Hiromaru Ogata

Differential effects of vecuronium on the thumb and great toe as measured by accelography and electromyography

We evaluated possible differential effects of vecuronium on the thumb and great toe using two types of neuromuscular transmission monitor. Train‐of‐four stimuli were simultaneously applied to the ulnar nerve and tibial nerves using cutaneous electrodes. The responses were quantified with accelographs (thumb and left great toe) and an electromyograph (right great toe). Twenty ASA 1 or 2 patients received, by random allocation, one of two types of anaesthesia: neuroleptanaesthesia or sevoflurane‐based anaesthesia. With both techniques, the shortest time to maximum block after vecuronium 0.1 mg.kg ‐1 occurred in the thumb as measured by accelography. The average (SD) values with neuroleptanaesthesia were: 173(23) s for thumb using accelography; 220(16) s for great toe using accelography; 205(44) s for great toe using electromyography. The average (SD) valuefs) with sevoflurane‐based anaesthesia were: 137(15) for thumb using accelography; 179(21) for great toe using accelography; 153(23) for great toe using electromyography. The differences between the thumb and great toe were statistically significant during both types of anaesthesia when measured with the accelograph (p < 0.01). The time from completion of maximal block to 25% recovery of twitch height in the thumb was significantly longer than that of the great toe as measured by accelography during both types of anaesthesia (p < 0.05). In contrast, there were no statistically significant differences between time to maximum block and 25% recovery of twitch height of the thumb as measured by accelography compared to the values measured for the great toe using electromyography during either anaesthetic technique. The fastest recovery, therefore, was measured in the tibial nerve using accelography. The time to 25% spontaneous recovery after vecuronium 0.1 mg.kg‐1 during sevoflurane anaesthesia was significantly longer than that during neuroleptanaesthesia (p < 0.01).

Superoxide radical generation and histopathological changes in hippocampal CA1 after ischaemia/ reperfusion in gerbils

PurposeWe investigated the relationship between the generation of Superoxide radicals and histopathological changes on delayed neuronal death in the hippocampal CA1 subfield.MethodsSeventy gerbils were randomly assigned to two groups, a sham group and an ischaemia/reperfusion (I/R) group. In the I/R group, transient forebrain ischaemia was induced by occluding the bilateral common carotid arteries for four minutes. The cerebrum was removed after reperfusion at intervals of one minute, six, twelve and twenty-four hr and at three, five and seven days. Each forebrain was cut into two portions including the hippocampus. The quantity of Superoxide radicals was measured by using chemiluminescence, and histopathological changes in the hippocampal CAI subfield were examined.ResultsIn the I/R group, Superoxide radicals increased on the 3rd and 5th days compared with the sham group (16.1 ±3.4vs3.2± 1.0 on the third day (P < 0.0001 ); 10.9 ± 1.9 vs 3.3 ± 0.8 on the fifth day (P < 0.0001)). In the I/R group, the pyramidal cells were atrophic and pycnotic; vacuolation, and structural disruption of the radial striated zone were observed from the third through the seventh day. In the sham group, these changes were not observed. There were differences of degenerative ratios in the pyramidal cells between the two groups from the third to seventh days (5.6 ± 2.0 vs 80.9 ± 3.3 on the third day (P < 0.05); 6.9 ± 0.4 vs 93.6 ± 2.4 on the fifth day (P < 0.05); 6.2 ± 1.5 vs 95.0 ± 1.3 on the seventh day (P < 0.05)).ConclusionThere is a correlation between the generation of Superoxide radicals and histopathological changes of the pyramidal cells in the hippocampal CAI subfield.RésuméObjectifInvestiguer la relation entre la production des radicaux superoxydes et les changements histopathologiques sur le décès neuronal retardé dans le champ hippocampique CAL.MéthodesSoixante-dix gerbilles ont été aléatoirement réparties en 2 groupes, un groupe contrôle et un groupe ischémie/reperfusion (I/R). Dans le groupe I/R, une ischémie transitoire du prosencéphale était induite par l’occlusion bilatérale des carotides communes pour quatre minutes. Après reperfusion, le cerveau était retiré de l’animal après une minute de même qu’à six, douze et vingt-quatre heures ainsi qu’à trois, cinq et sept jours. Chaque prosencéphale était coupé en deux parties incluant l’hippocampe. La quantité de radicaux superoxydes était mesurée par chemiluminescence et les changements histopathologiques dans le champ hippocampique CAI étaient observés.RésultatsDans le groupe I/R, les radicaux superoxydes ont augmenté aux jours 3 et 5 comparativement au groupe témoin (16,1 ±3,4 vs 3,2± 1,0 au jour 3 (P< 0,000l); 10,9 ± 1,9 vs 3,3 ± 0,8 au jour 5 (P< 0,000l)). Dans le groupe I/R, les cellules pyramidales étaient atrophiques et picnotiques; du 3e au 7e jour, on a observé de la vacuolisation et de la destruction structurale de la zone striée radiaire, et ces changements n’ont pas été retrouvés dans le groupe témoin. On a observé des différences dans le pourcentage dégénératif des cellules pyramidales entre les deux groupes à partir du jour 3 au jour 7 (5,6 ± 2,0 vs 80,9 ± 3,3 au jour 3 (P< 0,05); 6,9 ± 0,4 vs 93,6 ± 2,4 au jour 5 (P< 0,05); 6,2 ± 1,5vs 95,0 ± 1,3 au jour 7 (P< 0,05)).ConclusionIl y a une corrélation entre la production de radicaux superoxydes et les changements histopathologiques des cellules pyramidales du champ CAI de l’hippocampe.

Involvement of the glutamate transporter and the sodium–calcium exchanger in the hypoxia-induced increase in intracellular Ca2+ in rat hippocampal slices

Hippocampal slices prepared from adult rats were loaded with fura-2 and the intracellular free Ca2+ concentration ([Ca2+]i) in the CA1 pyramidal cell layer was measured. Hypoxia (oxygen-glucose deprivation) elicited a gradual increase in [Ca2+]i in normal Krebs solution. At high extracellular sodium concentrations ([Na+]o), the hypoxia-induced response was attenuated. In contrast, hypoxia in low [Na+]o elicited a significantly enhanced response. This exaggerated response to hypoxia at a low [Na+]o was reversed by pre-incubation of the slice at a low [Na+]o prior to the hypoxic insult. The attenuation of the response to hypoxia by high [Na+]o was no longer observed in the presence of antagonist to glutamate transporter. However, antagonist to Na+-Ca2+ exchanger only slightly influenced the effects of high [Na+]o. These observations suggest that disturbance of the transmembrane gradient of Na+ concentrations is an important factor in hypoxia-induced neuronal damage and corroborates the participation of the glutamate transporter in hypoxia-induced neuronal injury. In addition, the excess release of glutamate during hypoxia is due to a reversal of Na+-dependent glutamate transporter rather than an exocytotic process.

Assessment of neuromuscular block at the thumb and great toe using accelography in infants

We assessed neuromuscular block at the thumb and great toe using accelography after the administration of vecuronium in infants. Train‐of‐four stimuli were simultaneously applied to the ulnar and tibial nerves using cutaneous electrodes. Anaesthesia was maintained with nitrous oxide (66%) in oxygen and sevoflurane (1%). Vecuronium 0.1mg.kg‐1 was used for paralysis and reversed with intravenous neostigmine 0.04mg.kg‐1 with atropine 0.02mg.kg‐1 when the train‐of‐four ratio on the right great toe returned to 25%. The mean (SD) times from initial administration of vecuronium to completion of maximal block on the thumb and great toe were 78 (21.1) s and 75 (14.3) s, respectively (p>0.05). The times from maximal block to 25% recovery of twitch height at the thumb and great toe were 46 (9.1) min and 45 (9.0) min, respectively. The reversal time from 25% to 75% of the train‐of‐four ratio after the administration of neostigmine was 136 (49.1)s. We conclude that neuromuscular monitoring of the great toe in infants may be a suitable alternative when the thumb is inaccessible.

Does hypertonic saline have preventive effects against delayed neuronal death in gerbil hippocampus

This experiment was conducted to ascertain whether or not hypertonic saline solution (HSS) has preventive effects on delayed neuronal death in the hippocampal CA1 subfield of the gerbil. Twenty-eight gerbils were anesthetized with 1% halothane and 50% nitrous oxide during the experimental period. Their common carotid arteries were occluded bilaterally for 2.5 min, immediately after which 2 mL/kg of 10% NaCl was infused via the tail vein. Two mL/kg of physiological saline solution (PSS) was used for the control group in the same manner. 5 days later, after the cerebrum was removed, the hippocampus was stained with hematoxylin-eosin, and histopathological changes in the CA1 subfield were observed under the light microscope. Degenerative or necrotic pyramidal cells were compared among groups. The degeneration rates of the pyramidal cells were as follows; after sham operation with PSS, 4.2 ± 1.8%; after sham operation with HSS, 6.5 ± 3.3%; on ischemia-reperfusion with PSS, 95.6 ± 1.6%; on ischemia-reperfusion with HSS, 7.1 ± 3.0%. This study suggested that hypertonic saline might prevent delayed neuronal death in the hippocampal CA1 subfield of gerbils subjected to cerebral ischemia-reperfusion.

Edrophonium as an antagonist of vecuronium-induced neuromuscular block in the elderly

Train‐of‐four stimuli were applied to the ulnar nerve using an accelograph in 10 elderly patients (aged 70–82 years) and 10 younger patients (aged 27–54 years). Anaesthesia was induced with thiopentone 5mg.kg‐1 and was maintained with nitrous oxide (66%) oxygen and sevoflurane (1 MAC). Vecuronium 0.1mg.kg‐1 was used for paralysis, and reversed with intravenous edrophonium 0.75mg.kg‐1 and atropine 0.015mg.kg‐1 when the train‐of‐four ratio returned to 25%. The times from initial administration of vecuronium to completion of maximal block were 211.5 (SD 66.9) s and 154.0 (SD 39.7) s in the elderly and younger patients, respectively (p < 0.05). The times from maximal block to 25% recovery of train‐of‐four ratio were 64.8 (SD 36.3) min and 61.8 (SD 36.3) min in the elderly and younger patients, respectively. There was no statistically significant difference between them. The reversal times from 25% to 75% of the train‐of‐four ratio after the administration of edrophonium were 210.0 (SD 136.7) s and 177.0 (SD 100.4) s in the elderly and younger patients, respectively. There was no statistically significant difference between them. The authors were unable to show that healthy elderly patients differ significantly from younger patients in the neuromuscular blocking effect of vecuronium and the reversal effect of edrophonium.

Differential effects of vecuronium on the thumb and the big toe muscles evaluated by acceleration measurement

To clarify the differential effects of vecuronium on the thumb and on the big toe, train-of-four (TOF) stimuli were applied to the ulnar nerve at the wrist and the tibial nerve at the ankle in anesthetized patients using two acceleration transducers. Ten adult patients, aged 21–55 years, were studied. Anesthesia was induced by an intravenous injection of thiopental, and vecuronium 0.1 mg·kg−1 was used for paralysis. Anesthesia was maintained with nitrous oxide (66%)-oxygen-sevoflurane (1 MAC). The duration of time to the maximal twitch depression on the thumb and the big toe was 136.5±32.5 s and 183.0±40.1 s (P<0.05), respectively. The time to 25% recovery of the twitch height on the thumb and the big toe was 48.1±17.3 min and 39.1±11.6 min, respectively; the time to 50% recovery of twitch height on the thumb and the big toe was 54.1±16.1 min and 40.0±9.2 min (P<0.05), respectively. When paralysis was reversed at 25% of TOF ratio on the thumb, the value of the TOF ratio on the big toe was 58.5±18.2% (P<0.01).

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.

Epidural spinal cord stimulation for treatment of outpatients with intractable pain-report of three cases.

We devised a new needle for epidural spinal cord stimulation (ESCS) and have used it in outpatients with intractable pain. We now report three typical cases and introduce the procedure of ESCS with the new needle. ESCS was reported to be effective in various kinds of painl 7 , peripheral vascular8~12 and spastic muscular diseases13-15. The conventional method involves the insertion of a threadlike stainless steel wire through a catheter into the epidural space. It is a difficult technique. The tip of the wire has to be inserted into the epidulal space using a 17-gauge Tuohy needle. This conventional technique is so time-consuming that it can not be used in outpatients; of course, the indwelling electrical stimulating device can not be used in these patients. We therefore devised a new needle for ESCS and have successfully used it in the outpatients with various kinds of intractable pain. The needle is shown in figure 1. The surface of the outer needle (22-gauge, 7 cm) of the paired needles used for performing epidural block procedures was insulated with a teflon coating except at the tip. The head

407 A high extracellular sodium concentration inhibits the hypoxia-induced increase in intracellular Ca2+ concentration in rat hippocampal slices

DAIICHIRO NAKAHARA’, MASATO NAKAMURA’ , MASATOSHI TAKITA2 The extracellular concentration of glutamate (GLU) in the medial frontal cortex (MFC) was measured using microdialysis combined with on-line fluorometric detection of NADH resulting from the reaction of GLU and NAD+, catalyzed bu GLU dehydrogenase. Rewarding and stressful stimuli used here were self-stimulation of the medial forebrain bundle and immobilization, respectively. Self-stimulation caused a small decrease in extracellular GLU concentrations followed by a large increase returning to basal levels after cessation of the rewarding stimulation. Immobilization stress produced a rapid increase in extracellular GLU levels which peaked twice, during the period of immobilization and when rats were freed from the aversive manipulation. Thus, we observed a differnt pattern of changes in extracellular GLU in the MFC associated with different behavioral conditions.