Exaggerated anesthetic requirements.
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Biomedical subjects
Publications and source records attributed to T Adachi.
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Recent studies have shown that proto-oncogene c-fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain. Administration of 120 mg.kg-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C-Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c-Fos expression was observed in the hippocampus. In contrast, c-Fos expression following generalised convulsions induced by non-anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex. These results contradict those of previously reported local cerebral metabolic studies using 2-deoxyglucose as a metabolic marker, and suggest that lignocaine-induced convulsions, unlike those induced by non-anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.
The present study was undertaken to elucidate the physiological role and the regulation of insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) in human luteinizing granulosa cells. IGFBP-1 abolished IGF-I-stimulated estradiol production by luteinizing granulosa cells in a dose-dependent manner with a 50% inhibitory concentration (IC50) of 0.27 nM. Similarly, IGFBP-1 inhibited 125I-IGF-I binding to granulosa cells. IGFBP-1 was identified by Western immunoblot and specific enzyme immunoassay in the granulosa-cell-conditioned medium after 24 h culture. Immunoreactive IGFBP-1 released into the medium was inhibited by both IGF-I and follicle-stimulating hormone dose-dependently with an IC50 of 0.14 and 0.13 nM, respectively, while human chorionic gonadotropin-stimulated IGFBP-1 release with a 50% effective dose (ED50) of 0.6 nM. These results suggest that IGFBP-1 is involved in follicular development and granulosa cell differentiation in the human ovary and that gonadotropins may influence IGF-I action by modifying IGFBP-1 levels within the ovary.
BACKGROUND: The present study was performed to evaluate the effects of nitroglycerin (GTN) on plasma arteriovenous cGMP production and to compare its hemodynamic effects in patients with congestive heart failure (CHF). We also estimated the potential clinical value of plasma arteriovenous cGMP production as an indicator of nitrate tolerance. METHODS AND RESULTS: Plasma arterial and venous cGMP levels, atrial natriuretic peptide level, and hemodynamic parameters were measured before and after GTN infusion in 14 patients with CHF. Although the plasma levels of arterial cGMP and atrial natriuretic peptide decreased immediately after GTN, the plasma level of venous cGMP did not change. GTN infusion caused a dose-dependent increase in plasma arteriovenous cGMP production, and there was a positive correlation between the decrease of pulmonary capillary wedge pressure and the increase of plasma arteriovenous cGMP production immediately after GTN. Hemodynamic tolerance was observed after both 12 and 24 hours, when plasma arteriovenous GMP production was also attenuated. CONCLUSIONS: These findings indicate that the plasma arteriovenous cGMP difference is a clinical indicator of vasodilatory action of GTN and a useful indicator of nitrate tolerance in patients with CHF.
To provide a neurochemical basis for the central nervous system actions of nitrous oxide, the changes of brain dopamine (DA), serotonin (5-HT), norepinephrine (NE), and metabolites of DA and 5-HT were studied in rats. Thirty male Wistar rats were assigned to one of five groups according to the type of gas and the duration of gas exposure. The rats in one group, which served as control, were exposed to air for 30 min, and the rats in four other groups were exposed to 75% nitrous oxide in oxygen for 0.5, 1, 2, and 4 h, respectively. Animals were killed with microwave irradiation, and the brains were divided into seven sections: the cerebral cortex, cerebellum, striatum, hippocampus, midbrain-thalamus, hypothalamus, and medulla-pons. The contents of NE, DA, 3,4-dihydroxyphenyl-alanine (DOPAC), homovanillic acid (HVA), 5-HT, and 5-hydroxyindoleacetic acid (5-HIAA) in each discrete area were measured with high-performance liquid chromatography. Nitrous oxide had no significant effect on the contents of NE, 5-HT, nor 5-HIAA, but decreased that of DA in the striatum and midbrain-thalamus after 4 h of exposure (P < 0.05). Levels of DOPAC, but not DA, in the cerebral cortex and medulla-pons were increased significantly at exposures up to 2 h (P < 0.05), but were not significant from control levels after a 4-h exposure. Increased levels of DOPAC indicate that nitrous oxide increases dopaminergic neuronal activities in the mesocortical projection and the medullary network.(ABSTRACT TRUNCATED AT 250 WORDS)
Nitric oxide (NO) synthase inhibitor (N omega-nitro-L-arginine methyl ester [L-NAME]) has been reported to reduce minimum alveolar anesthetic concentration (MAC) of halothane when administered intravenously (i.v.) and to reduce thermal hyperalgesia, or produce antinociception in the formalin test, when administered intracerebroventricularly (ICV) or intrathecally (IT). This study attempts to identify the site(s) in the central nervous system (CNS) where L-NAME acts to reduce the halothane MAC. For this purpose, we examined the effects of i.v., ICV, and IT administration of L-NAME on the halothane MAC in rats. In contrast to an earlier study, we did not observe any decrease in the halothane MAC after i.v. (10-30 mg/kg) administration of L-NAME. ICV (100 micrograms) and IT (100 micrograms and 1 mg) administration of L-NAME also did not alter the halothane MAC. These findings indicate that the L-arginine-NO pathway is not involved in the mechanism of action of halothane to suppress mechanical nociceptive response or in the nociceptive neural mechanism of mechanical stimulation.
We analyzed the effect of a new volatile anesthetic, sevoflurane (2%-5% in oxygen) on the electroencephalogram (EEG) of the neocortex, amygdala, and hippocampus, cortical somatosensory evoked potential (SEP), and brainstem reticular multiunit activity (R-MUA) in cats. Sevoflurane suppressed the background activity of the neocortex more than the amygdala and hippocampus. With increasing concentration of sevoflurane, the cortical EEG progressed from high-amplitude slow waves to a suppression-burst pattern, which was followed by an isoelectric pattern and then spikes with isoelectricity. The amplitude of the SEP was augmented and the R-MUA was suppressed by sevoflurane in a dose-related manner. Repetitive peripheral electrical stimulation induced generalized seizures at 5% sevoflurane in 2 of 13 cats. These results suggest that sevoflurane suppresses the background central nervous system electrical activities in a dose-related manner, leaving the reactive capabilities facilitated at deep anesthesia.
The role of sensorimotor cortex (anterior and posterior sigmoid gyri) as the origin of enflurane-induced generalized seizures was examined and compared to that of lidocaine-induced seizures in cats. The inhaled enflurane concentration was adjusted at 3.5% in oxygen, the maximum potency to induce generalized seizures. Repetitive electrical stimulation with supramaximum intensity at a forepaw (2 Hz, 0.5 ms, 10 V) induced generalized seizures, which ended with a sudden appearance of isoelectricity in the electroencephalogram (EEG), the so-called "postictal depression." Repetitive auditory stimuli also induced similar grand mal-type EEGs. Unilateral ablation of the sensorimotor cortex completely blocked the induction of generalized seizures by contralateral somatosensory stimuli. However, it had little effect on the induction of seizures by ipsilateral somatosensory stimuli or bilateral auditory stimuli. In contrast, bilateral ablation of the sensorimotor cortex did not have a significant effect on the lidocaine-induced seizures. These findings indicate that the involvement of the sensorimotor cortex is essential for the development of enflurane-induced but not lidocaine-induced seizures.
Twenty male and 20 female Slc : SD rats were orally given lactitol, a hepatic encephalopathy drug, for 13 weeks at doses of 0, 0.625, 2.5 or 10 g/kg/day. A 5 week recovery test was conducted after the discontinuation of the drug treatment. Soft stool and decreased food consumption were seen in the 2.5 and 10 g/kg groups. In the 10 g/kg group, there were diarrhea, soiled fur, abdominal distention, salivation, piloerection, decreased body weight gain and increased water consumption. Urinalysis showed decreased urine volume and K+ excretion in the 10 g/kg group. In this dose group, biochemical examination showed decreased ALP, total cholesterol, triglyceride, glucose, Ca, Na+, Cl- and total protein. In the pathological examination, the cecum weight was increased in all dose groups. In the 2.5 and 10 g/kg groups, cecum distention with mucosal hyperplasia was observed. The adrenal weight was increased in the 10 g/kg group and hypertrophy of zona fasciculata of adrenal gland were seen in the 2.5 and 10 g/kg groups. The thymic weight was decreased in the 10 g/kg group. Ophthalmoscopic and hematologic examinations failed to reveal any drug induced changes. The increased cecum weight in the 0.625 g/kg group was regarded as toxicologically insignificant because of the failure of the association with any clinical or morphological findings. The above mentioned changes were satisfactorily reversible except for those in the cecum. Based on the results obtained, the NOAEL of this study was suggested to be 0.625 g/kg/day.
Magnesium (Mg) is an essential dietary element that plays important roles, acting as a cofactor of many enzymes. Rats fed a Mg-deficient diet have been reported to exhibit auricular and facial peripheral hyperemia and hemorrhage. Moreover, increased intake of calcium (Ca) or phosphorus (P) has been reported to impair apparent absorption of Mg. We tried to induce such typical inflammation in Mg-deficient rats by feeding low-Mg, high-Ca, and high-P diets. Increasing concentrations of Ca or P in the experimental diets significantly decreased the apparent absorption of Mg. And all rats fed the low-Mg (0.25 mg/g diet), high-Ca (10.4 mg/g diet), and high-P (12.0 mg/g diet) diet exhibited auricular and facial peripheral-hyperemia and hemorrhage. Then, we used the low-Mg, high-Ca, and high-P diet to investigate the effects of the fructooligosaccharides (FO) on absorption of Mg and skin inflammation. In the rats fed FO-containing (1 or 5%) diet, apparent absorption of Mg was significantly increased as compared with that of the control (FO 0%) group. In the rats fed a 5% FO-containing diet and sufficient Mg (0.50 mg/g), auricular and facial peripheral hyperemia and hemorrhage were significantly reduced. We concluded that FO increased the Mg absorption in rats fed a low-Mg, high-Ca, and high-P diet. Moreover, FO reduced inflammation in Mg-deficient rats, such as peripheral hyperemia and hemorrhage.
The effects of the frequency responses of hearing aids on speech discrimination scores were studied in 100 patients with sensori-neural hearing loss. Consonant discrimination scores of /s, z, m/ in frequency responses with high frequency amplification were better than those with low frequency amplification. On the other hand, consonant discrimination scores of /g/ were better in frequency responses with low frequency amplification. The discrimination scores of the other consonants were not affected by the frequency responses. In the fitting of the frequency response of a hearing aid, low frequency amplification is effective for improving sound quality through the hearing aid. However, there is a risk of decreasing the discrimination scores of /s, z, m/.
A new pre-B cell leukemia cell line, NALM-26, was established from the peripheral blood of a 24-year-old male patient with acute pre-B cell leukemia. NALM-26 is unique in its expression of T cell-associated CD5 and myeloid cell-associated CD13 antigens. Interleukin-7 (IL-7) receptor (CDw127) was detected by flow cytometric analysis. After PMA treatment, NALM-26 was induced to express CD20, CD25 and CD28, and to increase its expression of both CD5 and CD13. The expression of CDw127 was down-modulated.
The purpose of this study was to determine the etiology of peptic ulceration in patients with pulmonary emphysema. We performed endoscopy in 50 patients with chronic pulmonary emphysema, these were patients with and without peptic ulcer. There was no significant differences between the patients with and without ulcer, with respect to past history of pneumonia, degree of dyspnea, current drugs, nutritional status, the extent of gastric mucosal atrophy, gastric mucosal blood flow, gastric mucosal hexosamine content and serum pepsinogen levels. But patients with peptic ulcer were significantly younger than patients without peptic ulcer. Cigarettes per day in patients with peptic ulcer 29.3 +/- 11.6 cigarettes/day were significantly higher than those without peptic ulcer 22.5 +/- 10.0 cigarettes/day. We concluded that increased incidence of peptic ulceration in patients with chronic pulmonary emphysema is related to the quantity of cigarette smoking.
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Seven cell lines, MOLM-6, -7, -8, -9, -10, -11 and -12, were established from a single blood sample from a patient with chronic myelogenous leukemia (CML) in blastic phase having the Ph1 chromosome abnormality. Based on immunophenotyping, two of these seven cell lines, MOLM-7 and -11, represented the megakaryoblastoid lineage, and the other five cell lines represented two different maturation stages of the myeloid lineage.
We reported previously that feeding of fructooligosaccharides (FO) increased the apparent absorption of calcium (Ca), magnesium (Mg) and phosphorus (P) in rats. We suggested that there was an important correlation between this phenomenon and fermentation of FO in the large intestine. However, the precise mechanism remained to be characterized. Therefore, we performed a mineral-balance study to identify the segment of lumen in which FO affects mineral absorption, using cecectomized rats. Sham-operated rats and cecectomized rats were fed a control diet (without FO) or an FO-diet (containing 50 g of FO per kg of feed) for 28 days. Feeding of the FO-diet decreased the luminal pH in the cecum and colon in the sham-operated rats. In the cecectomized rats, feeding of the FO-diet also decreased the luminal pH in the colon. Thus, FO was fermented in the colon of the cecectomized rats. However, the acid composition of feces was altered by cecectomy. Feeding of the FO-diet increased the absorption of Ca and Mg in the sham-operated rats. In the cecectomized rats, the FO-diet increased the absorption of Mg but did not increase the absorption of Ca. These results suggest the mechanisms for the absorption of Ca and Mg when rats are fed an FO are different.
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