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K Kogure

Publications and source records attributed to K Kogure.

At least 379 records · Page 21Linked to original sources
PubMed1987

Comparative studies on clinical features and CSF proteins of motor neuron disease patients.

Clinical features such as types of diseases, sex ratio, age of onset, sites of initial involvement, the appearance of bulbar signs, and duration of illness were studied in 52 patients with motor neuron disease (MND) with a special reference to immunoglobulin in cerebrospinal fluid (CSF) and serum. Although MND has been thought to be a degenerative disease of unknown cause, our data suggested there are some immunological abnormalities in this disease. The duration of illness and the abnormalities of CSF immunoglobulins appeared to be correlated with the type of disease and the site of initial involvement. However, whether or not these abnormalities in CSF immunoglobulins are directly related to the pathogenesis of MND remains unclear.

Adult↗
PubMed1987

Importance of two iron-reducing systems in lipid peroxidation of rat brain: implications for oxygen toxicity in the central nervous system.

The mechanism of lipid peroxidation in the central nervous system has been studied using oxygen-flushed rat brain homogenates at pH 7.4. Brain lipid peroxidation was monitored by chemiluminescence and by determination of thiobarbituric acid-reactive substances. Less involvement of O2-., H2O2 and probably .OH in the initiation of lipid peroxidation was indicated. Deferroxamine was an extremely potent inhibitor of lipid peroxidation, suggesting that lipid peroxidation was catalyzed by endogenous iron. Brain tissues were shown to contain at least two iron-reducing systems for promotion of lipid peroxidation. One was ascorbate-dependent and the other NADPH-dependent. The former was much more potent than the latter with respect to iron-reducing activity.

Animals↗
PubMed1987

Protective effects of indeloxazine hydrochloride on cerebral ischemia in animals.

Effects of indeloxazine hydrochloride [(+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054] on cerebral ischemia were investigated in animals. Indeloxazine prolonged the gasping duration dose-dependently in decapitated mice. Bilateral occlusion of the carotid artery for 5 min shortened the latency of step-through in passive avoidance task 4 days following ischemia in mongolian gerbils. The i.p. administration of indeloxazine was started just after the surgical operation and repeated twice a day for 4 days. Indeloxazine (2 mg/kg) significantly prolonged the latency of step-through in this amnesic model, indicating a reversal effect on the ischemia-induced amnesia. In biochemical studies, decreases in brain ATP and total adenine nucleotide levels were inhibited by indeloxazine (2 mg/kg i.p., once a day for 7 days) in four-vessel occluded rats. These findings indicate that indeloxazine possesses protective effects on cerebral ischemia presumably due, in part, to improvement of the cerebral energy metabolism.

Animals↗
PubMed1987

[Effects of S-adenosyl-L-methionine on the cerebral energy metabolism and microcirculation in the rats subjected to transient forebrain ischemia].

Effects of S-adenosyl-L-methionine (SAM) on the improvement of cerebral energy metabolism and microcirculation were examined in postischemic rat brain. Male Wistar rats, whose vertebral arteries were electrically cauterized last day, were subjected to forebrain ischemia by temporary clipping of both common carotid arteries. After 60 min of ischemic insult, they were intravenously administered with SAM at doses of 30 or 100 mg/kg; this was followed by recirculation for 60 min. To determine cerebral concentrations of energy metabolites, the brain was frozen in situ. Adenine nucleotides (ATP, ADP, AMP) were assayed by anion-exchange HPLC system, and other metabolites (PCr, glucose, lactate, pyruvate) were analyzed by enzymatic fluorometry. In order to estimate regional cerebral blood flow (rCBF) and glucose utilization, double-tracer autoradiography was undertaken using 14C-iodoantipyrine (14C-IAP) and 18F-fluorodeoxyglucose (18F-FDG). In animals without SAM treatment (60-60 group), energy metabolites did not recover and neither CBF nor glucose uptake restored during 60 min of recirculation. In contrast, in SAM-treated animals (60-60 SAM group), values of the energy metabolites improved significantly and both CBF and glucose uptake recovered, though incompletely. These results indicate that SAM is able to improve postischemic cerebral microcirculation and energy metabolism. For mechanisms of the effects, it is suggested to the enhancement of erythrocyte deformability by phospholipid methylation, the stabilization of mitochondria, and the normalization of injured metabolic reactions. Therefore, we conclude that SAM is able to be effective clinically as a drug treated for the acute phase of cerebrovascular diseases.

Animals↗
PubMed1986

Biphasic effects of chlorpromazine on cell viability in a neuroblastoma cell line.

Although chlorpromazine was shown to greatly inhibit a Ca2+-mediated cell death at favorable concentrations (10(-6)-10(-5) M), it caused a drastic decrease in cell viability at higher concentrations (10(-4)-10(-3) M) in a human neuroblastoma cell line. The toxic effect of chlorpromazine also occurred in Ca2+-free medium and was not parallel to the amount of thiobarbituric acid-reactive substances produced. These results indicate that chlorpromazine has biphasic effects on cell viability according to the concentrations added, i.e. a protective effect against cell damage caused by Ca2+, and a direct toxic effect independent of extracellular Ca2+ or of lipid peroxidation.

Calcium↗
PubMed1986

Lesions to Schaffer collaterals prevent ischemic death of CA1 pyramidal cells.

The contribution of excitatory inputs to CA1 pyramidal cell death after ischemia was examined using rats with unilateral destruction of CA3 pyramidal cells. Intracerebroventricular injection of L-alpha-kainic acid (KA) was performed before the induction of transient forebrain ischemia. Five days after ischemic insult, pyramidal cells and L-glutamate binding sites in the CA1 region ipsilateral to the KA injection were preserved in spite of neuronal necrosis and a significant decrease in L-glutamate receptor density in the contralateral CA1 region, indicating the critical role of Schaffer collaterals in delayed neuronal death.

Animals↗
PubMed1986

Simplified enzymatic synthesis and biodistribution of 11C-S-adenosyl-L-methionine.

11C-S-Adenosyl-L-methionine (11C-SAM) was synthesized enzymatically from 11C-L-methionine using rat-liver extract [40%-50% saturated (NH4)2SO4 fraction] as the enzyme source. In biodistribution studies in rats, the highest uptake of 11C-SAM was found in the kidneys. 11C-SAM was also accumulated in the small intestine, pancreas, adrenal gland, liver, and spleen. The uptake of 11C-SAM in the brain increased with time, but remained low. At 30 min after injection, about 50%-60% of the 11C radioactivity was present in the acid-insoluble fraction of the kidneys and liver. When a high loading dose of 11C-SAM was administered, the kidney uptake was enhanced, but the proportion of the radioactivity present in the acid-insoluble fraction was lower. In a study of one rabbit, the kidney uptake was of 11-SAM clearly visualized using positron-emission tomography.

Animals↗
PubMed1986

Characterization of experimental ischemic brain edema utilizing proton nuclear magnetic resonance imaging.

Correlations between T1 and T2 relaxation times and water and electrolyte content in the normal and ischemic rat and gerbil brains were studied by means of both nuclear magnetic resonance (NMR) spectroscopic and imaging methods. In the spectroscopic experiment on excised rat brains, T1 was linearly dependent on tissue water content and T2 was prolonged in edematous tissue to a greater extent than expected by an increase in water content, showing that T2 possesses a greater sensitivity for edema identification and localization. Changes in Na+ and K+ content of the tissue mattered little in the prolongation of relaxation times. Serial NMR imaging of gerbil brains insulted with permanent hemispheric ischemia offered early lesion detection in T1- and especially T2-weighted images (detection as soon as 30 min after insult). The progressive nature of lesions was also imaged. Calculated T1 and T2 relaxation times in regions of interest correlated excellently with tissue water content (r = 0.892 and 0.744 for T1 and T2, respectively). As a result, detection of cerebral ischemia utilizing NMR imaging was strongly dependent on a change in tissue water content. The different nature of T1 and T2 relaxation times was also observed.

Animals↗
PubMed1986

Changes in levels of purine and pyrimidine nucleotides during acute hypoxia and recovery in neonatal rat brain.

Neonatal rat brains were examined for changes in levels of ATP, ADP, AMP, cyclic AMP, GTP, GDP, UTP, UDP, UMP, and CTP during exposure to 100% nitrogen for 20 min and subsequent recovery in air. During hypoxia, ATP, GTP, UTP, and CTP levels and the GTP/GDP ratio decreased to 38, 50, 26, 21, and 21%, respectively, of control levels. No significant change in cyclic AMP level was observed. The decrease in the total uridine nucleotide pool during hypoxia was markedly greater (to 53% of control levels) than that in the total adenine nucleotide pool (to 92% of control levels). During recovery, ATP and GTP levels were rapidly and almost completely restored. On the other hand, CTP levels returned slowly to control values after a 2-h recovery period. Restoration of the UTP level was slow and incomplete (87% of the control value even after a 3-h recovery period). The GTP/GDP ratio also did not return to normal. These data suggest that hypoxic insult to the neonate may have an effect on the synthesis of nucleotidyl sugars, phospholipids, and proteins in the brain, resulting in significant problems with developmental processes of the brain. The present study also showed that the delayed restorations of the UTP level and the GTP/GDP ratio were not seen in the brains of adult rats subjected to acute severe hypoxic insult.

Adenine Nucleotides↗
PubMed1986

Accurate evaluation of 1,2-diacylglycerol in gerbil forebrain using HPLC and in situ freezing technique.

Gerbil forebrains were frozen in situ to inactivate the tissues, and 1,2-diacylglycerols were first measured quantitatively by HPLC. Although 1,2-diacylglycerols were completely recovered from the HPLC column, the control amount of 1,2-diacylglycerol in gerbil forebrain was only 79.6 nmol/g wet weight, which is about one-fourth of that previously reported for gerbil brain inactivated by liquid N2 after decapitation instead of in situ freezing. The fatty acid composition of 1,2-diacylglycerols in gerbil forebrain was first reported and the control 1,2-diacylglycerols were richer in palmitic acid than in stearic acid or arachidonic acid, which is rather different from the data previously reported for mouse or rat brain obtained by decapitation and analyzed by traditional TLC methods. The amount of 1,2-diacylglycerol increased by 82.9% in gerbil forebrain during 5 min of ischemia induced by bilateral carotid ligation. Arachidonic acid and stearic acid were abundant in the 1,2-diacylglycerols produced by 5 min of ischemia. Thus we were able to obtain accurate values of the amount and the fatty acid composition of 1,2-diacylglycerols in gerbil forebrains using HPLC and in situ freezing technique.

Animals↗
PubMed1986

Mononucleotide metabolism in the rat brain after transient ischemia.

Nucleotide metabolism was studied in rats during and following the induction of 10 min of forebrain ischemia (four-vessel occlusion model). Purine and pyrimidine nucleotides, nucleotides, and bases in forebrain extracts were quantitated by HPLC with an ultraviolet detector. Ischemia resulted in a severe reduction in the concentration of nucleoside triphosphates (ATP, GTP, UTP, and CTP) and an increase in the concentration of AMP, IMP, adenosine, inosine, hypoxanthine, and guanosine. During the recovery period, both the phosphocreatine level and adenylate energy charge were rapidly and completely restored to the normal range. ATP was only 78% of the control value at 180 min after ischemic reperfusion. Levels of nucleosides and bases were elevated during ischemia but decreased to values close to those of control animals following recirculation. Both the decrease in the adenine nucleotide pool and the incomplete ATP recovery were caused by insufficient reutilization of hypoxanthine via the purine salvage system. The content of cyclic AMP, which transiently accumulated during the early recirculation period, returned to the control level, paralleling the decrease of adenosine concentration, which suggested that adenylate cyclase activity during reperfusion is modulated by adenosine A2 receptors. The recovery of CTP was slow but greater than that of ATP, GTP, and UTP. The GTP/GDP ratio was higher than that of the control animals following recirculation.

Adenosine↗
PubMed1986

Antishock effects of corticosterone on dextran-induced shock in rats.

To study the effects of glucocorticoid on the shock state, dextran-induced shock in rats was used as an experimental model system. The rats were divided into three groups, viz., control (group A), adrenalectomized (group B), and adrenalectomized corticosterone supplemented (2 mg/rat for 4 days; group C), and 5% dextran solution was given intravenously to each rat. In group B, remarkable increases in the histamine levels in both plasma and the paw cutaneous tissue, hemoconcentration, and intractable hypotension were observed. Most rats in group B died during the shock experiment without showing any recovery when the cannulas were inserted into the left carotid artery for the measurement of blood pressure. But in group C, most rats eventually survived and recovered to a normal state within 2 h, so that corticosterone clearly ameliorated the shock state of adrenalectomized rats by dextran administration. These results suggested that the ameliorating effects of corticosterone in the dextran-induced shock states are due to the acceleration of the rate of clearance of circulating chemical mediators that are represented by histamine and are due to the alteration of overall responsiveness of the animals to a complex array of factors that threaten the status of the animals, as represented by the amelioration of the vascular activity.

Adrenalectomy↗
PubMed1986

Sequential cerebral blood flow study by chrono-autoradiography.

A novel chrono-autoradiographic technique (sequential double label autoradiography) was established in order to evaluate regional cerebral blood flow (CBF) changes utilizing N-isopropyl-p-123I-iodoamphetamine (123I-IMP) and 14C-iodoantipyrine (14C-IAP). With sequential administration of 123I-IMP and 14C-IAP, two CBF images were obtained from the same brain section. By applying this method to focal cerebral ischemia, two sequential CBF images, one during ischemia and one after recirculation, were obtained. These results show that this method is useful in topographical evaluation of CBF changes. From a pathophysiological point of view, the result demonstrates a heterogeneous tissue perfusion after a transient ischemic insult.

Amphetamines↗
PubMed1986

[Retroperitoneal malignant fibrous histiocytoma--report of a case].

A 52-year-old man with a three-month history of left epigastralgia and body weight loss was referred to us for a possible abdominal tumor in March 1984. Retroperitoneal malignant tumor was suspected by ERCP, angiography, US, and CT. At laparotomy, a child's-head-sized retroperitoneal tumor, which weighed 1,800 g, was resected. Pathological examination revealed the diagnosis of retroperitoneal malignant fibrous histiocytoma (MFH). He died because of recurrence in the retroperitoneum six months after the operation. We selected 26 Japanese cases of retroperitoneal MFH and discussed their clinical findings and prognosis.

Female↗
PubMed1986

[Magnetic resonance imaging of experimental cerebral ischemia: correlations between NMR parameters and water content].

Recent studies on proton NMR imaging revealed its remarkable sensitivity for detecting cerebral ischemia. Since proton NMR reflects the distribution and state of water in the brain, an NMR imager becomes a sensitive in vivo detector of brain edema developing soon after the energy state is compromized by ischemia. To further clarify the usefulness of NMR imaging to characterize the ischemia-induced changes, correlations between T1 and T2 relaxation times and water content of the normal and ischemic rat and gerbil brain were studied by means of both spectroscopic and in vivo imaging methods. In the spectroscopic experiment on excised rat brain (cortex, white matter, hippocampus and thalamus for normal and ischemia-laden brain), T1 and T2 relaxation times and water content were determined. The ischemic insult was induced for 60 min by the method of Pulsinelli followed by 60 min of reperfusion. All of the T1, T2 and water content significantly increased in the ischemic tissue. Gray-white difference was evident in T1 and T1 was linearly correlated with the water content of the tissue. T2 was by far prolonged in the ischemic tissue compared with the increase in the water content, showing greater sensitivity of T2 for detection of ischemia. In the imaging experiment, coronal NMR imaging at 0.5 tesla was performed employing proton density-weighted saturation recovery (TR = 1.6 s, TE = 14 ms), T1-weighted inversion recovery (TR = 1.6 s, TI = 300 ms, TE = 14 ms) and T2-weighted spin echo (TR = 1.6 s, TE = 106 ms) pulse sequences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Effects of indeloxazine hydrochloride on brain energy and glucose metabolism in the four-vessel occlusion rat model].

Indeloxazine hydrochloride (Indeloxazine) has been known as a new type drug with enhancing effects on memory and learning processes in various experimental models. In the present studies, effects of Indeloxazine on brain energy and glucose metabolisms were determined in four-vessel occlusion rat model. Since a critical point of ischemic time for the recovery of brain energy levels existed between 30 min and 60 min in this model, effects of Indeloxazine were determined in the rat model of 60 min recirculation following 60 min ischemia. One-week dosing of Indeloxazine at 2 mg/kg showed slight increases in ATP and total adenine nucleotides levels. To elucidate the mechanism of improving action of Indeloxazine on brain energy levels, effects on glucose metabolism were determined. Non-treated group of 60 min ischemia-60 min recirculation showed severe reduction of 14C-2-deoxyglucose metabolism in comparison to normal control group. Indeloxazine-treated group showed a slight improvement of 14C-2-deoxyglucose metabolism in comparison to non-treated group. Furthermore, high 14C-2-deoxyglucose metabolism was observed in parts of hippocampus, cortex and thalamus. From these results, it seems possible that Indeloxazine has some protective effects on brain damage in four-vessel occlusion rat model.

Animals↗