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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The central histaminergic action on ischemia-induced neuronal damage was examined by evaluating the histological outcome and the direct current (DC) potential shift in the hippocampal CA1 region in gerbils. An intracerebroventricular administration of histamine (10–100 nmol) improved the delayed ischemic damage in hippocampal CA1 pyramidal cells produced by 3 min of transient forebrain ischemia. A high dose (75 nmol) of mepyramine, an H1 antagonist, aggravated ischemia-induced neuronal damage, but not a low dose (0.75 nmol). Administration of cimetidine (4 nmol) and ranitidine (3 nmol), H2 antagonists, aggravated the neuronal damage. An injection of histamine (100 nmol) prolonged the onset time of the ischemia-induced sudden shift in the extracellular DC potential (anoxic depolarization; AD) to 133% of that in control animals. Administration of mepyramine (75 nmol) did not markedly change the AD, whereas injections of cimetidine (40 nmol) and ranitidine (3 nmol) reduced the onset latency to 47 and 45%, respectively. These findings suggest that the central H2 action serves to protect neurons by delaying the onset of AD in gerbils.
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In vivo brain microdialysis experiments were performed in the gerbil to evaluate the origin of accumulation of extracellular glutamate under transient ischemia. Microdialysis probes were positioned in the CA1 field of the hippocampus in which proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals had been induced by 5-min ischemia 10–14 days before the microdialysis experiment; in the white matter of the cerebral cortex, which contained few neurons, few presynaptic terminals, and many astrocytes; or in the histologically normal CA1 field of the hippocampus, and then 5- or 20-min ischemia was induced. When 5-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter of the cerebral cortex, whereas a significant increase in glutamate (15-fold) was observed in the histologically normal CA1 field. When 20-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter during the first 10 min after the onset of 20-min ischemia, but remarkable ischemia-induced increases in glutamate were observed during the last 10 min of 20-min ischemia in both areas. An excessive increase in glutamate (100-fold) was observed during 20-min ischemia in the normal CA1 field of the hippocampus. When a probe was positioned in the CA1 field of the hippocampus in which presynaptic terminals of Schaffer collaterals and commissural fibers had been eliminated by bilateral kainate injections into the lateral ventricles 4–7 days before the microdialysis experiment and then 5-min ischemia was induced, a significant increase in glutamate was observed during the last half of 5-min ischemia. These results suggest that the efflux of glutamate from astrocytes does not contribute to the large ischemia-induced glutamate accumulation in the CA1 field of the hippocampus during 5-min ischemia but contributes to the ischemia-induced increase in glutamate level during ischemia with a longer duration and that ischemia-induced efflux of glutamate in the CA1 field during 5-min ischemia originates mainly from neuronal elements: presynaptic terminals and postsynaptic neurons.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of anesthesia 1 (1987), S. 203-205 
    ISSN: 1438-8359
    Keywords: Malignant hyperthermia ; Convulsion ; Postoperative
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of anesthesia 5 (1991), S. 412-415 
    ISSN: 1438-8359
    Keywords: Epidural buprenorphine ; Postoperative analgesia ; Nausea and vomiting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of anesthesia 4 (1990), S. 35-39 
    ISSN: 1438-8359
    Keywords: Epidural morphine ; Postsurgical pain ; Nausea and vomiting ; Minimum effective dose ; Linear discriminant analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine the optimum dose of epidural morphine for postoperative pain control, 0.5–4.0 mg of morphine was administered to 198 patients who had undergone operations on lower abdomen or lower extremities under continuous epidural anesthesia. Analgesic effect of morphine and incidence of nausea or vomiting were studied using linear discriminant analysis. As explanatory variables, age and dose of morphine were statistically significant in discriminating analgesic effect of morphine. Among indices for physique of patients, height was the most useful for predicting the analgesic effect. The dose which made the discriminant function zero corresponded to the minimum effective dose (MED) of morphine and it was expressed as follows; MED (mg·meter−1) = −0.0107 × age + 1.85. Predicting the incidence of nausea or vomiting in relation to the dose of morphine did not reach a level of statistical significance. (Ochi G, Yamane C, Arai T: Optimum dose of epidural morphine for postsurgical analgesia. J Anesth 4: 35–39, 1990)
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  • 6
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Cell death ; Hippocampus ; Brain temperature ; Normothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has not been discussed whether transient forebrain ischemia of 5-min duration, which is a model frequently used to evaluate pharmacological protection against ischemic injury, is an optimal model in the CA1 field of this animal whose brain temperature is maintained at normothermic levels. The temperature of the brain during an ischemic insult strongly affects the extent of the resulting neuronal injury. If the brain temperature is not regulated, it usually falls in the gerbil by 2°–4°C during 5-min ischemia. However, the brain temperature during ischemic insult was not regulated in many previous studies. In the present study, the effects of transient (1 to 5 min) forebrain ischemia on the development of neuronal degeneration in hippocampal regions of the gerbil whose brain temperature was maintained at 37°C were examined. In the CA1 field of the hippocampus, transient ischemia of 3- and 4-min duration caused almost the same maximal damage (88%–91% neuronal loss) as observed in the gerbils subjected to 5-min ischemia. Transient ischemia of 2-and 2.5-min duration provoked substantial neuronal damage in 25% and 55% of experimental gerbils, respectively. These results indicate that 5-min bilateral forebrain ischemia is more than is necessary to examine ischemiainduced neuronal degeneration in hippocampal CA1 field of the gerbil whose brain temperature is maintained at normothermic levels. In the normothermic gerbil brain, an ischemic period of 3-min already induces extensive neuronal death in the CA1 and, thus, constitutes a sensitive model to evaluate faint protective effects of drugs against ischemic injury in the normothermic gerbil.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1238
    Keywords: Hepatic encephalopathy Liver ischaemia Passive avoidance Prostaglandin E1 Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: To investigate the action of prostaglandin E1 on hepatic encephalopathy. Design: Prospective, randomised, controlled animal study. Setting: University animal laboratory. Subjects: Male Wistar rats. Interventions: After passive avoidance learning, acute liver failure was induced by occlusion of the left portal vein and the hepatic artery for 90 min. Then memory retention was evaluated 48 h later. The effects of prostaglandin E1 on memory retention were examined in animals treated with the agent systemically (intravenous injections with prostaglandin E1 twice before and after surgery, 20 µg/kg each time) and animals treated with the agent topically (intracerebroventricular injection with prostaglandin E1, 0.1 µg/h for 48 h beginning at liver ischaemia). Measurements and results: Marked damage was found on plasma analysis in animals subjected to liver ischaemia, and the memory retention was also impaired. Intravenous administration of prostaglandin E1 improved both the liver injury and memory retention. However, intracerebroventricular administration of prostaglandin E1 alleviated neither. Conclusion: These findings show that prostaglandin E1 contributes to the amelioration of hepatic encephalopathy by improving liver function.
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  • 8
    ISSN: 1438-8359
    Keywords: Pediatric intubation ; Fiberoptic bronchoscopy ; Infant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of anesthesia 6 (1992), S. 57-62 
    ISSN: 1438-8359
    Keywords: Preoperative evaluation ; Repiratory function ; Obesity ; Overweightness ; Underweightness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the influence of obesity and underweightness on the respiratory function of 228 patients over 65 ys. old undergoing elective surgery. The parameters we studied were preoperative PaO 2 (PaO 2-pre), PaO 2 under general anesthesia (PaO 2-op) and preoperative spirometric values including data from flow-volume curves and closing volumes. Triceps skinfold thickness (TSF), body mass index (BMI), Broca’s index (BI) and Onodera’s prognostic nutritional index (PNI) were measured or calculated. Respiratory parameters were compared between 3 groups; overweight (BMI ≫23), normal weight (BMI 20–22), underweight (BMI ≪19). Single and multiple correlations were analyzed between 3 nutritional parameters (BMI, TSF, PNI) and respiratory values. As a result, PaO 2-pre and PaO 2-op in overweight group were lower than those in the other groups. None of other parameters showed significant differences between the 3 groups. In multiple regression analysis, BMI correlated with PaO 2-pre (r = −0.24), PaO 2-op (r = −0.43), %VC (r = 0.18), peak flow rate (PFR, r = 0.17) and V¨50/HT (r = 0.18). TSF correlated with PaO 2-pre (r = −0.22), %MVV (r = −0.28) and RV/TLC (r = 0.28). PNI correlated with PFR (r = 0.23). We concluded that overweightness has greater influence on respiratory function of elderly patients than underweightness and that arterial blood gas analysis is essential in preoperative assessment of obese geriatric patients. (Ochi G and Arai T: The influence of obesity and underweightness on respiratory function of geriatric patients undergoing surgery. J Anesth 6, 57–62, 1992)
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of anesthesia 9 (1995), S. 209-209 
    ISSN: 1438-8359
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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