Biomedical subjects

H Abiko

Publications and source records attributed to H Abiko.

At least 19 recordsLinked to original sources

PubMed2006

Prevalence and risk factor analysis of microalbuminuria in Japanese general population: the Takahata study.

Microalbuminuria, an indicator of glomerular injury, is associated with increased risk of progressive renal deterioration, cardiovascular disease, and mortality. However, the prevalence of microalbuminuria in Japanese general population is less certain. Thus, we examined the prevalence of microalbuminuria and its associated risk factors in Japan. Subjects of this cross-sectional study were asymptomatic individuals over 40 years in Takahata, Japan. Urine albumin-creatinine ratio was calculated from a single-spot urine specimen collected in the morning. Creatinine clearance (CCr) was obtained by Cockcroft-Gault equation. Multivariate logistic regression analysis was used to determine which risk factors (i.e., age, hypertension, diabetes, obesity, and salt intake) might predict the presence of microalbuminuria. A total of 2321 subjects (mean age, 64 years; men, 1034; women, 1287) were entered into the final analysis. Among them, the prevalence of microalbuminuria, macroalbuminuria, and proteinuria by dipstick test (> or = 1+) were 317 (13.7%), 39 (1.7%), and 103 (4.4%), respectively. Age, hypertension, and diabetes were independently associated with microalbuminuria in men. In addition to the classical risk factors detected in men, estimated 24-h urinary sodium excretion and uric acid were also independently associated with microalbuminuria in women. Among the 668 subjects with renal insufficiency (CCr <60 ml/min/1.73 m(2)), the prevalence of microalbuminuria and macroalbuminuria were 119 (17.8%) and 18 (2.7%), respectively. In conclusion, microalbuminuria is prevalent across all age groups and is associated with lifestyle-related risk factors in Japanese general population. However, there are a substantial number of subjects with renal insufficiency accompanying no microalbuminuria.

Aged↗

PubMed1997

[Ewing's sarcoma at the occipital bone presenting as acute epidural hematoma: a case report].

Primary cranial Ewing's sarcoma is rare. We describe an exceptionally rare case of primary Ewing's sarcoma of the occipital bone, presenting as spontaneous acute epidural hematoma. A 19-year-old female was admitted to our hospital complaining of sudden onset of severe headache. There were no neurological deficit and no abnormal laboratory findings. Computerized tomographic (CT) scan revealed a lentiform shaped high density lesion at the left occipital epidural space. Magnetic resonance imaging (MRI) showed the lesion as iso to low intensity on T1-weighted image (T1WI) and mixed signal intensity on T2-weighted image (T2WI). There were no pathological findings at the adjacent brain. Cerebral angiography demonstrated mass effect. Right occipital craniotomy was performed. We found the tumor arising from the occipital bone and located at the epidural space. The tumor was resected totally. Histological examination revealed the tumor as Ewing's sarcoma with intratumoral hemorrhage. The postoperative course was uneventful. Radiation therapy (50Gy) was given. Follow-up examination six years after the treatment found no evidence of tumor recurrence or distant metastasis. It should be born in mind that primary Ewing's sarcoma of the skull can cause spontaneous acute epidural.

Acute Disease↗

PubMed1992

Effect of dichloroacetate on recovery of brain lactate, phosphorus energy metabolites, and glutamate during reperfusion after complete cerebral ischemia in rats.

The effects of dichloroacetate (DCA) on brain lactate, intracellular pH (pHi), phosphocreatine (PCr), and ATP during 60 min of complete cerebral ischemia and 2 h of reperfusion were investigated in rats by in vivo 1H and 31P magnetic resonance spectroscopy; brain lactate, water content, cations, and amino acids were measured in vitro after reperfusion. DCA, 100 mg/kg, or saline was infused before or immediately after the ischemic period. Preischemic treatment with DCA did not affect brain lactate or pHi during ischemia, but reduced lactate and increased pHi after 30 min of reperfusion (p < 0.05 vs. controls) and facilitated the recovery of PCr and ATP during reperfusion. Postischemic DCA treatment also reduced brain lactate and increased pHi during reperfusion compared with controls (p < 0.05), but had little effect on PCr, ATP, or Pi during reperfusion. After 30 min of reperfusion, serum lactate was 67% lower in the postischemic DCA group than in controls (p < 0.05). The brain lactate level in vitro was 46% lower in the postischemic DCA group than in controls (p < 0.05). DCA did not affect water content or cation concentrations in either group, but it increased brain glutamate by 40% in the preischemic treatment group (p < 0.05). The potential therapeutic effects of DCA on brain injury after complete ischemia may be mediated by reduced excitotoxin release related to decreased lactic acidosis during reperfusion.

Adenosine Triphosphate↗

PubMed1992

Effects of hyperglycemia on the time course of changes in energy metabolism and pH during global cerebral ischemia and reperfusion in rats: correlation of 1H and 31P NMR spectroscopy with fatty acid and excitatory amino acid levels.

The effects of hyperglycemia on the time course of changes in cerebral energy metabolite concentrations and intracellular pH were measured by nuclear magnetic resonance (NMR) spectroscopy in rats subjected to temporary complete brain ischemia. Interleaved 31P and 1H NMR spectra were obtained every 5 min before, during, and for 2 h after a 30-min bilateral carotid occlusion preceded by permanent occlusion of the basilar artery. The findings were compared with free fatty acid and excitatory amino acid levels as well as with cations and water content in funnel-frozen brain specimens. One hour before occlusion, nine rats received 50% glucose (12 ml/kg i.p.) and five received 7% saline (12 ml/kg i.p.). Before ischemia, there were no differences in cerebral metabolite levels or pH between hyperglycemic rats and controls. During the carotid occlusion, the lactate/N-acetylaspartate (Lac/NAA) peak ratio was higher (0.73-1.48 vs. 0.56-0.82; p less than 0.05) and pH was lower (less than 6.0 vs. 6.45 +/- 0.05; p less than 0.05) in the hyperglycemic rats than in the controls. Phosphocreatine and adenosine triphosphate were totally depleted in both groups. Within 5-15 min after the onset of reperfusion, the Lac/NAA peak ratio increased further in all rats; however, only in extremely hyperglycemic rats (serum glucose greater than 960 mg/dl) did the lactic acidosis progress rather than recover later during reperfusion. Total free fatty acid and excitatory amino acid levels, but not cation concentration or water content, in brain correlated with serum glucose levels during and after ischemia and with NMR findings after 2 h of reperfusion. Although profound hyperglycemia (serum glucose of 970-1,650 mg/dl) appears to be associated with progression of anaerobic glycolysis and failure of cerebral energy metabolism to recover after temporary complete brain ischemia and with postischemic excitotoxic and lipolytic reactions thought to participate in delayed cellular injury, severe hyperglycemia (490-720 mg/dl) was associated with recovery of energy metabolism.

Acidosis, Lactic↗

PubMed1988

Cerebral protective effect of flunarizine in a canine model of cerebral ischaemia.

To test the effect of flunarizine on cerebral ischaemia, 15 dogs were subjected to ischaemia, using the 'canine model of the completely ischaemic brain regulated with a perfusion method' in which the cerebral blood flow (CBF) can be fully regulated. Five animals served as untreated controls, 10 received flunarizine, a calcium antagonist (1 mg/kg in 5 dogs and 3 mg/kg in 5 dogs), before the ischaemic period. After 1 h CBF was restored and recovery of the electrical activity of the brain and the degree of brain swelling were observed for 3 h. At the end of the experiments, the degree of extravasation of Evans blue was examined. Remarkable recovery of EEG was found in the groups given flunarizine when compared with untreated controls. However, no significant difference was found between untreated controls and flunarizine treated groups for the degree of brain swelling and the degree of extravasation of Evans blue. These results suggest that the treatment of flunarizine is of benefit for functional recovery against cerebral ischaemia, but does not suppress ischaemic brain oedema.

Animals↗

PubMed1987

Protective effect of phenytoin and its enhanced action by combined administration with mannitol and vitamin E in cerebral ischaemia.

To study the therapeutic effect of phenytoin on cerebral ischaemia and confirm whether or not the effectiveness of phenytoin could be enhanced by combined administration with free radical scavengers, twenty-five dogs were subjected to ischaemia, using the "canine model of the completely ischaemic brain regulated with a perfusion method". Five animals served as untreated controls, fifteen received treatment with several doses of phenytoin and five were treated with 10 mg/kg phenytoin, 2 g/kg mannitol and 30 mg/kg vitamin E. These drugs were administered prior to the production of ischaemia. After one hour ischaemia, cerebral blood flow was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. With regard to the recovery of the EEG, the higher the administered dosage, the better was the degree of recovery of the EEG. And the group which was treated with a combination of phenytoin, mannitol and vitamin E exhibited remarkable recovery of the EEG. With regard to the degree of brain swelling, a similar dose-related suppressive effect was seen in the phenytoin-treated groups. Furthermore, in the combination therapy group, brain swelling was attenuated significantly. Based on these results, it is concluded that phenytoin has a protective effect in cerebral ischaemia and it shows its most remarkable effect when given together with radical scavengers, such as mannitol and vitamin E.

Animals↗

PubMed1987

Experimental study on the reversibility of cerebral ischemia. Residual blood flow and duration of ischemia.

The flow threshold and time threshold for reversibility of cerebral ischemia were studied using a canine model of cerebral ischemia regulated by controlled perfusion of cerebral blood flow (CBF). CBF was continuously monitored with a laser Doppler flow meter, the brain was brought to a constant level of ischemia for a defined period of time, after which recirculation was instituted. The electroencephalogram (EEG) and somatosensory evoked potentials (SEP) were monitored and used as an index of brain function. No recovery of brain function was found following recirculation if the CBF was reduced to a level below 20% of the normal state for more than one hour. When residual blood flow was 30% of the normal level, however, recirculation after one hour of ischemia resulted in nearly complete recovery of brain function. Significant functional recovery was not seen after two or more hours of such ischemia. Nearly complete recovery was also seen following reperfusion within three hours with 40% of normal CBF. It was demonstrated that the reversibility in the ischemic brain was critically correlated to the level of blood flow and its duration. If these results can be applied to the human brain, emergency cerebral revascularization for ischemic stroke should be attempted when critical flow and time thresholds have not been crossed, namely, in less than 1 hour and 3 hours of insult when the residual blood flow is reduced to 30 and 40% of the normal state, respectively. In clinical situations, this "critical time" may be too short for acute revascularization unless cerebral protective measures are applied pre-operatively to prolong the viability period of ischemic cerebral tissue.

Animals↗

PubMed1987

[Cerebral protective effect of flunarizine in a canine model of cerebral ischemia].

Recently there is the hypothesis proposing that ischemic brain damage is associated with intracellular accumulation of calcium (Ca++). Therefore a variety of experiments have been carried out to investigate whether a Ca++-entry blocker was able to protect against brain damage caused by ischemia. The purpose of the present experiment is to study the protective effects of a Ca++ antagonist, flunarizine, on cerebral ischemia. In this experiment fifteen dogs were subjected to ischemia, using the "canine model of the completely ischemic brain regulated with a perfusion method" in which the cerebral blood flow (CBF) can be fully regulated. Five animals served as untreated controls, ten received treatment with flunarizine (1 mg/kg in five dogs and 3 mg/kg in five dogs, respectively). This agent was administered intravenously 20 minutes prior to the production of ischemia, when cerebral blood flow was reduced to one-tenth its normal value while monitoring CBF by means of a laser-Doppler flow meter. After one hour CBF was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. At the end of the experiments, the degree of extravasation of Evans blue in the excised brain was examined. With regard to the recovery of EEG, no recovery of EEG was seen subsequent to recirculation except one dog in the control group. Whereas in the groups treated with flunarizine, remarkable recovery of EEG was found following recirculation in a dose dependent fasion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

[Protective effect of phenytoin and its enhanced action by combined administration of mannitol and vitamin E in cerebral ischemia].

Phenytoin is well known as the anticonvulsant agent and also said to protect the brain against ischemic damage. The purpose of the present experiment is to study the therapeutic effect of phenytoin on cerebral ischemia and confirm whether the effectiveness of phenytoin could be enhanced by combination of free radical scavengers such as mannitol and vitamin E. In this experiment, twenty-five dogs were subjected to ischemia, using the "canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump at will. Five animals served as untreated control, fifteen received treatment with phenytoin (7 mg/kg in five dogs, 10 mg/kg in five dogs and 30 mg/kg in five dogs) and five treated with 10 mg/kg phenytoin, 2 g/kg of mannitol and 30 mg/kg of vitamin E. These drugs were administered intravenously 20 minutes prior to the production of ischemia, when cerebral blood flow was reduced to one-tenth its normal volume. After one hour, cerebral blood flow was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. With regard to the recovery of EEG, no recovery of EEG was seen subsequent to recirculation except one dog in the control group. Whereas in the group treated with phenytoin, gradual emergence of slow wave ws observed soon after recirculation. The higher the administered dosage is, the better the degree of recovery of EEG was seen. Thus, the dose-related recovery of EEG was observed within the dose ranges tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

[Experimental study on reversibility of cerebral ischemia--residual blood flow and duration of ischemia].

This experimental study was designed to estimate the flow thresholds and the time thresholds for reversibility of cerebral ischemia. We used a "canine model of completely ischemic brain regulated with a perfusion method", in which the cerebral blood flow (CBF) could be controlled. The residual blood flow was reduced to 10%, 20%, 30% or 40% of normal CBF, and the recirculation was started after 1, 2, 3 or 4 hours of ischemia. CBF was measured by a laser doppler flow meter. EEG and somatosensory evoked potential (SEP) was monitored and used as a parameter expressing the brain function. In the 10% and 20% ischemia group, functional recovery could not be obtained even if reperfusion was started at 1 hour after the onset of ischemia. On the other hand, in the 30% ischemia group, nearly complete recovery of EEG and SEP could be seen when reperfusion was done at 1 hour from the onset of ischemia. But recirculation after 2 hours of ischemia did not lead to significant functional recovery. In the 40% ischemia group, reperfusion within 3 hours of ischemia allowed full recovery of ischemic brain. On the contrary, reperfusion after 4 hours of ischemia showed a gradual deterioration of EEG and SEP. Accordingly, it was clearly demonstrated that the reversibility of ischemic brain was critically correlated to severity and duration of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

[Agenesis of the corpus callosum associated with interhemispheric cyst. A case report].

A 7-year-old boy was admitted because of convulsive seizures. He was diagnosed as agenesis of corpus callosum associated with interhemispheric cyst by CT scan and angiography. Metrizamide CT cisternography and cystography disclosed no communication between interhemispheric cyst and the third ventricle. By means of metrizamide CT cisternography and cystography, the authors considered this interhemispheric cyst gradually increased by some kinds of ball-valve mechanism. Cysto-peritoneal shunt was carried out. Postoperative course was uneventful and follow-up CT revealed disappearance of interhemispheric cyst and typical findings of the acallosal brain. Improvement of clinical symptoms and EEG findings occurred after operation. Agenesis of the corpus callosum associated with interhemispheric cyst is rare. The authors can find only one case of this brain anomaly in the literature in which there is no communication between interhemispheric cyst and the third ventricle. Metrizamide CT cisternography and cystography was very useful in diagnosis and selection of treatment.

Brain Diseases↗

PubMed1984

[An experimental study on the protective effect of nizofenone in cerebral ischemia].

Using the "canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the protective effects of nizofenone against cerebral ischemia was investigated. After pre-treatment with nizofenone, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG activity were observed and the effect of nizofenone evaluated. In the control group, no recovery of EEG was seen following recirculation, but in the group treated with nizofenone, gradual emergence of slow waves was observed. And the degree of recovery of EEG was better in the group administered a large dosage than in those given a low dosage. Our study suggested that within the dose ranges tested, nizofenone ameliorated ischemic brain damage in a dose dependent fashion. But the application of this experimental results to the human clinical situation requires that particular note should be paid to the dangers of transient fall of blood pressure at higher dosages.

Animals↗

PubMed1978