Spontaneous haemorrhage in craniopharyngioma.
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Biomedical subjects
Publications and source records attributed to N Funatsu.
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The purpose of this study was to examine the effects of enflurane on local cerebral glucose utilization (LCGU), and to provide further insight into the mechanism of the epileptogenic properties of enflurane. Twenty-four male Wistar rats were divided into four groups; three groups with intact cortex received 0.5, 2, or 4% enflurane, and one group with unilateral cortex excised received 4% enflurane. LCGU was measured at each anesthetic concentration using the autoradiographic 2-[14C]deoxyglucose method. LCGU in ten of 33 structures examined during 2% enflurane decreased by 19-33%, and LCGU in 22 structures during 4% enflurane decreased by 19-65%, when compared with that during 0.5% enflurane. While LCGU, in most structures, decreased in a dose-related manner, LCGU in the corpus callosum, thalamic ventrobasal complex, and hippocampal CA3 field during 4% enflurane increased by 31-70%, compared with that during 0.5% and/or 2% enflurane. With unilateral cortical excision during 4% enflurane, the increase in LCGU in the ventrobasal complex was obliterated in the excision side, and the increase in the corpus callosum was attenuated. High LCGU in the hippocampal CA3 field and contralateral ventrobasal complex was not affected with cortical excision. These results indicate that intercortical and corticothalamic pathways are metabolically activated during deep enflurane anesthesia, suggesting that the epileptogenic property of enflurane is related to activation of these pathways.
A method for providing a saline drip during bipolar diathermy is described. Stainless steel tubing is incorporated in both blades of standard bipolar forceps and connected to the irrigating line. Irrigation is started when the forceps are closed and is stopped when they are open.
To examine the effects of hypotension induced either with trimethaphan (TMP) or nitroprusside (NTP) on blood-brain barrier (BBB), penetration of Evans blue (EB) was observed in dogs anesthetized with halothane. Dogs given TMP were divided into two groups: Group 1, seven dogs rendered hypotensive to mean cerebral perfusion pressure (CPP) of 45 mmHg for 45 min and then of 30 mmHg for 45 min; Group 2, three dogs examined 3 days after arterial hypotension identical to that in Group 1. Dogs given NTP were divided into four groups: Group 1, seven dogs rendered hypotensive with NTP (at dose less than 1 mg/kg) identical to the TMP-Group 1; Group 2, three dogs examined as the TMP-Group 2; Group 3, seven dogs rendered hypotensive to CPP 45 mmHg for 45 min; Group 4, seven dogs rendered hypotensive with NTP (at dose greater than 1 mg/kg) identical to the NTP-Group 1. In all dogs, the dorsal cortical surface and standardized serial coronal sections were examined for evidence of EB penetration. The mean EB penetration score (+/- SEM) for TMP-Groups 1 and 2 was 12 +/- 6, 0 +/- 0, respectively, and for NTP-Groups 1, 2, 3, and 4 was 105 +/- 14, 30 +/- 7, 6 +/- 6, and 125 +/- 26, respectively. These results suggest that dysfunction of the BBB in the NTP group was more pronounced than in the TMP group.
The effects of hypotension induced by trimetaphan (TMP) or nitroprusside (NTP) together with controlled haemorrhage on cerebral electrical activity, cerebrospinal fluid pressure (CSFP) and systemic circulatory and metabolic variables were measured in 10 mongrel dogs anaesthetized with halothane (end-tidal, 0.88 +/- 0.03%). Induced hypotension was maintained at cerebral perfusion pressure (CPP) of 45 mmHg for 45 min and then at 30 mmHg for 45 min. In five TMP dogs, there were significant decreases in EEG-power and slowing of peak power frequency from the frontal area, but not from the occipital area. The CSFP did not change significantly except for an increase during the induction stage of hypotension. In five NTP dogs, there were no significant changes in EEG-power and peak power frequency throughout the study from either frontal or occipital areas, but CSFP increased significantly. With both drugs, an increase in glucose, lactate and lactate pyruvate ratio (L/P), and a decrease in PaO2 were more pronounced at 30 mmHg than 45 mmHg. With NTP, there were sustained increases in lactate and L/P, even after restoration of arterial pressure. The same magnitude and duration of the decrease in CPP induced by either TMP or NTP produced different effects on cerebral and systemic function.
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