Mutsuo Mishio

Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Purpose: To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CAI subfield in gerbils.Methods: Forty gerbils were randomly assigned to five groups: Group I, control, sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg·kg−1 propofol; Group IV, ischemia/reperfusion treated with 100 mg·kg−1 propofol; Group V, ischemia/reperfusion treated with 150 mg·kg−1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N2O/O2/halothane anesthesia after propofol or PSS. Five days later, the cerebrum was removed and each forebrain was cut into two including the hippocampus. Lipid peroxidation was determined using the production of malondialdehyde (MDA), and histopathological changes in the hippocampal CAI subfield were examined.Results: In group II, the pyramidal cells were atrophic and pycnotic, vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. Degenerative ratios of pyramidal cells were: Group I: 4.9±2.3, Group II: 94.1±4.5 (P<0.01), Group III: 12.5±5.7, Group IV: 11.0±4.6, Group V: 9.6±4.9%. Production of MDA was: Group I: 83±22, Group II: 198±25 (P<0.01), Group III: 153±39, Group IV: 113±34, Group V: 106±27 nmol·g−1 wet tissue.Conclusion: Propofol attenuated delayed neuronal death by preventing lipid peroxidation induced by transient forebrain ischemia in the hippocampal CAI subfield in gerbils.RésuméObjectif: Vérfier si le propofol empêche la peroxydation lipidique qui survient à la mort neuronale différée induite par une ischémie transitoire du prosencéphale, dans le sous-champ CAI de l’hippocampe chez des gerbilles.Méthode: On a réparti au hasard 40 gerbilles en cinq groupes: dans le groupe I, témoin, elles ont subi une opération fictive traitée avec une solution physiologique salée (SPS); dans le groupe II, une ischémie/reperfusion traitée avec une SPS; dans le groupe III, une ischémie/reperfusion traitée avec 50 mg·kg−1 de propofol; dans le groupe IV, une ischémie/reperfusion traitée avec 100 mg·kg−1 de propofol et dans le groupe V, une ischémie/reperfusion traitée avec 150 mg·kg−1 de propofol. L’ischémie transitoire du cerveau antérieur a été induite par l’occlusion bilatérale des artères carotides communes pendant quatre minutes sous anesthésie au N2O/O2/halothane après l’administration de propofol ou de SPS. Cinq minutes plus tard, le cerveau a été retiré et chaque prosencéphale a été coupé en deux, induant l’hippocampe. La peroxydation lipidique a été déterminée en utilisant la production de malondialdéhyde (MDA), et les changements histopathologiques du sous-champ CAI de l’hippocampe ont été examinés.Résultats: Dans le groupe II, les cellules pyramidales étaient atrophiques et pycnotiques; une rupture vacuolaire et structurale de la zone radiale striée a été observée. Dans les autres groupes, ces changements n’ont pas été notés. Les taux de cellules pyramidales dégénératives ont été: groupe I: 5,8±2,5 %, groupe II: 94,1±4,5 (P<0,01), groupe III: 12,5±5,7 %, group IV: 11,0±4,6 %, groupe V: 9,4±6,6 %. La production de MDA a été dans le groupe I: 83±22, II: 198±25 (P<0,01), III: 153±39, IV: 113±34 et V: 106±27 nmol·g−1 de tissu.Conclusion: Le propofol a réduit la mort neuronale différée en empêchant la peroxydation lipidique induite par l’ischémie transitoire du prosencéphale dans le sous-champ CAI de l’hippocampe de gerbilles.

Delayed severe airway obstruction due to hematoma following stellate ganglion block

Background and Objectives. Delayed onset of airway obstruction following stellate ganglion block (SGB) may be life threatening. We treated a patient who developed a severe airway obstruction caused by a large hematoma several hours after an SGB. Methods. A 62‐year‐old woman suffering from sudden deafness developed dyspnea 2 hours after undergoing her fourth SGB, and evidenced swelling and tenderness in her anterior neck and chest. Her pharyngolaryngeal tissues were edematous, and the glottis was markedly narrowed. Computed tomograms and magnetic resonance images revealed a large soft tissue mass extending from the first cervical vertebra to the diaphragm. Results. Surgical tracheotomy was performed to maintain her airway. Swelling of the vocal cord disappeared on the eleventh day after the operation. Conclusions. We believe that the SGB needle injured the vertebral artery and caused massive hemorrhage anterior to the cervical vertebra, subsequently inducing pharyngolaryngeal edema by obstructing the venous and lymphatic drainage of the cervical region.

High concentration sevoflurane induction of anesthesia accelerates onset of vecuronium neuromuscular blockade

Purpose: To investigate neuromuscular block using accelography after administration of vecuronium under sevoflurane 8% induction and maintenance with sevoflurane 2% in adults.Methods: Patients were allocated to three groups: (1) group I: anesthesia was induced and maintained with propofol and fentanyl (n=15), (2) group II: anesthesia was induced with propofol and maintained with N2O(66%)-O2-sevoflurane 2% (n=15), (3) group III: anesthesia was induced with sevoflurane 8% using a vital capacity inhalation induction and maintained with N2O(66%)-O2-sevoflurane 2% (n=15). 0.1 mg·kg−1 vecuronium was used for paralysis three minutes after anesthetic induction and reversed using intravenous 0.04 mg·kg−1 neostigmine with 0.02 mg·kg−1 atropine when the train-of-four (TOF) ratio returned to 25%.Results: The onset time from initial administration of vecuronium to maximal block in the group III was shorter than that in the groups I and II (139±35, 193±35 and 188±47s, respectively:P<0.05). The clinical duration from maximal block to 25% recovery of TOF ratio in group II and III was longer than that in the group I (47±15, 48±14 and 36±10 min, respectively:P<0.05). The reversal times from administration of neostigmine to 75% of TOF ratio in groups II and III were longer than that in the group I (196±53, 208±64 and 136±28s, respectively:P<0.05).Conclusions: Vital capacity inhalation induction of anesthesia with sevoflurane accelerates onset and prolongs duration of vecuronium neuromuscular block compared with propofol-fentanyl anesthesia.RésuméObjectif: Étudier le blocage neuromusculaire à l’aide de l’accélographie après l’administration de vécuronium pendant l’anesthésie induite avec du sévoflurane à 8% et maintenue avec du sévoflurane à 2% chez des adultes.Méthode: Les patients ont été répartis en trois groupes: le groupe I: l’anesthésie est induite et maintenue avec du propofol et du fentanyl (n=15); le groupe II: l’anesthésie est induite avec du propofol et maintenue avec N2O(66%)-O2-sévoflurane 2% (n=15); le group III: l’anesthésie est induite avec du sévoflurane à 8% en utilisant la technique de la capacité vitale et maintenue avec N2O(66%)-O2-sévoflurane 2% (n=15). Une dose de 0,1 mg·kg−1de vécuronium a été utilisée pour provoquer le bloc, trois minutes après l’induction anesthésique. Ce bloc a été renversé avec une dose intraveineuse de 0,04 mg·kg−1 de néostigmine avec 0,02 mg·kg−1 d’atropine quand le train-de-quatre (TDQ) était revenu à 25%.Résultats: Le délai d’installation, de l’administration initiale de vécuronium jusqu’au bloc maximal, a été plus court dans le groupe III que dans les groupes I et II (139±35, 193±35 et 188±47s, respectivement:P<0,05). La durée clinique, du bloc maximal jusqu’à une récupération de 25% du ratio du TDQ, a été plus longue dans les groupes II et III que dans le groupe I (47±15, 48±14 et 36±10 min, respectivement:P<0,05). Le temps de renversement du bloc, de l’administration de néostigmine jusqu’au retour de 75% du ratio du TDQ, a été plus long dans les groupes II et III que dans le groupe I (196±53, 208±64 et 136±28s, respectivement:P<0,05).Conclusion: L’induction de l’anesthésie par inhalation avec du sévoflurane, selon la technique de la capacité vitale, permet un début d’action plus rapide et prolonge la durée du bloc neuromusculaire réalisé avec du vécuronium comparé au mélange de propofol et de fentanyl.

Bispectral monitoring during vital capacity rapid inhalation induction with sevoflurane

STUDY OBJECTIVE To evaluate the variables of bispectral index (BIS) values during vital capacity rapid inhalation induction (VCRII) with sevoflurane. DESIGN Randomized, prospective study. SETTING University hospital. PATIENTS 40 ASA physical status I and II patients scheduled for elective orthopedic surgery with general anesthesia. INTERVENTIONS Patients was divided into two groups, both of which received intravenous (IV) injection of propofol 2 mg/kg followed by inhalation of sevoflurane 3% (Group P), or vital capacity inhalation induction with sevoflurane 8% (Group S). After loss of consciousness, tracheal intubation was performed with vecuronium 0.1 mg/kg. MEASUREMENTS AND MAIN RESULTS The induction times in Group P were significantly shorter than those in Group S (p < 0.01). In Group S, BIS values were gradually decreased and maintained the adequate hypnotic levels were maintained during induction. In Group P, although BIS values were rapidly decreased, the values remained higher compared with Group S. The BIS value before intubation in Group S was significantly lower than that in Group P (25 +/- 9 and 38 +/- 7, respectively; p < 0.01). Five of 20 Group P patients had BIS values exceeding 60 before tracheal intubation, but no patient in Group S had a BIS value as high. Mean arterial pressure immediately after intubation in Group S was significantly lower than that in Group P (p < 0.05). CONCLUSION VCRII with a high concentration of sevoflurane provided adequate BIS values during induction, suggesting that it may allow smoother transition from anesthesia induction to maintenance, and also maintain an adequate hypnotic level in readiness for certain stimuli such as laryngoscopy and tracheal intubation.

Pediatric caudal block with mepivacaine, bupivacaine or a mixture of both drugs: requirement for postoperative analgesia and plasma concentration of local anesthetics

STUDY OBJECTIVES To assess the effects of pediatric caudal block using mepivacaine, bupivacaine, or a mixture of both drugs on postoperative analgesia, and to examine plasma concentrations of the local anesthetics after caudal injection. DESIGN Prospective, randomized, double-blind study. SETTING Operating room and pediatric surgical ward. PATIENTS 60 ASA physical status I children weighing 10 to 20 kg (26 females, 34 males), and scheduled for inguinal herniorrhaphy. INTERVENTIONS Patients randomly received caudal block with 1 mL/kg of mepivacaine 1% (Group M, n = 20), 1 mL/kg of bupivacaine 0.25% (Group B, n = 20), or a mixture of 0.5 mL/kg of mepivacaine 1% and 0.5 mL/kg of bupivacaine 0.25% (Group MB, n = 20) after induction of anesthesia with sevoflurane in 50% oxygen (O2). Anesthesia was maintained with 66% nitrous oxide in O2 supplemented with sevoflurane at an end-tidal concentration of less than 1%. MEASUREMENTS AND MAIN RESULTS Postoperative pain scores using a pediatric pain scale and plasma concentration of each local anesthetic were measured. In Group M, four patients required postoperative analgesics within the first 24 hours. However, no patients required postoperative analgesics in Groups B and MB. In Group M, the plasma concentration of mepivacaine of two patients exceeded 5 microg/kg of the level of toxicity. However, these patients did not show any toxic symptoms. Because a mixture of two local anesthetics halves the concentration of each local anesthetic, the plasma concentrations of mepivacaine and bupivacaine in Group MB were significantly lower than those of Groups M and B. CONCLUSIONS Pediatric caudal block with a mixture of mepivacaine and bupivacaine is effective for intraoperative and postoperative analgesia.

Significance of elevated cytochrome aa3 in a state of endotoxemia in dogs

It is now possible to detect quantitative changes in cytochrome aa3 by means of near-infrared spectrophotometry. This technique is also suitable for determining oxidised hemoglobin (HbO2), reduced hemoglobin (Hb), cerebral blood volume, and the redox state of cytochrome aa3 (cyt aa3) in the tissues. The significance of elevated cyt aa3, measured by near-infrared spectrophotometry, is still unclear, so we investigated this question using both near-infrared spectrophotometry and oxygen saturation meters in endotoxemic dogs. Ten anaesthetised mongrel dogs were injected with endotoxin (E. coli 0111: B4 Difco 2 mg/kg i.v.) and the redox state of Hb and cyt aa3 was determined in real time by near-infrared spectrophotometry. The levels of arterial and cisternal venous oxygen saturation were recorded simultaneously by two Oximetrix 3 saturation meters to calculate the cerebral arterial and venous oxygen saturation difference (Sata-vO2D) in real time. HbO2 decreased along with the fall in mean arterial pressure and remained at a low level, while Hb increased and remained at a high level. The cerebral blood volume decreased in the endotoxic early stage and then returned gradually towards baseline. Cyt aa3 showed an increase following endotoxin injection and maintained an oxidised form. The cerebral Sata-vO2D rose to about three times the control level. From these observations, an increase of oxidised cytochrome aa3 after endotoxin administration seems to be a compensatory protective effect in response to the cerebral oxygen demand rather than over-oxygenation or hyperoxia.