Biomedical subjects
Publications and source records attributed to H Kuyama.
We have proposed a field-inversion electrophoresis on a microchip for a shorter effective length, and investigated the external frequency for the DNA analysis based on the field-inversion electrophoresis device. By using the optimized frequency, we demonstrated that the field-inversion electrophoresis has great potentials for the separation of DNA fragments with shorter effective length.
The therapeutic significance of moderate hypothermia and cerebral monitorings was assessed in the 10 patients with severe head injury. Cooling was begun as soon as possible after admission, using water blankets under general anesthesia. Jugular venous or tympanic temperature of patients was maintained at 32 degrees C for 3 to 5 days, then rewarming at the rate of 1 degree C a day was started. The intracranial pressure was controllable less than 20 mmHg under hypothermia. Moderate hypothermia reduced the jugular venous lactate (33.5%) as well as the cerebral blood flow velocity at M1 portion of middle cerebral artery (CBFV-M1) measured by transcranial Doppler (7.2%), while increase of the jugular venous oxygen saturation (SjO2) (17.9%) was observed in a majority of the patients. Our results demonstrated that moderate therapeutic hypothermia significantly reduced cerebral circulation and metabolism. Measurement of SjO2 and CBFV-M1 seems to be useful for estimation of cerebral circulation and metabolism in therapeutic hypothermia.
A 41-year-old man presented with subarachnoid hemorrhage (SAH) caused by a cervical spinal cord hemangioblastoma. There were no features to distinguish the SAH from that due to an intracranial lesion. The diagnosis was established by cerebral angiography, computed tomography, and magnetic resonance imaging. The tumor was located in the right dorsolateral aspect of the cervical spinal cord. Hemilaminectomy was performed, and the tumor was completely removed. No postoperative neurological deficit was observed. The possibility of a spinal origin for SAH should be considered if no cranial origin can be detected.
We examined the effect of orally administered OPC-21268, a nonpeptide Arginine Vasopressin V1 receptor antagonist, on cold induced vasogenic brain edema in rat. Cold brain injury was induced by applying a copper rode cooled with liquid nitrogen for one minute. To mimic clinical use, one hour after induction of the cold lesion, rats were treated with orally administered OPC-21268 at doses of 100 mg, 200 mg, and 300 mg/kg every 8 hr for 24 hours. Two percent Evans blue in saline, in a volume of 1 ml/kg was given intravenously prior to cold injury. Twenty four hours after induction the cold lesion, brain water, brain tissue electrolytes, and plasma osmolality and electrolytes were measured. Quantitative evaluation of BBB permeability was performed using the Evans blue fluorescence method. The injury resulted in significant increases in the brain water and brain tissue sodium, and Evans blue concentration in both the lesioned and contralateral hemispheres (p < 0.01). OPC-21268 at doses of 200 mg and 300 mg/kg significantly decreased brain water and Evans blue concentrations in both the lesioned and contralateral hemispheres (p < 0.01). Brain tissue sodium content was significantly reduced at a dose of 300 mg/kg in the lesioned side (p < 0.05). There were no significant changes in other parameters throughout the experiments. Our results indicate that OPC-21268 exerts a protective effect in areas where the maximal amount of BBB breakdown occurs.
RU 51599, a selective kappa opioid agonist which is a potent aquaretic, was studied for its effect on acute intracranial hypertension. In ketamine anesthetized cats acute intracranial hypertension was induced by progressive inflation of an epidural balloon with physiological saline at a constant rate of 0.5 ml/hr for three hours. In the control group (n = 8), the balloon was maintained inflated for another an hour after which it was deflated. In the post deflation period monitoring was continued for one hour. In the treatment group (n = 8), cats were treated by an intravenous (i.v.) injection of RU 51599, at a dose of 1 mg/kg every hour at the beginning of balloon inflation, during balloon inflation, at the completion of inflation, and after deflation. Changes in intracranial pressure (ICP), mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), blood gases, serum electrolytes and osmolality, and brain water content water content were studied in both groups. In the control group, epidural brain compression resulted in significant increases in the mean ICP up to 80.7 +/- 9.8 mmHg at 3 hrs (during balloon inflation), 68.6 +/- 8.3 after complete inflation, and 62.1 +/- 11.4 mmHg after deflation (P < 0.01), and significant decreases in CPP to 55.5 +/- 14.0 mmHg at 3 hrs (during balloon inflation), 43.0 +/- 11.2 mmHg after inflation, and 36.3 +/- 9.9 mmHg after deflation (P < 0.01). In the treatment group there were significant decreases in the mean ICP to 35.2 +/- 6.8 mmHg at 3 hrs (during balloon inflation), 32.3 +/- 7.9 after inflation, and 16.1 +/- 3.6 mmHg after deflation (P < 0.01), and significant increases in CPP to 103.2 +/- 6.1 mmHg at 3 hrs (during balloon inflation), 109.0 +/- 8.8 mmHg after inflation, and 102.7 +/- 8.2 mmHg after deflation (P < 0.01). Brain water content was also significantly reduced (P < 0.05). There were no significant changes in the serum electrolytes and osmolality throughout the experiments. Our results suggest that, the mechanism by which RU 51599 reduces ICP is related to reduction in the brain water content.
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Systemic and focal cerebral acidosis is considered deleterious to cell metabolism and neuronal recovery. We investigated the immediate effect of tris-(hydroxymethyl)-aminomethane (THAM), an alkalizing agent, on focal cerebral ischemia produced by occlusion of the left middle cerebral artery (MCA) in cats with systemic acidosis. Occlusion of MCA resulted in prompt decreases in local cerebral blood flow of the ipsilateral marginal and ectosylvian gyri from 47.7 ml/100 g per minute in control to 32.3 ml/100 g per minute and 8.3 ml/100 g per minute, respectively. In the control group, physiological saline was infused continuously and the treated group received 0.3 M THAM to normalize systemic and focal cerebral acidosis. There were no significant changes in the systemic arterial pressure, arterial PO2 and PCO2 throughout the experiments in the two groups. Arterial pH decreased from 7.42 to 7.30 in the control, while it remained normal during THAM treatment. Extracellular pH of the marginal gyrus (peri-infarct zone) decreased from 7.39 to 6.87 with 6 h ischemia in the control group. In THAM infusion, extracellular pH was kept between 7.26 and 7.29, which was significantly higher than the control group. THAM significantly decreased infarct volume and lactate and water contents of the gray matter in the marginal gyrus at 6 h after occlusion. It is concluded that THAM infusion immediately after ischemia onset is considered effective in improving acidosis at the site of ischemic penumbra and consequently reduces lactate production, brain edema, and infarct volume.
An attempt at transarterial balloon embolization of a traumatic carotid cavernous fistula was made but the carotid artery rent was too small for this approach. The patient was then treated by antegrade embolization through a superior ophthalmic vein using mechanical detachable coils. Successful obliteration of the fistula was achieved with preservation of the carotid artery. Transvenous embolization is an alternative technique to treat patients with traumatic carotid cavernous fistulas, especially when a transarterial approach has failed.
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Intraoperative radiotherapy (IORT) was performed in 20 of 36 patients with glioma; 11 glioblastomas, 7 malignant astrocytomas, 2 benign astrocytomas. Twenty or 25 Gy of irradiation was delivered in a single fraction intraoperatively, followed by external beam irradiation. The electron beam energy was selected so that the 80% isodose line fell at 2 or 3 cm below the residual tumor surface. Median survival time of IORT group was 14 months and that of the control group was 10 months. Difference of survival curve was significant. There were 6 incidences of complication caused by IORT; 1 radionecrosis, 1 convulsion, 1 abscess, and 3 severe brain edemas. IORT is suited for the treatment of malignant gliomas.
BACKGROUND: Intraarterial chemotherapy with carboplatin for malignant gliomas has been tried recently, but its therapeutic efficacy and toxicity have not yet been elucidated. METHODS: We treated patients with malignant glioma by intraarterial chemotherapy using carboplatin, and compared the efficacy as well as the side effects with intraarterial ACNU. RESULTS: Twenty patients were treated with carboplatin (300 mg/m2) and 22 patients were treated with ACNU (80-200 mg/m2). Response (complete remission+partial response) rate for carboplatin was 12.5% compared to 45% for ACNU. Despite higher response rate for ACNU, the difference in the survival curves of the two groups was not significant. Three patients who were treated with high dose (150-200 mg/m2) of ACNU developed hemiparesis and aphasia. Seven patients treated with carboplatin developed 10 incidences of neurotoxicities; two hemiparesis, one aphasia, one blindness, one visual field disturbance, three convulsions, and two developed incidences of disturbances of consciousness. CONCLUSIONS: Intraarterial carboplatin was not superior to intraarterial ACNU in achieving remissions, and showed much greater tendency to produce neurotoxicities.
A case of neurinoma from the spinal accessory nerve which is located in the cisterna magna is reported. A 54-year-old woman was admitted to the institute in 1990 with complaints of headache, nausea and ataxic gait for several months. Plain CT showed dilation of the lateral ventricles and a mass of lower density in the cisterna magna. The capsule and septa of the mass were enhanced with contrast medium. MRI showed the mass was low intense on T1-weighted images and high intense on T2-weighted images. Gadolinium visualized the mass multicystic. V-P shunt was performed before tumor resection. Through suboccipital craniectomy and C1 laminectomy the tumor was removed. The tumor had a long neck attached to the right spinal accessory nerve and extended to the cisterna magna.
We determined the effect of a centrally administered V1 receptor antagonist of arginine vasopressin on the brain water content in an animal model of vasogenic brain edema. Using adult rats, a cold injury was induced in the left hemisphere of the brain by applying a frozen copper rod. 50 ng of V1 receptor antagonist was administered into the left lateral ventricle 10 minutes prior to and/or 1 hour after injury. Twenty four hours after the cold injury, the brain water and sodium contents and plasma osmolality were measured. The V1 receptor antagonist significantly suppressed the increase of the brain water and sodium contents in the cortical structure adjacent to the lesion without any changes in plasma osmolality. Our results demonstrate the effectiveness of a V1 receptor antagonist of vasopressin on vasogenic brain edema.
We investigated the immediate effect of tris (hydroxymethyl) aminomethane (THAM) and NaHCO3 on focal cerebral ischemia produced by occlusion of the left middle cerebral artery (MCA) in cats. The animals were divided into three groups. In the control group, physiological saline was infused continuously. The THAM and NaHCO3 groups received continuous administration of 0.3 mol THAM and 7% NaHCO3, respectively, to normalize arterial pH. Local CBF measured in the marginal and suprasylvian gyri decreased less than 30 ml/100 g/min after the MCA occlusion and there were no significant differences among the three groups. Extracellular pH of the marginal gyrus (peri-infarct zone) decreased from 7.21 to 6.86 in the control group. However, extracellular pH did not show significant changes in the THAM and NaHCO3 groups. Intracellular pH of the infarct area decreased from 7.23 to 6.13 in the control group within 6 hours after occlusion. THAM had a tendency to normalize intracellular pH compared with that in the control and NaHCO3 groups. THAM significantly (p < 0.05) decreased water content of the gray matter in the marginal gyrus at 6 hours after occlusion and the infarct size compared with those in the control and NaHCO3 groups. Therefore, normalization of systemic and perifocal acidosis with THAM is effective for reducing cortical edema and infarct size in the early stage of focal cerebral ischemia probably due to the improvement of intracellular acidosis.
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Using a newly devised model of dural sinus occlusion, we investigated the pathophysiology of venous haemorrhage as well as venous circulatory disturbance. The superior sagittal sinus (SSS) and diploic veins (DV) were occluded in 16 cats. Intracranial pressure (ICP), cerebral blood volume (CBV) and regional cerebral blood flow (rCBF) were measured for 12 hours after the occlusion. At the end of the experiment, cerebral water content was estimated. In another 8 cats additional occlusions of cortical veins were carried out. In both groups, the blood-brain barrier permeability was evaluated with Evans blue or horseradish peroxidase. The SSS and DV occlusion produced a significant increase in ICP and CBV concomitant with a significant decrease in rCBF. Cerebral water content also increased significantly. However, there was no transition of Evans blue and horseradish peroxidase through the cerebral vessels, and no haemorrhages could be observed. In contrast, the additional occlusion of cortical veins produced haemorrhagic infarctions with Evans blue extravasation in 6 out of the 8 cats. These data suggest that dural sinus occlusion may lead to an increase in CBV and cerebral water content resulting in intracranial hypertension and decreased rCBF. The brain oedema in this model seemed to be mainly hydrostatic oedema, and might also be contributed by cytotoxic oedema. The additional occlusion of cortical veins might be essential in the development of haemorrhage in this model, and the blood-brain barrier was also disrupted in these areas.
The authors describe the first reported case of dissecting aneurysm presenting with hemifacial spasm. The patient was a 58-year-old woman with left hemifacial spasm of 2 years' duration. Cranial nerve examination was otherwise normal and no other clinical symptoms were observed. Vertebral angiography revealed a fusiform enlargement of the left vertebral artery and contrast medium remaining in the intramural false lumen in the venous phase. Microvascular decompression of the facial nerve with wrapping of the aneurysm resulted in complete relief of the hemifacial spasm.
This study was carried out to study the effect of stimulation of the reticular formation of the medulla oblongata on intracranial pressure (ICP) and cerebral blood volume (CBV) in injured brain with increased ICP. CBV was measured by the photoelectric method from the parietal lobe. Seventeen hours prior to the experiments, cold induced edema was produced to increase basal ICP. In 15 cats, electric stimulation produced temporary increases in BP, ICP and CBV and progressive intracranial hypertension was never observed (Group A). In 9 animals, progressive increases in CBV and ICP up to 50 to 100 mmHg were evoked after cessation of stimulation (Group B). Prestimulation ICP in Group B was significantly higher than that of Group A. Rapid and simultaneous increases in ICP and CBV following stimulation strongly suggested that global increments of CBV secondary to loss of cerebral vasomotor tonus were responsible for producing progressive intracranial hypertension. In Group B, the stimulation electrodes were invariably located at the area of the nucleus reticularis parvocellularis and gigantocellularis. Our experimental results show that in increased ICP a stimulated or irritable condition of the medullary reticular formation will cause acute progressive intracranial hypertension.