood pressure (BP), were compared over the entire perioperative period between remifentanil and fentanyl groups.
The remifentanil group exhibited significantly lower intraoperative arterial BP than the fentanyl group. Intraoperative blood loss was also significantly lower in the remifentanil group (125 +/- 67 mL vs. 165 +/- 82 mL, P = 0.035).
Intraoperative blood loss during spinal surgery was decreased in patients who received remifentanil as an opioid adjuvant, possibly because of lower intraoperative BP. A larger-scale prospective randomized controlled trial is warranted to confirm our results and to test whether remifentanil can decrease intraoperative blood loss during other surgical procedures.
[show abstract][hide abstract] ABSTRACT: Background: Hyperkalemia has multimodal effects on myocardial protection during ischemia/reperfusion. The preservation of Na(+)/K(+)-ATPase activity induced by hyperkalemia may have critical impact on myocardial protection. Methods: To elucidate the roles of hyperkalemia (16 mM) and Na(+)/K(+)-ATPase inhibition (100 µM ouabain) in myocardial protection during simulated ischemia (5 mM NaCN and 5.5 mM 2-deoxyglucose)/reperfusion, we measured loss of membrane integrity and bleb formation using a vital dye calcein AM in cultured neonatal rat cardiomyocytes. The control perfusate was switched to treatment solution for 15 min, followed by reperfusion for 30 min. In a second set of experiments, myocardial excitability and diastolic intracellular calcium ion concentration ([Ca(2+)]i) were measured during a 45-min treatment using a calcium-sensitive fluorescent dye fluo-4 AM. Results: Simulated ischemia/reperfusion under ouabain treatment induced loss of membrane integrity, which was suppressed by hyperkalemia. Simulated ischemia/reperfusion induced bleb formation, which was accelerated by ouabain. Hyperkalemia delayed and inhibited the increase in diastolic [Ca(2+)]i induced by simulated ischemia. Furthermore, hyperkalemia almost completely inhibited the effects of ouabain on the diastolic [Ca(2+)]i during ischemia. Conclusions: These results suggest that hyperkalemia during ischemia is cardioprotective against ischemia/reperfusion insults and that hyperkalemia inhibits the effects of ouabain during ischemia. J. Med. Invest. 60: 66-76, February, 2013.
The Journal of Medical Investigation 01/2013; 60(1-2):66-76.
[show abstract][hide abstract] ABSTRACT: For anesthetic management during renal transplantation, it is necessary to maintain the blood flow and function of the transplanted kidney by performing massive fluid management and stabilizing blood pressure. We report anesthetic management for renal transplantation with a less-invasive circulatory monitoring system (Edwards Life Sciences Co., Ltd., Irvine, California, U.S.A.). In November 2010, renal transplantation was started in our hospital, and performed in 6 patients. In the first patient, fluid/circulatory management was conducted by connecting a standard arterial line and a standard central venous (CV) line. In the second patient, a FloTrac(TM) system and a standard CV line were used. In the third patient, a standard arterial line and a PreSep(TM) CV Oximetry Catheter were used. In the fourth and fifth patients, a FloTrac(TM) and a PreSep(TM) were used. In the latest patient, FloTrac(TM) and PreSep(TM) were connected to an EV1000(TM) Clinical Platform for fluid/circulatory management. The establishment of high-visibility monitors was useful for evaluating the condition and confirming the effects. As there are marked changes in hemodynamics, the CV pressure, which has been used as a parameter of fluid management, is not reliable in renal failure patients with a high incidence of cardiovascular complications. Advances in noninvasive circulatory monitoring with dynamic indices may improve the safety of anesthetic management during renal transplantation. J. Med. Invest. 60: 159-163, February, 2013.
The Journal of Medical Investigation 01/2013; 60(1-2):159-63.
[show abstract][hide abstract] ABSTRACT: Background: The purpose of this study was to evaluate the usefulness of the closed-loop system (STG-22; Nikkiso, Tokyo, Japan), a type of artificial endocrine pancreas for the continuous monitoring and control of intraoperative blood glucose in patients undergoing liver transplantation. Methods: Sixteen patients undergoing living-donor liver transplantation were enrolled in this study. Glucose levels were controlled with either a manual injection of insulin based on a commonly used sliding scale (manual insulin group, n=8) or a programmed infusion of insulin determined by the control algorithm of the artificial endocrine pancreas (programmed insulin group, n=8). The target glucose level range was set at 80-150 mg/dl. Results: The mean and SD of blood glucose concentration during surgery (Glu-Ave and Glu-SD, respectively) for the programmed insulin group were lower than for the manual insulin group. The coefficient of variability (Glu-CV=Glu-SD×100 /Glu-Ave) for the programmed insulin group was also lower than for the manual insulin group (20.1±4.9% vs. 26.9±6.1%; mean±SD). No hypoglycemia was detected in either group. Conclusion: The STG-22 closed-loop system is effective for maintaining strict blood glucose control during liver transplantation with minimal variability in blood glucose concentration. J. Med. Invest. 60: 205-212, August, 2013.
The Journal of Medical Investigation 01/2013; 60(3-4):205-12.
[show abstract][hide abstract] ABSTRACT: We describe a case of dextran-induced anaphylactic shock during general anesthesia. A 34-year-old woman was scheduled for partial hepatic resection under general anesthesia. General anesthesia was induced with intravenous remifentanil, thiamylal and rocuronium, and was maintained with oxygen, air, sevoflurane and remifentanil. The patient developed hypotension (from 90/50 to 49/27 mmHg in 20 min) together with tachycardia (111 beats x min(-1)) and desaturation (83%) subsequent to intravenous infusion of Saviosol (dextran 40). We made a diagnosis of anaphylactic shock on the basis of clinical manifestations and administered adrenaline and hydrocortisone. The patient's blood pressure and oxygen saturation immediately improved, and the operation was resumed. No postoperative complications were evident, and the postoperative course was uneventful. Although low molecular weight dextran is often used as plasma expander or to prevent thromboembolism, it can cause severe hypotension or bronchospasm during general anesthesia.
Masui. The Japanese journal of anesthesiology 11/2012; 61(11):1265-8.
[show abstract][hide abstract] ABSTRACT: A 31-year-old woman with amyotrophic lateral sclerosis (ALS) with respiratory muscle paralysis was scheduled for tracheotomy. After applying standard neuromuscular monitoring devices, general anesthesia was induced and maintained with propofol, remifentanil, rocuronium, and sevoflurane. Sugammadex is a potent agent for reversal of neuromuscular blockade by rocuronium. The patient emerged from general anesthesia smoothly using sugammadex; however, assisted respiration was continued for possible prolongation of the effect of muscle relaxant. The postoperative course was uneventful, and she was discharged without any discomfort.
Masui. The Japanese journal of anesthesiology 09/2012; 61(9):1006-8.
[show abstract][hide abstract] ABSTRACT: We describe anesthetic management of a patient with airway stenosis due to a tracheal tumor involving the carina. A 68-year-old man developed dyspnea and was scheduled for YAG laser surgery under general anesthesia. Awake fiberoptic intubation was selected for anesthesia induction, and percutaneous cardiopulmonary support (PCPS) was ready to be established prior to induction of anesthesia. Anesthesia was maintained with remifentanil (0.05 microg x kg(-1) x min(-1)) and propofol (2 mg x kg(-1) x hr(-1)), and spontaneous breathing was preserved throughout the surgical procedure. The operation was completed successfully without any adverse events, and PCPS was not used. In this patient, preservation of spontaneous breathing using remifentanil was found to be useful for airway management.
Masui. The Japanese journal of anesthesiology 02/2012; 61(2):182-5.
[show abstract][hide abstract] ABSTRACT: We investigated the effects of the imidazoline-derived α2-adrenoceptor agonist clonidine on vascular adenosine triphosphate-sensitive potassium (K(ATP)) channel activity in rat vascular smooth muscle cells and recombinant vascular K(ATP) channels transiently expressed in COS-7 cells.
Using the patch-clamp method, we investigated the effects of clonidine on the following: (1) native vascular K(ATP) channels; (2) recombinant K(ATP) channels with different combinations of various types of inwardly rectifying potassium channel (Kir6.0 family: Kir6.1, 6.2) and sulfonylurea receptor (SUR1, 2A, 2B) subunits; (3) SUR-deficient channels derived from a truncated isoform of the Kir6.2 subunit (Kir6.2ΔC36 channels); and (4) mutant Kir6.2ΔC36 channels with diminished sensitivity to ATP (Kir6.2ΔC36-K185Q channels).
Clonidine (≥3 × 10(-8) M) inhibited native K(ATP) channel activity in cell-attached configurations with a half-maximal inhibitory concentration value of 1.21 × 10(-6) M and in inside-out configurations with a half-maximal inhibitory concentration value of 0.89 × 10(-6) M. With similar potency, clonidine (10(-6) or 10(-3) M) also inhibited the activities of various recombinant SUR/Kir6.0 K(ATP) channels, the Kir6.2ΔC36 channel, and the Kir6.2ΔC36-K185Q channel.
Clinically relevant concentrations of clonidine inhibit K(ATP) channel activity in vascular smooth muscle cells. This inhibition seems to be the result of its effect on the Kir6.0 subunit and not on the SUR subunit.
Anesthesia and analgesia 12/2011; 113(6):1374-80. · 3.08 Impact Factor
[show abstract][hide abstract] ABSTRACT: Tracheobronchial compression is a well-recognized complication of thoracic aortic aneurysm. We describe the anesthetic management of a patient with severe tracheal stenosis due to thoracic aortic aneurysm. An 81-year-old woman was scheduled for endovascular aortic stent graft placement. Computed tomographic (CT) scans showed that the narrowest diameter of the trachea was 3 x 18 mm. Awake fiberoptic intubation was selected for anesthesia induction, and percutaneous cardiopulmonary support (PCPS) was ready to be established prior to induction of anesthesia. We successfully inserted ID 6.0 mm spiral tube beyond the tracheal compression using bronchoscope and induced hypotension. The operation was completed successfully without any adverse events. We conclude that, in patients with thoracic aortic aneurysm, careful attention should be paid not only to circulation but to respiration.
Masui. The Japanese journal of anesthesiology 10/2011; 60(10):1195-8.
[show abstract][hide abstract] ABSTRACT: An 80-year-old woman with chronic atrial flutter/fibrillation, and chronic renal failure underwent ileocecal resection. The preoperative electrocadiogram showed normal QT interval. Temporary pacemaker catheter was inserted for sinus arrest (5-6 sec) the day before operation. Anesthesia was induced with remifentanil 0.5 micro x kg(-1) min(-1), thiamylal 125 mg, and rocuronium 30 mg after intravenous atropine sulfate 0.5 mg. Because the heart rate was increased with atropine sulfate, the pacemaker was not started. Anesthesia was then maintained with intravenous remifentanil and sevoflurane-air-oxygen. Just after induction of anesthesia, sinus bradycardia occurred, and 9 minutes after tracheal intubation, ECG suddenly showed torsade de pointes (TdP) and the arterial blood pressure decreased leading to asystole. We immediately started cardiopulmonary resuscitation, and TdP stopped spontaneously within 1 minute. We started pacemaker (VVI, 60 beats x min(-1)) and intravenous injection of lidocaine, and TdP did not recur. In this case, TdP seemed to have occurred because of bradycardia-induced abnormal QT prolongation. This should be considered the risk of lethal arrhythmia in patients with severe bradycardia including TdP.
Masui. The Japanese journal of anesthesiology 09/2011; 60(9):1097-100.
[show abstract][hide abstract] ABSTRACT: Cardiac protection by volatile anesthetic-induced preconditioning and ischemic preconditioning have similar signaling pathways. Recently, it was reported that augmentation of protein modified with O-linked β-N-acetylglucosamine (O-GlcNAc) contributes to cardiac protection. This study investigated the role of O-GlcNAc in cardiac protection induced by anesthetic-induced preconditioning.
O-GlcNAc-modified proteins were visualized by immunoblotting. Tolerance against ischemia or reperfusion was tested in vivo (n = 8) and in vitro (n = 6). The opening of the mitochondrial permeability transition pore (mPTP) upon oxidative stress was examined in myocytes treated with calcein AM (n = 5). Coimmunoprecipitation and enzymatic labeling were performed to detect the mitochondrial protein responsible for the mPTP opening.
Isoflurane treatment and the consequent augmentation of O-GlcNAc concentrations reduced the infarct size (26 ± 5% [mean ± SD], P < 0.001) compared with the control. The protective effect of O-GlcNAc was eliminated in the group pretreated with the O-GlcNAc transferase inhibitor alloxan (39 ± 5%, P < 0.001). Myocyte survival also showed the same result in vitro. Formation of the mPTP was abrogated in the isoflurane-treated cells (86 ± 4%, P < 0.001) compared with the control and alloxan-plus-isoflurane-treated cells (57 ± 7%, P < 0.001). Coimmunoprecipitation and enzymatic labeling studies revealed that the O-GlcNAc-modified, voltage-dependent anion channel restained the mPTP opening.
Isoflurane induced O-GlcNAc modification of mitochondrial voltage-dependent anion channel. This modification inhibited the opening of the mPTP and conferred resistance to ischemia-reperfusion stress.
[show abstract][hide abstract] ABSTRACT: Brugada syndrome is characterized by an electrocardiograph pattern of right bundle-branch block and has an increased risk for cardiac arrest due to malignant arrhythmia. We describe the successful anesthetic management for electroconvulsive therapy in a patient with Brugada electrocardiograph pattern. Patients with Brugada ECG pattern are not recommended to use neostigmine which augments ST elevation. Sugammadex was administered as a neuromuscular reversal agent in this case. Sugammadex provides rapid reversal of profound rocuronium-induced neuromuscular blockade under propofol anesthesia.
The Journal of Medical Investigation 08/2011; 58(3-4):273-6.
[show abstract][hide abstract] ABSTRACT: Post-operative nausea and vomiting (PONV) remains the most frequently reported patient complaint after anesthesia. Aprepitant is the first neurokinin-1(NK1) receptor antagonism available for use as an antiemetic. We investigated whether aprepitant can effectively decrease PONV in patients undergoing laparoscopic gynecological surgery.
Sixty four patients receiving general anesthesia for laparoscopic gynecological surgery were randomly assigned to either receive a preoperative dose of 80 mg aprepitant or no drug. Efficacy was assessed in 2 and 24 hours after surgery. Primary and secondary endpoints were analyzed for the time intervals 0-2 hours (acute phase) and 2-24 hours (delayed phase). Vomiting, nausea, use of rescue anti-emetic, and visual analog scale (VAS) were assessed. Nausea was assessed on a 4-point scale, from 0 to 3.
Sixty patients participated in the study. At acute phase, PONV was present in both control and NK1 group and were 63% and 43% respectively. The severity of nausea was much less in the NK1 group. PONV prevalence at delayed phase was present in control but absent in NK1 group 27% vs. 0%, respectively. The amount of pain medication used by patients in the NK1 group was significantly less for diclofenac and pentazocine suggesting increase pain tolerance.
Neurokinin-1 receptor antagonism effectively lowered PONV increased pain tolerance, and expedited recovery in patients undergoing laparoscopic gynecological surgery.
The Journal of Medical Investigation 08/2011; 58(3-4):246-51.
[show abstract][hide abstract] ABSTRACT: We experienced anesthetic management of a patient with Becker muscular dystrophy. He had advanced dilated cardiomyopathy and high serum CK in the preoperative examinations. Anesthesia was planned to avoid triggering malignant hyperthermia or rhabdomyolysis and hemodynamic changes. Propofol, remifentanil and a minimum dose of rocuronium bromide were used for anesthetic induction and maintainance. Arterial pressure, cardiac output and stroke volume variation were monitored by Flotrac sensor. There were no adverse events observed during the anesthetic management. In conclusion, total intravenous anesthesia with the administration of rocuronium and circulatory monitoring by Flotrac sensor could be safe and efficient for anesthetic management of patients with Becker muscular dystrophy.
Masui. The Japanese journal of anesthesiology 08/2011; 60(8):950-2.
[show abstract][hide abstract] ABSTRACT: Compound K (C-K; 20-O-D-glucopyranosyl-20(S)-protopanaxadiol) is a novel ginsenoside metabolite formed by intestinal bacteria and does not occur naturally in ginseng. In this study, we investigated whether administration of C-K has protective effects on myocardial ischemia-reperfusion injury and its potential mechanisms.
We used in vivo mouse models of ischemia-reperfusion injury and performed biochemical assays in excised hearts.
C-K reduced infarct size compared with the control group after ischemia-reperfusion. Immunoblot analysis showed that C-K significantly enhanced protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) activity. Wortmannin, a phosphoinositide 3-kinase (PI3K) inhibitor, blocked cardiac protection in vivo and attenuated phosphorylation of Akt and eNOS. Additionally, the hearts of C-K pretreated mice showed inhibition of mitochondrial swelling induced by Ca(2+).
This study showed that Compound K pretreatment has protective effects on myocardial ischemia-reperfusion injury, partly by mediating the activation of PI3K pathway and phosphorylation of Akt and eNOS.
Life sciences 02/2011; 88(15-16):725-9. · 2.56 Impact Factor
[show abstract][hide abstract] ABSTRACT: We present a case where immediate muscle relaxation was needed following sugammadex administration. A 72 year-old female underwent surgery for a cerebral artery aneurysm. Upon conclusion of the operation sugammadex (9.3 mg/kg) was administered and the patient was noted to have left hemiplegia. Rocuronium (1.2 mg/kg × 2 doses) was given in order to gain neuromuscular block approximately 25 minutes after sugammadex had been injected. Although TOF monitoring was not utilized in this case and assessing residual muscular block was difficult, spontaneous respirations continued and breathing had to be controlled with sevoflurane and remifentanil. Sugammadex is a potent reversal agent for rocuronium-induced neuromuscular block, however, certain situations require immediate neuromuscular blockade following sugammadex. In this case, rocuronium was unable to induce neuromuscular blockade immediately after sugammadex and that higher concentrations were necessary in addition to intravenous analgesics and inhaled anesthetics.
The Journal of Medical Investigation 02/2011; 58(1-2):163-5.
[show abstract][hide abstract] ABSTRACT: Volatile anesthetics, such as isoflurane, reverse glucose-induced inhibition of pancreatic adenosine triphosphate-sensitive potassium (K(ATP)) channel activity, resulting in reduced insulin secretion and impaired glucose tolerance. No previous studies have investigated the effects of intravenous anesthetics, such as propofol, on pancreatic K(ATP) channels. We investigated the cellular mechanisms underlying the effects of isoflurane and propofol on pancreatic K(ATP) channels and insulin secretion.
Intravenous glucose tolerance tests (IVGTT) were performed on male rabbits. Pancreatic islets were isolated from male rats and used for a perifusion study, measurement of intracellular ATP concentration ([ATP](i)), and patch clamp experiments.
Glucose stimulus significantly increased insulin secretion during propofol anesthesia, but not isoflurane anesthesia, in IVGTT study. In perifusion experiments, both islets exposed to propofol and control islets not exposed to anesthetic had a biphasic insulin secretory response to a high dose of glucose. However, isoflurane markedly inhibited glucose-induced insulin secretion. In a patch clamp study, the relationship between ATP concentration and channel activity could be fitted by the Hill equation with a half-maximal inhibition of 22.4, 15.8, and 218.8 μM in the absence of anesthetic, and with propofol, and isoflurane, respectively. [ATP](i) and single K(ATP) channel conductance did not differ in islets exposed to isoflurane or propofol.
Our results indicate that isoflurane, but not propofol, decreases the ATP sensitivity of K(ATP) channels and impairs glucose-stimulated insulin release. These differential actions of isoflurane and propofol on ATP sensitivity may explain the differential effects of isoflurane and propofol on insulin release.
Life sciences 11/2010; 88(1-2):96-103. · 2.56 Impact Factor
[show abstract][hide abstract] ABSTRACT: Isoflurane activates protein kinase A (PKA) in vascular smooth muscle cells (VSMCs), which in turn activates ATP-sensitive potassium (K(ATP)) channels and causes vasodilation. The present study was undertaken to examine whether advanced age influences the effect of isoflurane on K(ATP) channel activity in cultured VSMCs. We used VSMCs obtained from 12- to 15-week-old (adult) and 24- to 25-month-old (aged) male Wistar rats. Electrophysiological experiments were performed using cell-attached and inside-out patch-clamp techniques to monitor the K(ATP) channel activity. Application of isoflurane or forskolin to the bath solution in cell-attached recordings induced a significant increase in K(ATP) channel activity in the VSMCs from the adult group. However, K(ATP) channel opening induced by isoflurane, but not forskolin, was significantly suppressed by aging. On the other hand, cell-free recordings showed similar pharmacologic sensitivity to the K(ATP) channel opener pinacidil, inward rectification, and unitary conductance (40–45 pS) between groups. In addition, direct K(ATP) channel activation by c-PKA in the inside-out patches was similar in both groups. Furthermore, increasing PKA activation in cell-attached patches by CPT-cAMP restored isoflurane's effects in the aged group. These results suggest that aging decreases isoflurane-induced PKA activation, resulting in attenuation of K(ATP) channel opening.
Journal of cardiovascular pharmacology 09/2010; 56(6):676-85. · 2.83 Impact Factor
[show abstract][hide abstract] ABSTRACT: Nicorandil opens adenosine triphosphate-sensitive potassium (K(ATP)) channels in the cardiovascular system and is being increasingly used for the treatment of angina pectoris. In the present study, we tested whether intravenous anesthetic agent ketamine affected nicorandil-induced native vascular K(ATP) channel activation.
We used excised inside-out patch clamp configurations to investigate the direct effects of ketamine racemate and S-(+)-ketamine on the activities of K(ATP) channels in cultured rat aortic smooth muscle cells. Furthermore, we also investigated whether intracellular MgADP could modulate ketamine inhibition.
Nicorandil significantly activated K(ATP) channel activity, whereas this channel activity was completely blocked by glibenclamide, a specific K(ATP) channel blocker. Ketamine racemate inhibited the nicorandil induced K(ATP) channel activity (IC(50)=34±1 µM, n=14), but S-(+)-ketamine was less potent than ketamine racemate in blocking nicorandil induced K(ATP) channel activities (IC(50)=226±7 µM, n=10). Application of MgADP to the intracellular side of the channel was able to decrease the inhibitory potency of ketamine racemate on nicorandil induced K(ATP) channel activities.
Our results indicate that ketamine inhibits nicorandil induced K(ATP) channel activities in a dose dependent and stereoselective manner. Furthermore, increase of intracellular MgADP attenuates the inhibitory potency of ketamine racemate. J. Med. Invest. 57: 237-244, August, 2010.
The Journal of Medical Investigation 08/2010; 57(3-4):237-44.