Biomedical subjects

H Chigasaki

Publications and source records attributed to H Chigasaki.

At least 19 recordsLinked to original sources

PubMed2000

Hepatocyte growth factor reduces infarct volume after transient focal cerebral ischemia in rats.

Hepatocyte growth factor (HGF) was originally discovered as a powerful mitogen for hepatocytes. HGF functions both as a neurotrophic factor as well as an angiogenetic factor. Furthermore, HGF has an anti-apoptotic effect on vascular endothelial cells. The present study examined the neuroprotective effect of HGF after transient focal cerebral ischemia in rats, in which an anti-apoptotic and an angiogenetic effect of HGF was assumed to contribute to the reduction of the infarct volume. The intraventricular administration of human recombinant HGF (90 micrograms) significantly reduced the infarct volume after 120 minutes occlusion of both the right middle cerebral artery (MCA) and the bilateral common carotid arteries (CCAs). In a separate series of experiments, we investigated both the anti-apoptotic effect on neurons and the angiogenetic effect of HGF histopathologically. The number of survival neurons and vascular lumina in the HGF group were significantly higher than those in the vehicle group. A large number of TUNEL positive neurons were observed in the inner boundary of the infarct area in the vehicle group, whereas only a few TUNEL positive neurons were observed in a corresponding area in the HGF group. In the HGF group, Bcl-2 protein was obviously represented in survival neurons as well as in vascular endothelial cells and in glial cells subjected to ischemia. These data suggest that HGF prevents apoptotic neuronal cell death by upregulating the production of Bcl-2 protein and by an angiogenetic effect in the central nervous system which affected transient focal cerebral ischemia.

Animals↗

PubMed1998

Selective hippocampal damage to hypoxia after mild closed head injury in the rat.

Our previous studies have shown selective neuronal damage in the CA3 region after mild closed head injury (CHI) combined with hypoxia. In the present studies, we examined (1) extracellular concentrations of neuroactive amino acids using in vivo microdialysis technique and (2) neuroactive amino acid binding to their receptors using quantitative autoradiography. Male SD rats were divided into five groups; sham control, mild CHI (sacrificed at 1 h or 24 h after CHI), mild CHI followed by hypoxia (1 h or 24 h). [3H]-Glutamate binding to NMDA receptors, [3H]-muscimol binding to GABAA receptors and [3H]-kainate binding to KA receptors were measured in hippocampus and cortex by quantitative autoradiography. With CHI alone, GLU and TAU levels were transiently increased by 15 min posttrauma. In the CHI with hypoxia, increases in GLU and TAU levels were sustained until 60 min following CHI. GABA level was also increased until 75 min posttrauma Pretreatment of MK-801 significantly diminished the prolonged elevation in GLU and TAU levels. (2) CHI alone did not produce prominent change in the measured receptor binding. When hypoxia was combined with CHI, significant increase in [3H] GLU binding to NMDA receptors and significant decrease in [3H]-muscimol binding to GABAA receptors were observed in CA1 and CA3 at 1 h and 24 h post-insult. These results demonstrate that selective hippocampal damage to hypoxia after mild CHI may be mediated through an increase in NMDA receptor activation and the further release of GLU and that NMDA antagonist may be beneficial in preventing secondary neuronal damage by hypoxia.

Animals↗

PubMed1997

The effect of MK-801 on extracellular neuroactive amino acids in hippocampus after closed head injury followed by hypoxia in rats.

Increased neuronal vulnerability to ischemia or hypoxia has been demonstrated following traumatic brain injury but not explained. Animal data suggest that neuronal damage after traumatic brain injury is caused mainly by massive glutamate release that activates N-methyl-D-aspartate (NMDA) receptors. Using rat models with controlled closed head injury (CHI) followed by hypoxia, we investigated extracellular concentrations of neuroactive amino acids in the hippocampus by in vivo microdialysis. CHI alone produced an immediate increase of glutamate and taurine; hypoxia alone did not alter amino acid concentrations. CHI followed by hypoxia produced a biphasic increase in extracellular glutamate and taurine, with an immediate peak after CHI and a prolonged plateau after hypoxia. Though changes in gamma-aminobutylic acid (GABA) concentration is also prolonged by combined traumatic and hypoxic insults, it showed less alteration than glutamate. Pre-treatment with dizocilpine maleate (MK-801), a non-competitive NMDA antagonist, did not affect the immediate peak of glutamate after CHI but significantly diminished the prolonged plateau after hypoxia. These findings suggest that traumatic brain injury may increase hypoxic release of glutamate, contributing to increased vulnerability to hypoxia. Our data suggest that MK-801 may be beneficial in preventing secondary neuronal damages by hypoxia.

Amino Acids↗

PubMed1997

Intraischemic hypothermia during pretreatment with sublethal ischemia reduces the induction of ischemic tolerance in the gerbil hippocampus.

We examined whether mild brain hypothermia during pretreatment with sublethal 2-min ischemia affected the tolerance to subsequent lethal 5-min ischemia. The neuronal densities in the hippocampal CA1 sector of gerbils preconditioned at mild brain hypothermia (32% of normal) were significantly lower than those in gerbils preconditioned at brain normothermia (70% of normal). 72-kDa heat-shock protein immunoreactivity in the CA1 sector preconditioned at mild hypothermia was reduced. These results suggests that mild brain hypothermia during pretreatment with sublethal ischemia reduces the tolerance to subsequent lethal ischemia.

Animals↗

PubMed1997

Intraischemic hypothermia during pretreatment with sublethal ischemia reduces the induction of ischemic tolerance in the gerbil hippocampus.

We examined whether mild brain hypothermia during pretreatment with sublethal 2-min ischemia affected the tolerance to subsequent lethal 5-min ischemia. The neuronal densities in the hippocampal CA1 sector of gerbils preconditioned at mild brain hypothermia (32% of normal) were significantly lower than those in gerbils preconditioned at brain normothermia (70% of normal). 72-kDa heat-shock protein immunoreactivity in the CA1 sector preconditioned at mild hypothermia was reduced. These results suggest that mild brain hypothermia during pretreatment with sublethal ischemia reduces the tolerance to subsequent lethal ischemia.

Animals↗

PubMed1997

Pathologic significance of meningeal enhancement ("flare sign") of meningiomas on MRI.

BACKGROUND: The purpose of this study was to clarify the pathologic features and clinical significance of the meningeal enhancement surrounding meningiomas ("flare sign") on contrast-enhanced T1-weighted magnetic resonance images (MRI). METHODS: The marginal dura mater of tumors was resected from nine cases of meningioma exhibiting a flare sign and used for histopathologic evaluation. RESULTS: Connective tissue proliferation was found in the dura mater in all cases, vascular proliferation was found in three, and tumor cell nests were observed in four cases. In one case, tumor cells were found 4.5 mm from the edge of the tumor. In another case, a meningothelial cell cluster was found. CONCLUSIONS: These results suggest that tumor cell nests are present frequently in dura mater that exhibits the flare sign, and that the dura mater near these lesions should be resected as widely as possible.

Aged↗

PubMed1997

[A case of jugular foramen neurinoma originating from glossopharyngeal nerve].

A 39-year-old man was admitted with right hearing loss, tinnitus and vertigo. Neurological examination on admission revealed right facial palsy, right acoustic nerve disturbance and cerebellar ataxia. CT scan demonstrated a mass with intra-and extracranial extension in the pyramid bone concomitant with enlarged jugular foramen. MRI showed a ring-like enhanced, extra-axial mass in the right CP angle. Cerebral angiography showed no tumor stain. Venous phase of VAG revealed lateral displacement of the right sigmoidal sinus and obstruction of the internal jugular vein. Three dimensional CT was very useful to reveal enlarged jugular foramen. The tumor was resected totally and was approached through a right suboccipital craniectomy and mastoidectomy on July, 1994. Surgery confirmed that the tumor was a neurinoma originating from the glossopharyngeal nerve. After the operation, right facial palsy developed and transient fugitive CSF leakage was observed, but the patient is doing well. There was no amelioration of right hearing loss. JFN originating from the glossopharyngeal nerve is rare. Twenty-five cases of glossopharyngeal neurinoma are reviewed.

Adult↗

PubMed1997

[Dural arteriovenous fistula presenting as acute-onset dementia: a case report].

We report here a unique case of acute-onset dementia caused by a posterior fossa dural arteriovenous fistula (AVF), which was successfully treated by surgical resection of the isolated transverse-sigmoid sinus combined with endovascular procedures. A 70-year-old female was admitted to our hospital with acute-onset dementia and pulsatile tinnitus on the left side. CT scan revealed a low-density area in the parieto-temporal region. Cerebral angiography revealed a dural AVF of the transverse-sigmoid sinus with retrograde drainage into cerebral cortical veins. After transarterial endovascular embolization of the dural AVF, a xenon-CT scan revealed increased cerebral blood flow. Four months postoperatively, however, she was admitted to our hospital again with seizure and aphasia due to recanalizaion of the dural AVF. After trans-arterial embolization, transvenous embolization was attempted, but was unsuccessful due to inaccessibility of the isolated sinus segment. Since this patient could not be cured by endovascular embolization, an open surgical resection of the isolated sinus segment was performed. Following this, CT scans revealed that the low density area present on the first admission had disappeared. The patient's dementia resolved postoperatively. We discuss the pathophysiological mechanism by which venous ischemia due to dural AVF can cause reversible dementia.

Acute Disease↗

PubMed1996

Repeated hyperbaric oxygen induces ischemic tolerance in gerbil hippocampus.

Hyperbaric oxygen (HBO; 100% oxygen at 2 atmospheres absolute) was administered for 1 h to male Mongolian gerbils either for a single session or every other day for five sessions. Two days after HBO pretreatment, the gerbils were subjected to 5 min of forebrain ischemia by occlusion of both common carotid arteries under anesthesia. Seven days after recirculation, neuronal density per 1-mm length of the CA1 sector in the hippocampus was significantly better preserved in the five-session HBO pretreatment group (n = 10: 175.7 (47.8/mm, 54.9% of normal) than in the ischemic control group (n = 10: 26.2 (11.6/mm, 8.0% of normal) and in the single-session HBO pretreatment group (n = 7: 37.3 (21.7/mm, 11.4% of normal). Immunohistochemical staining for the 72-kDa heat-shock protein (HSP-72) in the CA1 sector performed 2 days following pretreatment revealed that the five-session HBO pretreatment increased the amount of HSP-72 present compared with that in the ischemic control group and in the single HBO pretreatment group. These results suggest that tolerance against ischemic neuronal damage was induced by repeated HBO pretreatment, which is thought to occur through the induction of HSP-72 synthesis.

Animals↗

PubMed1996

Delayed neuronal damage following focal ischemic injury in stroke-prone spontaneously hypertensive rats.

We detected the delayed accumulation of 45Ca in the lateral part of the striatum 3 days after distal middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats (SHRSP). However, the mechanism of delayed neuronal damage in the striatum, which is not supplied by the occluded MCA, remains unknown. The aim of this study was to evaluate whether the delayed damage involves alterations in the extracellular release of neurotransmitter monoamines and amino acids. Chronological changes in the distribution of neuronal damage were determined by 45Ca autoradiography. The microdialysis probes were inserted into either the medial or lateral part of the striatum. The dialysate content of monoamines, their metabolites and amino acids was determined by analytical techniques. 45Ca accumulation was detected only in the cortex and corpus callosum by 24 hours postischemia and extended to the pyramidal tract, thalamus and lateral portion of the striatum by 3 days. A 3-fold increase in glutamate content, and a 2-fold increase in dopamine content were observed only in the lateral part of the striatum following ischemia. The results suggest that excessive release of glutamate and dopamine is related to delayed neuronal damage that occurs in the lateral part of the striatum in this ischemic model.

Amino Acids↗

PubMed1996

Immunohistochemical analysis of the nm23 gene product (NDP kinase) expression in astrocytic neoplasms.

The expression levels of nm23-H1 have been reported to correlate with the metastatic potential of some tumours. We have treated a child with a rare case of astrocytoma with diffuse osteoblastic metastases. We therefore decided to examine the expression of the nm23 gene product in 24 gliomas in order to clarify the association of its expression with the clinical features of the disease. A polyclonal antibody against a GST/nm23-H1 fusion protein was raised in rabbits. Twenty-four specimens, including 5 recurrent gliomas and one extraneural metastasis, were obtained from 19 patients treated surgically between 1990 and 1993 in our hospital. Immunohistochemical staining was performed on paraffin sections using an avidin-biotinyl peroxidase complex method. Of the 24 astrocytic neoplasms, 3 (12.5%) specimens from one patient with diffuse bony metastases stained intensely with nm23-H1. Two specimens obtained from glioblastoma multiforme patients stained weakly. The other 19 specimens were negative for nm23-H1 expression. Little or no nm23 expression was observed in adjacent nontumourous cerebral tissues. The results suggest that high levels of nm23 expression might correlate with extraneural metastatic potential in astrocytic neoplasms.

Adolescent↗

PubMed1996

Pontine glioma with osteoblastic skeletal metastases in a child.

BACKGROUND: The development of systemic metastases from primary intracranial gliomas is rare. We report here a rare case of pontine glioma with osteoblastic skeletal metastases. CASE: This 12-year-old boy presented with a 4-month history of hoarseness, dysphagia, and a progressively ataxic gait. Cranial computed tomography (CT) and magnetic resonance imaging (MRI) revealed a brain stem tumor that was diagnosed as a low grade glioma by stereotactic biopsy. Twelve months later following chemotherapy and radiotherapy, neurologic examination and neuroradiologic studies disclosed a recurrence of the pontine glioma. Skeletal roentgenograms revealed widespread osteoblastic metastases in the skull, vertebral bodies, pelvis, and long bones. A specimen from the iliac bone demonstrated cells that were immunoreactive glial fibrillary acidic protein (GFAP). DISCUSSION: The mechanism of how glioma cells determine their biologic behavior at bony metastatic sites is not known. Infratentorial gliomas, which occur frequently in young patients and demonstrate active bony metabolism, may stimulate osteoblastic cells, and induce osteoblastic changes.

Bone Neoplasms↗

PubMed1996

Fatal subarachnoid hemorrhage from an inflammatory cavernous carotid artery aneurysm: failure of conservative treatment after early diagnosis--case report.

Inflammatory carotid artery aneurysm is a rare complication of acute paranasal sinusitis. A 50-year-old female presented with a ruptured giant carotid artery aneurysm secondary to infection of the sphenoid sinus and cavernous sinus. She had been healthy until 5 days before admission, when she developed orbital phlegmon and meningitis. She received antibiotic therapy for 10 days. Computed tomography (CT) of the brain 2 days after admission showed no abnormality. However, repeat CT on day 6 showed a round isodense mass in the suprasellar cistern suggesting a cerebral aneurysm. Twelve days after admission, she suffered a fatal subarachnoid hemorrhage. Cerebral angiography revealed a giant left cavernous carotid artery aneurysm with a very irregular shape. Autopsy found sphenoid sinusitis and osteomyelitis extending into the cavernous sinuses. Diagnosis of bacterial inflammatory aneurysms before rupture is very important. Appropriate surgical intervention should be considered if there is enlargement of the original aneurysm or appearance of a new aneurysm indicating a potentially dangerous situation.

Anti-Bacterial Agents↗

PubMed1995

Stable prostacyclin improves postischaemic microcirculatory changes in hypertensive rats.

The prostacyclin analogue TTC-909 is incorporated in lipid microspheres and is chemically very stable. We examined the efficacy of TTC-909 on cerebral microcirculation following focal cerebral ischaemia. Focal cerebral ischaemia was produced by the occlusion of the distal middle cerebral artery in stroke-prone spontaneously hypertensive rats. Intravenous administration of TTC-909 (100 ng/kg/day) or vehicle was started 30 minutes after the occlusion and repeated for 7 days. On day 7, cerebral blood flow and blood-brain barrier permeability were measured autoradiographically. Brain oedema was estimated by the gravimetric method. The size of the infarction was calculated from area measurements on serial histologic sections. Treatment with TTC-909 resulted in significant improvement in regional blood flow in the ischaemic rim (p < 0.01) and the surrounding area (p < 0.05). With TTC-909 treatment, the increased permeability was significantly reduced in the ischaemic centre (p < 0.01) and rim (p < 0.05). A decrease in specific gravity in the ischaemic region and the remote non-ischaemic regions was prevented by the treatment (p < 0.01). We assumed that the efficacy of TTC-909 maintains the blood supply in the ischaemic area, improves disruption of the blood-brain barrier and prevents development of ischaemic oedema.

Animals↗

PubMed1995

Cerebral blood flow and glucose metabolism of the ischemic rim in spontaneously hypertensive stroke-prone rats with occlusion of the middle cerebral artery.

To determine acute postischemic metabolic changes of the ischemic rim under conditions of poor collateral circulation, we examined cerebral blood flow and glucose metabolism in the area of the brain around the ischemic tissue in 36 male spontaneously hypertensive stroke-prone rats (SHRSP) in the acute stage of focal ischemia. The right middle cerebral artery (MCA) was occluded dorsal to the rhinal fissure. Four hours after occlusion, local cerebral blood flow (LCBF), glucose content (LCGC), and glucose utilization (LCGU) were measured by quantitative autoradiographic techniques. The lumped constant was determined from the corresponding LCGC. LCBF showed a widespread and marked decrease in the cortex surrounding the ischemic core, in the thalamus, and in the medial portion of the striatum in the MCA-occluded hemisphere, while the lateral segment of the striatum showed an increase of 36%, compared with findings on the contralateral side. LCGC showed little regional variation, but there was an increase of 38% in the zone bordering the ischemic area. LCGU at the cortex surrounding the ischemic core and in the external capsule showed an increase of 55%. The cortex surrounding the ischemic core, the thalamus, and the lateral segment of the striatum in the MCA-occluded hemisphere showed significant decreases in LCGU. It has been speculated that a high accumulation of glucose reflects a demand for glucose for anaerobic glycolysis in the border areas and that such a demand is probably greater in cases of impaired oxygen delivery due to the presence of microcirculatory disturbances in the MCA-occluded SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Immediate cerebrovascular responses to closed head injury in the rat.

Changes in cerebrovascular dynamics were investigated immediately after closed head injury in the rat using a newly developed closed head injury model developed by Marmarou et al. Intracranial pressure (ICP) and mean arterial blood pressure (MABP) were monitored before and after trauma. Regional cerebral blood flow (rCBF), regional cerebral plasma volume (rCPV), and blood-brain barrier (BBB) permeability were measured autoradiographically with iodo[14C]antipyrine [14C]sucrose, and [alpha-14C]aminoisobutyric acid, respectively. rCBF responses to induced hypertension after trauma were measured by laser-Doppler flowmetry to investigate the status of autoregulation. Before injury, baseline ICP values ranged from 6 to 10 mm Hg in all animals. Immediately after trauma, ICP increased synchronously with MABP to > 100 mm Hg and then rapidly returned to baseline values: MABP increased rapidly by 20% after trauma and returned to baseline values within 30 sec. At 30 sec after injury, a significant increase in rCBF was observed in five subcortical regions (p < 0.05), and a significant increase in rCPV was observed in the frontal cortex, parietal cortex, thalamus, and hypothalamus (p < 0.05). At 10 min after injury, BBB permeability (the transfer constant for [alpha 14C]aminoisobutyric acid) was < 0.1 mL/kg/min for all regions except those with a relatively permeable BBB, for example, median eminence, choroidal plexus, pineal body, and pituitary gland. Induced hypertension resulted in a prolonged increase in rCBF after trauma. Thus, in this closed head injury model, which is not associated with marked hypertension or prolonged BBB disruption, widespread increases in rCBF and impaired cerebral autoregulation were apparent immediately after injury.

Animals↗

PubMed1995

In vivo studies of extracellular metabolites in the striatum after distal middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: We demonstrated in a previous study that 45Ca accumulation in the lateral part of the striatum was detected 3 days after distal middle cerebral artery (MCA) occlusion using a 45Ca autoradiographic technique in stroke-prone spontaneously hypertensive rats. However, the mechanism of delayed neuronal damage that occurred in the lateral part of the striatum is unknown. We examined changes in amino acids and monoamines in the striatums of rat brains after MCA occlusion in stroke-prone spontaneously hypertensive rats using an in vivo brain microdialysis technique. METHODS: Microdialysis probes were inserted into the lateral or medial part of the striatum 24 hours before the experiment. The dialysis probe was perfused continuously at 2 microL/min with Ringer's solution, and the dialysate samples were collected every 20 minutes. After a 3-hour period for baseline stabilization, the right MCA was occluded. The dialysate count of monoamines and amino acids was determined by high-performance liquid chromatography. RESULTS: After MCA occlusion, a threefold transient increase in glutamate was observed in the lateral part of the striatum. The level returned to its baseline value 60 minutes after MCA occlusion. Dopamine in the lateral part increased twofold to its peak value. This release persisted for 2 hours after MCA occlusion. There were no significant changes in these components in the extracellular fluid of the medial part of the striatum. CONCLUSIONS: Our study demonstrated that changes of neurotransmitters in the lateral part of the striatum after MCA occlusion differed from those in the medial part. These results suggest that excessive release of glutamate and dopamine is related to delayed neuronal damage that occurs in the lateral part of the striatum in this model.

Animals↗

PubMed1995

[A penetrating injury of the extracranial vertebral artery: a case report].

Penetrating injury to the vertebral artery is a very rare accident and no case except ours has been reported to date in Japan. We reported a case of successful treatment of a penetrating injury by a nail to the left vertebral artery with the use of interventional radiologic procedure. A 27-year-old man was admitted to our hospital with a complaint of penetrating injury in his neck. Left vertebral angiography revealed that a nail had penetrated into the vertebral artery at the C6 level. Considering the possibility of thrombus formation around the metallic foreign body and the risk of uncontrollable bleeding, we performed embolization of the injured vertebral artery with Interlocking Detachable Coil.

Adult↗