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Biomedical subjects

T Egashira

Publications and source records attributed to T Egashira.

At least 73 records · Page 4Linked to original sources

[An injury of the liver caused by ischemia-reperfusion in rat liver. Report 2: Relationship between the damage of the liver and during the period of reperfusion].

Liver injury by 30-min ischemia following reperfusion was examined biochemically and histopathologically. A greater increase in the level of LDH was observed after 1-hr reperfusion. However, the level of LDH decreased in proportion to the period of reperfusion, while the levels of GOT and GPT were also increased rapidly and reached its peak at 12 hr following reperfusion and were almost restored to the control level by 48 hr. A similar increase was obtained in the lipid peroxides of the liver. In addition, cyt. P-450 content and NADPH cyt. c reductase activity decreased in proportion to the period of reperfusion up to 12 hr and then recovered by 96 hr. On the other hand, heme oxygenase activity was significantly increased by ischemia-reperfusion. The ischemia-reperfused liver resulted in various morphological changes with the period of reperfusion. The destruction of Disse's space, vacuolization of the cytoplasm and nonviable hepatocytes were observed after 12-hr reperfusion. These results indicate the greatest damages of the liver induced by 30-min ischemia following reperfusion is observed after 12-hr or 24-hr reperfusion. The liver injury by ischemia-reperfusion could be a useful experimental model to develop for future studies.

Alanine Transaminase↗

Attenuation of dysfunction in the ischemia-reperfused liver by glycyrrhizin.

The present study evaluated the effect of glycyrrhizin (GR) on an injury of the liver caused by ischemia-reperfusion in rats. In the liver ischemia-reperfusion model, levels of serum GOT, GPT and LDH activities and lipid peroxides in the liver tissue were significantly increased. On the contrary, total glutathione content in the liver tissue and NADPH cytochrome P-450 reductase activity of liver microsomes were decreased. Pretreatment with GR 20 mg/kg, i.v. 10 min before induction of ischemia resulted in significant decreases in serum GOT, GPT, LDH activities and the lipid peroxide level and a higher tissue glutathione content during the period of reperfusion. Electron microscopic studies revealed various hepatocellular damages with an almost intact sinusoidal endothelium in ischemia-reperfused livers. However, the degree of damage was less severe in the livers from the rats pretreated with 20 mg/kg GR. The results indicate that GR is able to provide partial protection against ischemia-reperfused damage.

Animals↗

Protective effect of ulinastatin against liver injury caused by ischemia-reperfusion in rats.

The effects of ulinastatin (ULN), a human urinary protease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strongly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN's membrane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver's lipid peroxidation caused by ischemia-reperfusion.

Animals↗

[A case of asymptomatic Dandy-Walker syndrome with cerebellar hemorrhage].

A case of asymptomatic Dandy-Walker syndrome (DWS) complicated by cerebellar hemorrhage is reported. A 65 year-old man was hospitalized for investigation and treatment of disturbance of consciousness. CT scan and MRI showed a large hematoma in the posterior fossa cyst. Postoperative CT scan and MRI revealed the DWS and cerebellar hemorrhage on the left side. This patient had no symptom until 65 years of age, in spite of having DWS. There has been no such case reported in the literature to our knowledge. Derangement of secretion and absorption of cerebrospinal fluid seem to have been the cause of late-onset symptoms after a long well balanced symptom-free period.

Aged↗

The protective effect of glycyrrhizin against injury of the liver caused by ischemia-reperfusion.

Effects of glycyrrhizin (GR) on an injury of the liver caused by ischemia-reperfusion in rats were determined. In the liver ischemia-reperfusion model, levels of serum AST, ALT and LDH, lipid peroxides in the liver tissue, and blood superoxide dismutase activity were significantly increased. On the contrary, total glutathione content in the liver tissue was decreased. When rats were given GR 100 mg/kg for 10 days, GR suppressed the elevation of the lipid peroxide level, serum AST, ALT, LDH level, and the decrease in glutathione content during the period of reperfusion. The suppressive effect of GR was similar with that of alpha-tocopherol (VE). GR showed neither 1,1-diphenyl-2-picrylhydrazyl (DPPH) nor 5,5-dimethyl-1-pyrroline-N-oxide(DMPO)-OOH radical-trapping ability, but exhibited DMPO-OH radical-trapping action, while, VE exhibited both DPPH and DMPO-OOH radical-trapping ability. These results indicate that the hydroxyl radical trapping action of GR is the likely mechanism suppressing liver injury caused by ischemia-reperfusion.

Alanine Transaminase↗

[An injury of the liver caused by ischemia-reperfusion in rat liver].

Cellular damage of various organs by ischemia following reperfusion is assumed to be at least in part due to lipid peroxidation in biomembranes, and oxygen-derived free radicals play a major role. The level of lipid peroxides in liver tissue increased during 90-min ischemia. When reflow of hepatic blood was allowed, a greater increase in the lipid peroxides was observed. Similar increases were obtained in several serum markers (GOT, GPT and LDH) during the period of ischemia or ischemia-reperfusion. In addition, levels of cytochrome p-450 and NADPH cyt. c reductase activity decreased in proportion to the decrease in microsomal proteins during ischemia or ischemia-reperfusion. On the other hand, superoxide dismutase in blood was significantly increased by ischemia-reperfusion. Rats died within 2 days after liver ischemia of 90 min, while all animals subjected to 30-min ischemia survived. Histopathological examinations indicated that extensive coagulation with erythrocytes occurred and the extent was dependent on the time of ischemia. The liver injury by ischemia-reperfusion could be a useful experimental model for studying liver injury induced by free radicals, for developing hepatoprotective drugs, or for investigating liver transplantation.

Alanine Transaminase↗

[Effects of kamikihi-to, a Chinese traditional medicine, on various cholinergic biochemical markers in the brains of aged rats].

The effects of kamikihi-to (EK-49) on various cholinergic biochemical markers, muscarinic receptors, acetylcholinesterase (AChE), choline acetyltransferase (CAT) and choline uptake, in aged rat brains were examined. Administration of kamikihi-to in daily doses of 200 mg/kg, p.o. for 4 weeks to aged rats (24-months-old) significantly increased the density of muscarinic receptors (Bmax) for 3H-QNB (quinuclidinyl benzilate), but did not affect the apparent dissociation constant (Kd). After repeated administration of kamikihi-to to aged rats, AChE activity and choline uptake were not significantly different in the kamikihi-to treated aged rats as compared with the control aged rats. However, administration of kamikihi-to for 4 weeks resulted in a significant increase in Vmax values of CAT in kamikihi-to treated aged rats as compared with those of the control rats. These results indicate that long-term treatment with kamikihi-to enhances both the Bmax and Vmax for QNB binding and CAT activity in aged rats, respectively.

Acetylcholinesterase↗

Evidence for the existence of serotonin uptake inhibitor-like substances in human cerebrospinal fluid.

Addition of human cerebrospinal fluid (CSF) induced a marked inhibition of 3H-paroxetine binding to the monkey cortical membranes, while the specific binding of 3H-imipramine was slightly inhibited. Moreover, 3H-serotonin (5-hydroxy-tryptamine, 5-HT) uptake inhibition in the monkey cortical synaptosomes was also increased as the volume of added CSF was increased. Scatchard analysis of specific 3H-paroxetine binding with human CSF showed non-competitive kinetics, although CSF was competitive with 3H-imipramine binding. The inhibitory effect of human CSF on 5-HT uptake was non-competitive in nature. The endogenous substances in human CSF most probably act at the recognition site labeled with 3H-paroxetine. Moreover, occupation of this site by the endogenous substances is likely to inhibit the 5-HT uptake process.

Animals↗

[Bilateral traumatic hemorrhage in the basal ganglia: report of two cases].

Hematomas of the basal ganglia in head injury have long been recognized by pathologists with an interest in head injury but their mechanism has not been revealed clearly. We report two cases of bilateral traumatic hemorrhage in the basal ganglia. Case #1, a 17-year-old male was admitted to our hospital immediately after a traffic accident. Neurological examination revealed that the patient was comatose and had right hemiparesis. CT scan showed bilateral hemorrhage of the basal ganglia and subarachnoid hemorrhage in the perimesencephalic cistern. MRI showed high signal intensity areas in the bilateral basal ganglia, perimesencephalic cistern, cerebral white matter and corpus callosum. The patient was diagnosed as having diffuse axonal injury coinciding with bilateral hemorrhage of the basal ganglia. Stereotactic aspiration for the hematoma of the left basal ganglia was carried out. Case #2, a 75-year-old male was admitted immediately after falling from the roof of his house. Neurological examination revealed no neurological deficit except for headache and nausea. CT scan on the day of injury revealed no abnormality. But CT scan 12 hours following the injury showed bilateral hemorrhage of the basal ganglia. Blood pressure of the patient was within normal range and he was diagnosed as having traumatic bilateral intracerebral hematoma. Conservative treatment was carried out and the patient was discharged 7 days after injury with no neurological deficit. The mechanism of traumatic hemorrhage of the basal ganglia has not been clear. In case #1, diffuse axonal injury (DAI) may have played an important role in the bilateral hemorrhage. But in case #2, non-DAI factor such as vasoparalysis syndrome may have existed.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidental Falls↗

Isoelectric focusing of isoenzymes of monkey platelet monoamine oxidase.

Monkey platelet monoamine oxidase (MAO) was preferentially found as the B-form of the enzyme as observed from differences in substrate specificities, as well as liver MAO. The isoelectric points and molecular weights of platelet MAO subunits were compared with those of monkey liver using sodium dodecyl sulfate-disc polyacrylamide gel electrophoresis and isoelectric focusing-disc gel electrophoresis. The pI value of monkey liver was a single peak at 6.5, but the pI values of monkey platelets were triple peaks at 5.5, 6.5 and 7.0. The molecular weight of MAO subunits in monkey platelets was similar to that of liver, and was found to be about 60,000. These results indicate that MAO-B of monkey platelets differs from MAO-B of the liver, and that it has different electrophoretic properties.

Animals↗

Inhibition of MAO activity, 3H-imipramine binding, 3H-paroxetine binding and 3H-5-HT uptake by human cerebrospinal fluid.

Addition of small amount of human cerebrospinal fluid (CSF) inhibited both types of MAO in monkey brain mitochondria. The specific binding of 3H-paroxetine decreased remarkably with increasing CSF volumes, while 3H-imipramine binding was slightly inhibited. Scatchard analysis of 3H-paroxetine binding in the presence and absence of CSF indicated that the inhibitory effect was associated with a decreased Bmax without an appreciable change in Kd. Addition of CSF induced an inhibition of uncompetitive 3H-5-HT uptake to monkey cerebral membranes. These results indicate that the materials in human CSF inhibit 3H-paroxetine binding, and modulate the uptake system for 5-HT.

Animals↗

Effect of bifemelane hydrochloride on an injury of the liver caused by ischemia-reperfusion in rats.

In the liver ischemia-reperfusion model, the lipid peroxide level increased during ischemic periods, while a greater increase was observed during reflow periods. The increase in the cytochrome b5 content was observed during ischemia and reflow periods. On the contrary, the cytochrome P-450 content remained unchanged during ischemic periods, but decreased during reflow periods. Bifemelane suppressed the elevation of the lipid peroxide level, the cytochrome b5 content and the decrease in cytochrome P-450 content during the period of reperfusion.

Animals↗

Avian adenovirus isolated from pigeons affected with inclusion body hepatitis.

Avian adenoviruses were isolated from two pigeons affected with inclusion body hepatitis (IBH) by using chicken embryo liver cell cultures. One of the isolates, designated strain S-PL1, replicated in the cell nuclei forming intranuclear inclusion bodies, showed adenovirus-like morphology by electron microscopy, and cross-reacted serologically with strain SR-48 known as serotype 2 of fowl adenovirus. The strain S-PL1 killed day-old chicks by subcutaneous inoculation, and its 50% chicken lethal dose was 10(3.8) plaque forming units per bird. Severe lesions characterized with IBH and pancreatitis, were produced in chicks inoculated with the virus. Intranuclear inclusion bodies were also recognized in the liver, pancreas, kidney, proventriculus, small intestine, and caecum. By indirect immunofluorescence test, intranuclear viral antigens were detected in the liver, pancreas and other tissues.

Adenoviridae↗

Suppressive effect of bifemelane on lipid peroxidation in rat liver.

The effects of Bifemelane (BF) on lipid peroxidation, the activities of hepatic drug metabolizing enzymes, and the function of cell membranes were examined in rats. In the liver ischemia-reperfusion model, BF suppressed the elevation of the lipid peroxidation level during the period of reperfusion. BF did not exhibit a radical-trapping action using a stable free radical, 1,1-diphenyl-2-picrylhydrazyl (DPPH), which was estimated by electron spin resonance (ESR). BF remarkably inhibited NADPH-dependent lipid peroxidation in vitro. BF had no effect on the contents of cytochrome P-450 and b5 and the activities of NADPH cytochrome P-450 reductase and Cu,Zn-superoxide dismutase (SOD). BF suppressed phorbol myristate acetate (PMA)-induced superoxide formation of polymorphonuclear leukocytes (PMNs), protected hypotonic hemolysis of erythrocyte and inhibited platelet aggregation induced by adenosine diphosphate (ADP) and serum phospholipase A activity. These results suggest that BF has neither radical-trapping activity nor any influence on the drug metabolizing enzymes, but BF has a membrane-stabilizing action and it attributes to the suppressive effect of lipid peroxidation.

Animals↗