Morio Uchida

Enflurane-induced Release of an Excitatory Amino Acid, Glutamate, from Mouse Brain Synaptosomes

To clarify the mechanisms of enflurane-induced convulsions, we examined the effects of enflurane, halothane, and diethyl ether on the release of an excitatory neurotransmitter, glutamate, from isolated pinched-off nerve terminals (synaptosomes) of the mouse cerebral cortex. At concentrations corresponding to those used clinically (0.75 and 1.25 mM), enflurane released more glutamate than did halothane. Diethyl ether (10 and 58 mM) had no effect on glutamate release. Enflurane (0.75-15 mM) increased glutamate and aspartate release in a dose-dependent manner but had little effect on the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid or on the release of glutamine. A glutamate uptake inhibitor, kainic acid (1 mM), did not affect enflurane-induced glutamate release. Replacement of the mediums Ca2+ by Co2+, or exposure to cold (about 2 degrees C), suppressed the enflurane-induced glutamate release. Depolarization caused by 40 mM K+ increased the basal level of glutamate released, and enflurane-induced glutamate release was lower after depolarization. Enflurane had no effect in synaptosomes prepared from the cerebellum, diencephalon and pons, or medulla oblongata. Thus, enflurane increased Ca(2+)- and temperature-dependent glutamate release, especially from synaptosomes of the cerebral cortex. These data provide a pathophysiologic explanation for enflurane-induced convulsions.

Changes in the cerebral arteriovenous oxygen content difference by surgical incision are similar during sevoflurane and isoflurane anaesthesia

PurposeTo investigate changes of cerebral arteriovenous oxygen content difference (AVDO2) induced by surgical incision and to determine carbon dioxide (CO2) reactivity of the cerebral circulation during sevoflurane and isoflurane anaesthesia.MethodsTwenty-one ASA 1–2 patients undergoing elective surgery for supratentorial tumours were randomly allocated to receive either 1.3 MAC sevoflurane/N2O anaesthesia (n =10) or equi-MAC isoflurane/N2O anaesthesia (n = 11). Before and after incision, haemodynamic measurements and AVDO2 determinations were performed. After opening the dura, AVDO2 was determined before and after the respiration rate was increased by 50%.ResultsIncision produced an increase in mean arterial pressure from 69 ±11 to 97 ±22 mmHg (mean ±SD) (P < 0.0005) and from 71 ±6 to 89 ±12 mmHg (P < 0.0001) in the sevoflurane and isoflurane groups, respectively, whereas the heart rate increased from 60 ±9 to 72 ±8 bpm (P < 0.001) and from 65 ±6 to 70 ±7 bpm (P < 0.001), respectively. Arterial carbon dioxide tension (PaCO2) was increased from 33.6 ±2.3 to 34.6 ±1.8 mmHg (P < 0.05) with incision in the sevoflurane group. The AVDO2 was decreased from 6.5 ±1.6 to 5.3 ±1.6 vol% (P < 0.0005) in the sevoflurane group and from 6.7 ±1.1 to 6.0 ±1.1 vol% (P < 0.01) in the isoflurane group. The % change of AVDO2 was larger in the sevoflurane group than in the isoflurane group (−18.3 ±8.4% vs −9.1 ±9.0%; P < 0.05) but no difference remained after the postincisional AVDO2 value of the sevoflurane group was corrected for pre-incisional PaCO2. Carbon dioxide reactivity, calculated as the percent change in AVDO2 per mmHg change in PaCO2, was 6.1 ±3.0% mmHg−1 in the sevoflurane group and 5.9 ±2.4% · mmHg−1 in the isoflurane group (P = NS).ConclusionsSevoflurane and isoflurane are associated with similar impairment of cerebral flow-metabolism coupling at incision, while CO2 reactivity is maintained during both anaesthetics.ObjectifÉtudier les changements de la différence artérioveineuse du contenu en oxygène cérébral (AVDO2) produits par l’incision et déterminer la réactivité au gaz carbonique (CO2) de la circulation cérébrale sous anesthésie au sévoflurane et à l’isoflurane.MéthodesVingt et un patients ASA 1 et 2 subissant une chirurgie non urgente pour tumeur supratentorielle ont été aléatoirement assignés à recevoir soit une anesthésie au sévoflurane/N2O 1,3 MAC (n = 10) soit une anesthésie à l’isoflurane/N2O équi-MAC (n = 11). Avant et après l’incision, les mesures hémodynamiques ont été effectuées et AVDO2 déterminée. Après l’ouverture de la dure-mère, AVDO2 a été calculée avant et après une augmentation de la fréquence respiratoire de 50%.RésultatsL’incision a provoqué une augmentation de la pression artérielle moyenne respective de 69 ±11 à 97 ±22 mmHg (moyenne ±ET) (P < 0,0005) et 71 ±6 à 89 ±12 (P < 0,0001) dans les groupes sévoflurane et isoflurane; la fréquence cardiaque augmentait respectivement de 60 ±9 à 72 ±8 bpm (P < 0,001) et de 65 ±6 à 70 ±7 bpm (P < 0,001). Dans le groupe sévoflurane, la PaCO2 augmentait de 33,6 ±2,3 à 34,6 ±1,8 (P < 0,05) avec l’incision. Dans le groupe sévoflurane, AVDO2 diminuait de 6,5 ±1,6 à 5,3 ±1,6 vol% (P < 0,0005) et dans le groupe isoflurane, de 6,7 ±1,1 à 6,0 ±1,1 vol% (P < 0,01). Le pourcentage de changement de AVDO2 était plus important dans le groupe sévoflurane que dans le groupe isoflurane (−18,3 ±8,4% vs −9,1 ±9,0%; P < 0,05); cette différence est disparue une fois la valeur post-incision du groupe sévoflurane corrigée pour la valeur de PaCO2 pré-incision. La réactivité du gaz carbonique, calculée en pourcentage de changement en AVDO2 par mmHg de changement de PaCO2 était 6,1 ±3,0% · mmHg−1 dans le groupe sévoflurane et 5,9 ±2,4% · mmHg−1 dans le groupe isoflurane (P = NS).ConclusionLe sévoflurane et l’isoflurane sont associés à une perturbation identique du couplage débit-métabolisme à l’incision, alors que la réactivité au CO2 est maintenue avec les deux anesthésiques.

Laryngeal mask and tracheal stenosis

The use of the laryngeal mask with controlled ventilation in a child with tracheal stenosis has been published previously [I]. One of the disadvantages of using the laryngeal mask in this population is air leakage, as high inflation pressures may be required during controlled ventilation. We report a patient with tracheal stenosis in whom the laryngeal mask was successfully used by maintaining spontaneous breathing. A 49-year-old man was scheduled for wedge resection of a femoral head. Pre-operative chest X ray revealed a tracheal stenosis, starting at the level of the sternum and extending to the tracheal carina (Fig. 1). The narrowest calibre was about 8 mm. Computed tomography showed a deformed trachea, in which the coronal diameter was less than one half of the sagittal diameter. The diagnosis of ‘sabre-sheath’ trachea was made. Pulmonary function studies indicated obstructive airway disease with the ratio of FEV, to FVC of 53%; vital capacity was 87% of predicted. Analysis of arterial blood gases revealed Pao, 9.5 kPa, Paco, 5.8 kPa, and pH 7.4. Despite the tracheal stenosis, he had no symptomatic respiratory complications. Clear breath sounds were heard equally over both lung fields. No chest wall retraction was observed. At the preoperative consultation he strongly requested general anaesthesia during surgery. After epidural anaesthesia was established, general anaesthesia was induced by allowing the patient to inhale nitrous oxide, oxygen, and increasing concentrations of halothane up to 1.5%, supplemented with diazepam 2.5 mg. A size 3 laryngeal mask was easily inserted without interruption to spontaneous respiration. The correct position of the mask was confirmed by passing a fibreoptic bronchoscope down the lumen. During induction of anaesthesia and surgery the stenosis did not appear to worsen. End-expiratory carbon dioxide tension and arterial oxygen saturation were continuously within normal limits; analyses of arterial blood gases taken during surgery were also normal. After an uneventful intra-operative course, the laryngeal mask was removed without complications. ‘Sabre-sheath’ trachea is defined as a deformed trachea with an internal coronal diameter two-thirds of, or less than, its internal sagittal diameter only in the intrathoracic part of the trachea [2]. The deformed trachea is usually densely ossified and is unlikely to collapse. The advantages of maintaining spontaneous respiration over controlled ventilation are threefold: first, since the inflation pressures are negative during spontaneous inspiration, air leakage is unlikely to occur. Second, while air trapping might be a problem during controlled ventilation, this is likely to be mild during spontaneous respiration. Furthermore, if ventilation is controlled in patients with severe tracheal stenosis, turbulent flow will occur distal to the stenosis, Fig. 1. Postero-anterior view of a high kilovoltage film of the trachea showing marked coronal narrowing of the intrathoracic trachea with an abrupt return to normal at the thoracic inlet.

Model of electrocardiographic changes seen with subarachnoid hemorrhage in rabbits.

We developed a new method for introducing drugs into the basal cistern of rabbits. With minimal surgical invasion, we used either the opening of the craniopharyngeal duct to access the chiasmatic cistern or the suture between the basisphenoid and basioccipital bones to access the interpeduncular cistern. With our method, 0.5 ml contrast medium injected into three rabbits was determined roentgenographically to remain in the basal cistern; histologically, all the brain tissue remained intact. Intracisternal injection of 0.5 ml physiological saline into five rabbits had no effect on the cardiovascular system. In 23 rabbits, injection of 0.5 ml 0.1% prostaglandin F2 alpha led to a variety of electrocardiographic changes, including sinus bradycardia (in 43.5%), premature atrial contractions (in 17.4%), and premature ventricular contractions (in 39.1%). In 15 rabbits with severe changes, arrhythmia was followed by ST depression (in 30.4%), ST elevation (in 8.7%), T wave inversion (in 4.3%), ventricular tachycardia (in 17.4%), or ventricular fibrillation (in 4.3%). Intracisternal injection of 0.5 ml 1.0% lidocaine into the 23 rabbits was very effective in overcoming bradycardia and arrhythmias. We conclude that the clinical features of electrocardiographic changes seen in patients with subarachnoid hemorrhage are reproducible in this rabbit model.

Anaesthesia for cardiac surgery in children with nemaline myopathy.

Nemaline myopathy is a rare congenital myopathy associated with skeletal deformities and respiratory complications. Three children with nemaline myopathy who underwent cardiac surgery are described where the heart rate decreased during induction of anaesthesia and body temperature increased during or after the surgery. The anaesthetic implications in the management of patients with nemaline myopathy are discussed.

Severe cardiovascular changes associated with pancuronium after cardiopulmonary resuscitation and after brain injury

Severe hypertension, tachycardia or ECG changes have been reported following i.v. administration of pancuronium to patients with pheochromocytoma or bronchial asthma. These cardiovascular changes were explained by an interaction between autonomic effects of pancuronium and elevated serum catecholamines or aminophylline. We noted similar cardiovascular changes associated with i.v. administration of pancuronium in two patients after successful cardiopulmonary resuscitation and in two with midbrain hemorrhage and epidural hematoma. In these patients, pancuronium produced no abnormal cardiovascular changes when given during elective surgery or before the occurrence of midbrain hemorrhage. Thus, ischemic brain damage may play a role in producing the severe cardiovascular changes associated with pancuronium.

Changes in the Cerebral Arteriovenous Oxygen Content Difference by Surgical Incision Are Similar During Sevoflurane and Isoflurane Anaesthesia

PURPOSE To investigate changes of cerebral arteriovenous oxygen content difference (AVDO2) induced by surgical incision and to determine carbon dioxide (CO2) reactivity of the cerebral circulation during sevoflurane and isoflurane anaesthesia. METHODS Twenty-one ASA 1-2 patients undergoing elective surgery for supratentorial tumours were randomly allocated to receive either 1.3 MAC sevoflurane/N2O anaesthesia (n = 10) or equi-MAC isoflurane/N2O anaesthesia (n = 11). Before and after incision, haemodynamic measurements and AVDO2 determinations were performed. After opening the dura, AVDO2 was determined before and after the respiration rate was increased by 50%. RESULTS Incision produced an increase in mean arterial pressure from 69 +/- 11 to 97 +/- 22 mmHg (mean +/- SD) (P < 0.0005) and from 71 +/- 6 to 89 +/- 12 mmHg (P < 0.0001) in the sevoflurane and isoflurane groups, respectively, whereas the heart rate increased from 60 +/- 9 to 72 +/- 8 bpm (P < 0.001) and from 65 +/- 6 to 70 +/- 7 bpm (P < 0.001), respectively. Arterial carbon dioxide tension (PaCO2) was increased from 33.6 +/- 2.3 to 34.6 +/- 1.8 mmHg (P < 0.05) with incision in the sevoflurane group. The AVDO2 was decreased from 6.5 +/- 1.6 to 5.3 +/- 1.6 vol% (P < 0.0005) in the sevoflurane group and from 6.7 +/- 1.1 to 6.0 +/- 1.1 vol% (P < 0.01) in the isoflurane group. The % change of AVDO2 was larger in the sevoflurane group than in the isoflurane group (-18.3 +/- 8.4% vs -9.1 +/- 9.0%; P < 0.05) but no difference remained after the post-incisional AVDO2 value of the sevoflurane group was corrected for pre-incisional PaCO2. Carbon dioxide reactivity, calculated as the percent change in AVDO2 per mmHg change in PaCO2, was 6.1 +/- 3.0%.mmHg-1 in the sevoflurane group and 5.9 +/- 2.4%.mmHg-1 in the isoflurane group (P = NS). CONCLUSIONS Sevoflurane and isoflurane are associated with similar impairment of cerebral flow-metabolism coupling at incision, while CO2 reactivity is maintained during both anaesthetics.

Contribution of brain injury to hypertension following intravenously-administered pancuronium in rats

Abnormal hypertension sometimes occurs following intravenous administration (i.v.) of pancuronium in patients with brain injury. The present experiment was designed to determine whether brain injury contributes to the hypertensive response of i.v. pancuronium. Forty-six Wister strain rats were studied, of which 39 had induced brain injury at (a) upper pons (b) midbrain (c) thalamus region (excluding hypothalamus) and (d) cerebellum or a combination of these sites. The injury was made by single insertion of a 22 Gauge needle through the skull surface. The quantity of pancuronium solution administered i.v. in each case was 1.0 ml containing either 0.8 mg/kg or 8 mg/kg of pancuronium. Group A (n = 7) had no brain injury and the mean arterial pressure (MAP) did not change following i.v. administration of pancuronium. In Group B (n = 9) (a+b+c, 8.0 mg/kg) MAP rose from 90.9 +/- 15.4 to 102 +/- 22.0 mmHg and in Group C (n = 7) (a+b+c, 0.8 mg/kg) MAP rose from 148.4 +/- 13.3 to 160 +/- 14.4 mmHg. In Group D (n = 5) (b+c, 8.0 mg/kg) MAP remained unchanged. In Group E (n = 5) (a, 8.0 mg/kg) MAP rose from 130.3 +/- 18.7 to 146 +/- 27.6 mmHg and in Group F (n = 6) (a, 0.8 mg/kg) MAP rose from 129.7 +/- 15.6 to 135.8 +/- 13.8 mmHg. In Group G (n = 7) (d, 8.0 mg/kg) MAP remained unchanged. Since the MAP was elevated in only those groups that received injury in the upper pons, we concluded that injury in the upper pons can lead to hypertension following i.v. administration of pancuronium.

A Computer Control System of Applying Anesthesia Using Fuzzy Logic for Medical Operation

Operations are basically performed in the order as some phases. The periods in which the anesthesiologist is most active are the induction phase and the extubation phase. It is believed that automation of this phase is very difficult. The objective of this system is the management of blood pressure during the stable phase of using enflurane. The way that anesthesiologist thinks when deciding the concentration of inhalation anesthesia for management of blood pressure was represented on this system.

Changes in plasma catecholamine levels following injection of prostaglandin F2α into the basal cistern in rabbits

We measured plasma epinephrine and norepinephrine concentrations in a rabbit model simulating subarachnoid hemorrhage (SAH), following the injection of prostaglandin F2α (PGF2α) into the basal cistern. In this model, plasma epinephrine values increased significantly (to 4.2-fold those before injection), substantially more than norepinephrine (which increased 1.3-fold) at 5 minutes (min) after PGF2α injection. Dissection of autonomic outflow from the cervical spinal cord or ligation of the suprarenal veins reduced the changes in plasma catecholamine concentrations associated with PGF2α injection. These results suggest that the sympathetic discharge seen after PGF2α injection into the basal cistern in rabbits occurred through the sympatho-adrenal pathways.