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Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

At least 361 records · Page 20Linked to original sources
PubMed1988

Recovery from edema and of protein synthesis differs between the cortex and caudate following transient focal cerebral ischemia in rats.

Postischemic recovery from brain edema and of protein synthesis was examined following 1 h of middle cerebral artery (MCA) occlusion in rats. Recovery from brain edema and of protein synthesis showed a good correlation until 7 days after reperfusion in each area (cerebral cortex or lateral caudate) in the occluded MCA side. However, regional differences in the above types of recovery in the cortex and in the lateral caudate were found for the first time in this experiment. A profound inhibition of protein synthesis and formation of brain edema began sooner in the lateral caudate than in the cortex and continued long after reperfusion. Grades of cerebral blood flow during ischemia and the early period of reperfusion were almost the same in the two regions. Therefore, the regional differences in the above recoveries may not be due to the difference in the blood flow during ischemia and reperfusion, but may be partly attributable to the imbalance of excitatory and inhibitory innervation in the above two areas of the brain, may be due to a distinctive response to ischemic stress, and may be caused also by the potentiative effect of free arachidonate on the excitotoxic mechanism.

Animals↗
PubMed1988

Effect of dihydroergotoxine mesylate (Hydergine) on delayed neuronal death in the gerbil hippocampus.

The CA 1 neurons in the gerbil hippocampus exhibiting necrosis with delayed onset following 5 min ischemia were reduced markedly by the systemic administration of dihydroergotoxine mesylate (Hydergine; HYG). Immediately after 5 min of forebrain ischemia, the animals were injected intraperitoneally with HYG. Seven days after ischemia, perfusion-fixed brains were processed by conventional histology. The number of neurons per millimeter in the CA 1 pyramidal cell layer were calculated and they were labelled neuronal density. In the control group, the neuronal density was 66.03 +/- 7.37 (mean +/- SEM), in the vehicle group, it was 11.25 +/- 4.93. The neuronal density in the HYG group was 69.19 +/- 6.49. The difference in the neuronal density between the HYG group and the control group was not statistically significant. These data indicate that HYG protects on the CA 1 neurons, and this suggest that the suppression of adrenoceptors by this drugs may be the main mechanism of action. This morphologic outcome may explain the functional amelioration of mental impairment by HYG.

Animals↗
PubMed1988

Strong attenuation of ischemic and postischemic brain edema in rats by a novel free radical scavenger.

Regional changes in the amount of free fatty acids, polyphosphoinositides, and water content in the cerebral cortex were examined using a middle cerebral artery occlusion model of rats. The amount of various free fatty acids increased as polyphosphoinositides decreased during 3 and 6 hours of ischemia in the occluded middle cerebral artery territory. After 3 hours of reperfusion following 3 hours of ischemia, free fatty acids partially recovered while polyphosphoinositides did not. Water content increased significantly after 3 and 6 hours of ischemia, and a further increase was found after 3 hours of reperfusion following 3 hours of ischemia. The change of polyenoic fatty acids in this occluded middle cerebral artery territory was much smaller than that in the case of decapitation ischemia, although the amounts of polyphosphoinositides and monoenoic and saturated fatty acids showed almost identical changes in both cases, probably because polyenoic fatty acids may be washed out and/or peroxidatively consumed in the middle cerebral artery occlusion model due to its residual blood flow. Changes in the area surrounding the occluded middle cerebral artery territory were similar to the above results, although less dramatic. However, there was no change in free fatty acids, polyphosphoinositides, and water content in the contralateral cortex. A novel free radical scavenger (MCI-186), which prevents both nonenzymatic peroxidation and lipoxygenase activity in vitro, markedly attenuated the ischemic and postischemic brain swelling. These results suggest that free radical mechanisms may be involved in ischemic and postischemic brain edema.

Animals↗
PubMed1988

Prevention of delayed neuronal death in gerbil hippocampus by ion channel blockers.

We used a gerbil model of cerebral ischemia to study the effects of ion channel blockers on neuronal death resulting from enhanced glutamate release and calcium ion influx. The common carotid arteries of gerbils were occluded for 5 minutes and injected intraperitoneally immediately after ischemia with an alkylene iminopropylene derivative (glutamate blocker) or a piperazinyl ethanol derivative (calcium blocker) given at high or low doses. Two vehicle groups received saline or 0.2% methyl cellulose solution. Seven days later, the gerbils were perfusion-fixed and their brains were processed for histologic study. The number of neurons per millimeter (neuronal density) of the CA1 region was calculated, and the neuronal density in each group was statistically compared using the Mann-Whitney U test. Compared with a control group not subjected to carotid ligation, neurons of the two vehicle groups and the low-dose calcium blocker group were almost nonexistent in the CA1 region. Neuronal densities of the glutamate blocker group and the high-dose calcium blocker group were similar and were found to be within normal limits by statistical analysis. Our study shows that detrimental membrane phenomena and the incidence of delayed neuronal death may be counteracted by the systemic administration of these ion channel blockers after ischemic insult.

Animals↗
PubMed1987

Recovery from calcium-induced damage in a neuroblastoma cell line.

Calcium may act as a second messenger in normal cellular signal transduction systems. However, an excessive influx of calcium into the cytoplasm is well known to be a final common pathway causing cell death under various pathological conditions. The purpose of this study was to investigate the effect of a transient treatment with the calcium ionophore A23187 on the recovery process of cell viability, energy metabolism, amino acid incorporation and calcium uptake in a neuroblastoma cell line. When neuroblastoma cells were treated with 20 microM of the calcium ionophore A23187 in combination with extracellular calcium, rapid energy failure and marked inhibition of amino acid incorporation by the cells occurred together with a massive influx of calcium, and finally resulted in cell death. Recovery from this calcium-induced damage with regards to energy metabolism and prognosis of cell viability was better after a 10-min treatment than after a 30-min treatment with A23187. After a 10-min treatment, the viability was higher in calcium-free medium than in calcium-containing medium in contrast with the cases after treatment for 30 min. The above difference in viability after treatment for 10 min had a very significant correlation with the degree of exclusion of excessive calcium and the recovery of CTP, indicating that the recovery of CTP and the rate of calcium exclusion may be final markers of the recovery of cells from calcium-induced damage rather than the recovery of ATP or amino acid incorporation. Amino acid incorporation was restricted to a level lower than that of the control long after the recovery of GTP and the GTP/GDP ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcimycin↗
PubMed1987

Prevention of an increase in susceptibility to calcium in a neuroblastoma cell line.

An increase in susceptibility of neuroblastoma cells to calcium was inhibited when the cells were treated with hypothermia, diphenylhydantoin, chlorpromazine or pentobarbital; all of these treatments affect membrane permeability to calcium or membrane-associated cell metabolism. Diphenylhydantoin and chlorpromazine were found to have positive effects only when they were administered before the addition of calcium. This was in contrast to flunarizine, which showed a protective effect only in combination with calcium. However, leupeptin did not show any positive effect, indicating that calcium-activated neutral protease may be only slightly involved in this type of calcium-induced cell damage.

Calcium↗
PubMed1987

Quantitative analysis of glucose after transient ischemia in the gerbil hippocampus by light and electron microscope radioautography.

Changes in glucose uptake in the gerbil hippocampus were studied by high-resolution [3H]2-deoxyglucose radioautography under sham and postischemic conditions. Sections of dorsal hippocampi were fixed by chemical fixatives or rapid-freezing and freeze-substitution techniques. Light and electron microscope radioautograms showed that the cell soma of each CA1 neuron subjected to transient ischemia revealed various degrees of glucose uptake. In the neuropil of the CA1 stratum radiatum, glucose uptake was higher in the thin dendrites of the ischemic group. Cell damage due to transsynaptic stimulation is suggested by these results.

Animals↗
PubMed1987

Quantitative autoradiographic analysis of muscarinic cholinergic and adenosine A1 binding sites after transient forebrain ischemia in the gerbil.

The influence of transient forebrain ischemia on adenosine A1 and muscarinic cholinergic receptors in the gerbil brain 1-27 days after recirculation was studied. The topographical distribution and the alteration in the adenosine A1 and muscarinic receptor sites were analyzed by means of quantitative receptor autoradiography using [3H]cyclohexyladenosine ([3H]CHA) and [3H]quinuclidinyl benzilate ([3H]QNB), respectively. In most regions examined, the temporal profiles of the alteration of the receptor density were in accordance with the histopathological findings. [3H]CHA binding activity decreased suddenly after neuronal damage, while [3H]QNB grain density showed a gradual decrease in the dorsolateral caudate-putamen and in the CA1 subfield of the hippocampus. In the caudate-putamen, [3H]CHA and [3H]QNB binding activity in the dorsal aspect was markedly reduced 1-27 days after ischemia. [3H]CHA binding activity in the ventromedial region of the caudate-putamen also decreased 1-3 days after ischemia, though neuronal damage was restricted to the dorsolateral aspect. Neuronal death in CA1 was preceded by the decrease in [3H]QNB binding activity in the stratum radiatum 1 and 2 days after ischemia. Marked decrease in [3H]QNB and [3H]CHA binding activity was noted in the CA1 subfield 3-27 days after recirculation. Three to 27 days after ischemia, the A1 binding activities in the CA3 subfield of the hippocampus and in the dentate gyrus were reduced despite the normal appearance of these areas throughout the reperfusion period. Muscarinic binding sites in the CA3 subfield were also reduced 27 days after ischemia. Despite minimal neuronal damage in the lateral septal nucleus and in the substantia nigra, the A1 binding activity in these regions was reduced by 70% and 50%, respectively. These results provide further evidence that the muscarinic receptors in the dorsolateral region of the caudate-putamen are localized postsynaptically on small and medium-sized neurons and that those in the CA1 subfield of the hippocampus are localized on the CA1 pyramidal cells.

Adenosine↗
PubMed1987

Greater disturbance of water and ion homeostasis in the periphery of experimental focal cerebral ischemia.

Differences in disturbed water and ion homeostasis in the periphery and the center of focal cerebral ischemia were investigated. Focal cerebral ischemia was induced by occlusion of the right common carotid artery in gerbils. Water and electrolyte content were determined using punched-out samples. In 2 h of ischemia, water content of the cerebral cortex was 79.0 +/- 0.3, 82.0 +/- 0.4, and 80.7 +/- 0.4% (means +/- SE) for the nonischemic region, the periphery, and the center of the ischemic region, respectively (significantly different). Na+ content was increased and K+ content was decreased most prominently in the periphery of the ischemic region. K+ depletion and exogenous Ca2+ accumulation in the peripheral region were visualized by K+ staining and 45Ca autoradiography, respectively. Thus, water and electrolyte changes in the periphery of ischemia were different from those in the center. Brain edema was developed initially in the marginal region of the focal cerebral ischemia.

Adenosine Triphosphate↗
PubMed1987

GABA and benzodiazepine receptors in the gerbil brain after transient ischemia: demonstration by quantitative receptor autoradiography.

Quantitative receptor autoradiography was used to measure the binding of gamma-aminobutyric acid (GABA) and benzodiazepine receptors after ischemia by means of transient occlusion of bilateral common carotid arteries in the gerbil. [3H]Muscimol was used to label the GABAA receptors and [3H]flunitrazepam to label central type benzodiazepine receptors. In the superolateral convexities of the frontal cortices, [3H]muscimol binding was increased in 60% of the animals killed 3 days after ischemia, and decreased in 67% of the animals killed 27 days after ischemia. Twenty-seven days after ischemia, [3H]flunitrazepam binding in the substantia nigra pars reticulata increased to 252% of the control, though the increase in [3H]muscimol binding was not significant. In the dorsolateral region of the caudate putamen, marked neuronal necrosis and depletion of both [3H]muscimol and [3H]flunitrazepam binding sites were observed 27 days after ischemia, the ventromedial region being left intact. In spite of the depletion of pyramidal cells in the CA1 region of the hippocampus, both [3H]muscimol and [3H]flunitrazepam binding sites were preserved 27 days after ischemia. Since our previous study revealed that adenosine A1 binding sites were depleted in the CA1 subfield of the hippocampus after ischemia correlating with neuronal damage, GABAA and benzodiazepine receptors may not be distributed predominantly on the pyramidal cells in the CA1 region.

Animals↗
PubMed1987

Activation autoradiography: imaging and quantitative determination of endogenous and exogenous oxygen in the rat brain.

Endogenous and exogenous oxygen in the rat brain were quantitatively determined using an autoradiographic technique. The oxygen images of frozen and dried rat brain sections were obtained as 18F images by using the 16O (3He,p)18F reaction for endogenous 16O images and the 18O(p,n)18F reaction for endogenous and exogenous 18O images. These autoradiograms demonstrated the different distribution of oxygen between gray and white matter. These images also allowed differentiation of the individual structures of hippocampal formation, owing to the differing water content of the various structures. Local oxygen contents were quantitatively determined from autoradiograms of brain sections and standard sections with known oxygen contents. The estimated values were 75.6 +/- 4.6 wt% in gray matter and 72.2 +/- 4.0 wt% in white matter. The systematic error in the present method was estimated to be 4.9%.

Activation Analysis↗
PubMed1987

Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex.

Once brain ischemia was induced in the gerbil cerebral fronto-parietal cortex, serial changes occurred in energy metabolites and various lipids. The amounts of inositol-containing phospholipids began to decrease immediately after energy failure, followed by an increase in the amount of 1,2-diacylglycerol with a subsequent liberation of arachidonic acid and other free fatty acids. The fatty acid compositions of inositol-containing phospholipids, of 1,2-diacylglycerols produced by ischemia, and of free fatty acids liberated during ischemia were quite similar. The amount of stearic acid liberated was much larger than that of arachidonic acid between 30 s and 1 min of ischemia. On the other hand, there was no significant decrease in the amount of the other phospholipids except for phosphatidic acid. Furthermore, there was also no change in the fatty acid composition of phosphatidylcholine or phosphatidylethanolamine throughout 15 min of ischemia. The amount of cytidine-monophosphate reached a peak (36.7 nmol/g wet wt) at 2 min of ischemia. These results indicated that arachidonic acid was predominantly liberated from inositol-containing phospholipids by phospholipase C, and by the diglyceride lipase and monoglyceride lipase system rather than from phosphatidylcholine or phosphatidylethanolamine by phospholipase A2 or plasmalogenase or choline phosphotransferase during the early period of ischemia.

Animals↗
PubMed1987

Correlation of direct viable counts with heterotrophic activity for marine bacteria.

Viable-bacteria counts, heterotrophic activity, and substrate responsiveness of viable bacteria have been used to measure microbial activity. However, the relationship between these parameters is not clear. Thus, the direct viable count (DVC) method was used to analyze seawater samples collected from several different geographical locations. Samples collected from offshore waters of the South China Sea and western Pacific Ocean yielded DVC that indicated the presence of surface and subsurface peaks of viable, substrate-responsive bacteria which could be correlated with turnover rates of amino acids obtained by using uniformly C-labeled amino acids. DVC were always less than total viable counts (acridine orange direct counts), and the DVC subsurface peak occurred close to and within the chlorophyll a zone, suggesting algal-bacterial interactions within the layer. For comparison with the open-ocean samples, selected substrates were used to determine the response of viable bacteria present in seawater samples collected near an ocean outfall of the Barceloneta Regional Waste Treatment Plant, Barceloneta, Puerto Rico. The number of specific substrate-responsive bacteria at the outfall stations varied depending on the substrate used and the sampling location. Changes in the population size or physiological condition of the bacteria were detected and found to be associated with the presence of pharmaceutical waste.

Journal Article↗
PubMed1987

Particle counter determination of bacterial biomass in seawater.

The applicability of the Elzone particle counter to the determination of marine bacterial biomass was investigated. The biomass of bacterial pure cultures and a mixed natural population were followed by using the particle counter, a CHN analyzer, and an ATP analyzer. The particle counter showed the precise size distribution of number and volume of submicron-size particles in seawater. For the pure cultured bacterial strains, the conversion factor from volume to carbon is 0.209 mg of C per mm, and for natural bacterial cells of >0.6 mum in diameter, it is 0.184 mg of C per mm. It is recommended that 0.2 be used as the conversion factor for both pure cultured marine bacterial cells and natural bacteria from coastal and near-shore marine environments.

Journal Article↗