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Biomedical subjects

H Mogami

Publications and source records attributed to H Mogami.

At least 235 records · Page 13Linked to original sources
PubMed1983

[Intracranial hypertension].

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.

Brain Neoplasms↗
PubMed1982

Distribution of bleomycin in ethylnitrosourea-induced gliomas in rats.

We used a microbioassay to study the distribution of bleomycin in rat brain tumors induced in newborn Sprague-Dawley rats with 1-ethyl-1-nitrosourea (ENU, 50 mg/kg s.c.). Upon suspected successful tumor induction bleomycin (0.1 g/kg i.v.) was administered, and 2 hr later bleomycin concentrations in major organs and tumor tissues were bioassayed using Bacillus subtilis PCI 219 IMC. To determine their histology, the tumors were stained by the immunofluorescence- or immunoperoxidase method using antiserum to astroprotein in addition to the conventional staining methods. There were 11 gliomas each of the brain and spinal cord, 14 schwannomas of the trigeminal nerve and 4 adenomas of the pituitary gland; they developed within 8 (gliomas), 7.3 (schwannomas) and 15 (adenomas) months on average after ENU treatment. The bleomycin concentration and the tumor:plasma concentration ratio were 7.69 +/- 2.84 micrograms/g and 0.13 +/- 0.05 (brain gliomas), 7.10 +/- 3.15 micrograms/g and 0.27 +/- 0.12 (spinal cord gliomas), 5.40 +/- 1.41 micrograms/g and 0.23 +/- 0.05 (schwannomas), 4.83 +/- 1.05 micrograms/g and 0.21 +/- 0.08 (adenomas). Normal brain- and spinal cord tissues scarcely contained bleomycin.

Animals↗
PubMed1982

Cellular level of purine compounds in ischemic gerbil brain by high performance liquid chromatography.

The cellular level of AtP and related compounds in ischemic gerbil brain was investigated by high performance liquid chromatography (HPLC). Brain samples were obtained in situ following ligation of the common carotid artery. AMP and ADP peaks in the brain extracts in the ischemic group became much larger whereas the ATP peak decreased dramatically. The most striking finding was an extensive increase of adenosine: 50-100 fold. The levels of inosine and hypoxanthine also increased greatly in typical symptomatic gerbil.

Adenine Nucleotides↗
PubMed1982

Quantitative autoradiographic measurements of blood-brain barrier permeability in the rat glioma model.

Quantitative autoradiographic technique was applied in measuring blood-brain barrier (BBB) permeability of autochthonous gliomas in rats. In small tumors (less than 2 mm in diameter), no increase in BBB permeability was noted. As the tumor grew and neovascularization occurred, BBB permeability increased in the center of the tumor, and it was suggested that the BBB was partly disrupted in the neovascularized vessels. In the fully grown tumors, BBB permeability was markedly increased in the viable part of the tumor to levels similar to the choroid plexus. Yet, the BBB was partly preserved at the periphery of the tumor and in the brain adjacent to the tumor. The heterogeneity of the BBB phenomenon according to the stage of tumor growth may be a major obstacle for uptake of chemotherapeutic drugs that do not cross the BBB easily.

Animals↗
PubMed1982

[Combined effect of intravenous hyperalimentation and chemotherapy on experimental meningioma].

Combination effects of intravenous hyperalimentation (IVH) and chemotherapy were studied in rats with meningeal carcinomatosis. Sprague-Dawley rats were inoculated intracisternally with 1 X 10(4) Walker 256 carcinosarcoma cells. Animals were divided into five groups of 10 to 12 animals per group: 1) no treatment; 2) cyclophosphamide 30 mg/kg i.v. at 5 days after tumor inoculation (Day 5); 3) IVH (Day 5 to Day 10); 4) cyclophosphamide (Day 5) and IVH (Day 5 to Day 10); and 5) cyclophosphamide (Day 5) and IVH (Day 10 to Day 15). The group of IVH alone reduced survival time significantly (p less than 0.001) compared with no treatment group. Cyclophosphamide alone increased survival time significantly (p less than 0.001) in comparison with no treatment group. Combination of cyclophosphamide (Day 5) and IVH (Day 5 to Day 10) did not prolong survival time compared with cyclophosphamide alone. However, IVH (Day 10 to 15) in combination with cyclophosphamide (Day 5) prolonged survival time significantly (p less than 0.001) in comparison with cyclophosphamide alone. Mean body weight was reduced maximally at 5 to 10 days after cyclophosphamide injection. However, no reduction of body weight was noted while animals were on IVH. The present data appears to indicate that IVH may reduce the side effects of cyclophosphamide and may prolong the survival time.

Animals↗
PubMed1982

[Local cerebral glucose utilization in the ethylnitrosourea-induced rat glioma].

Local cerebral glucose utilization (LCGU) of anesthetized rats bearing ethylnitrosourea (ENU)-induced gliomas was studied with 14C-deoxyglucose autoradiography. Single subcutaneous injection of ethylnitrosourea (50 mg/kg) was made to the newborn rats, and animals were used for experiment at 150 to 300 days after birth. Under ketamine anesthesia, 14C-deoxyglucose was injected through a venous catheter, and timed arterial sampling was made. Brains were removed at 45 min after injection, and prepared for macro-autoradiography. LCGU values were measured by the equation developed by Sokoloff et al. In the microtumors (less than 2 mm in diameter), mean LCGU value was 30 mumol/100 g/min, which was significantly (p less than 0.01) lower than mean value of normal cortex (63 mumol/100 g/min). In the macrotumors (greater than 2 mm in diameter). LCGU values in the tumor were separated to high part (mean; 49 mumol/100 g/min) and low part (mean; 38 mumol/100 g/min), which were still lower than mean cortical value and higher than mean white matter value (corpus callosum; 26 mumol/100 g/min). No LCGU changes were noted in the brain tissue adjacent to the microtumors. Whereas, macrotumor significantly reduced LCGU in the adjacent cortex. The present data may indicate that glucose metabolism of the ENU induced glioma and edematous peritumoral brain tissue is lower than that of normal cortex.

Animals↗
PubMed1981

Alteration of blood-CSF barrier by tumor invasion into the meninges.

Cyclophosphamide and 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) were found to have an equivalent cytostatic effect in rats with subcutaneous transplants of Walker 256 carcinosarcoma. Rats with meningeal carcinomatosis received a single intravenous dose of cyclophosphamide (30 mg/kg) or ACNU (15 mg/kg) at various times after intracisternal inoculation of 1 X 10(4) Walker 256 carcinosarcoma cells. Cyclophosphamide, administered 1 day after tumor inoculation, failed to prevent tumor growth in the subarachnoid space. The survival time of these rats was prolonged only 10% to 14% compared to the controls, while ACNU produced a maximum increased survival time of 180%. If administered 2, 3, 4, and 5 days after tumor inoculation, both drugs were effective; cyclophosphamide yielded a maximum increase in median survival time of 109%, 94%, 90%, and 52%, and ACNU 127%, 139%, 240%, and 100%, respectively. These results indicate that the blood-cerebrospinal fluid (CSF) barrier was circumvented in the early stage of subarachnoid tumor growth, although some areas remained where the infiltrating tumor cells were protected from systemically administered drugs by the intact barrier.

Animals↗
PubMed1981

Regional blood flow and capillary permeability in the ethylnitrosourea-induced rat glioma.

Regional cerebral blood flow and capillary permeability of rat brains bearing ethylnitrosourea-induced gliomas of various size were investigated with 14C-antipyrine autoradiography and Evans blue staining. In the small tumors (less than 2 mm in diameter), blood flow was uniformly reduced when compared to the adjacent brain. Even in tiny tumors (0.3 to 0.4 mm in diameter), reduction in blood flow was evident. In the medium (2 to 4 mm in diameter) and large (greater than 4 mm in diameter) tumors, the blood flow increased or decreased depending on the part of the tumor examined. The necrotic center and peripheral edge had low blood flows, whereas the viable portion adjacent to the necrotic center had high blood flows. Blood flow in the brain tissue adjacent to medium and large tumors was lower than control brain tissue, probably due to local edema. Leakage of intravenous Evans blue in the tissue was only evident in the large tumors with central necrosis. The present findings suggest that neovascularization of the tumor may occur when the tumor reaches a certain size, and leaky new vessels may be the cause of brain edema associated with tumor.

Animals↗
PubMed1981

[Changes of blood-brain barrier in the ethylnitrosourea induced rat glioma (author's transl)].

Capillary permeability of rat brains bearing ethylnitrosourea induced rat glioma was measured with quantitative autoradiography. In the small tumors (less than 2mm in diameter), no changes in capillary permeability was noted. When tumors became larger and neovascularization of the tumor occurred, increase in capillary permeability was evident. This change was more prominent in the center of the tumor than in the periphery. In the large tumors, the capillary permeability was markedly increases, and the value was similar to that in the choroid plexus. This indicates that blood-brain barrier(BBB) completely disappeared in the large tumors. This BBB change may be the main cause of tumor induced brain edema. The data also provide the information about pharmacokinetics of water soluble drugs in the brain tumors.

Animals↗
PubMed1981

[Regional blood flow in the ethylnitrosourea induced rat glioma (author's transl)].

Regional cerebral blood flow of rat brains bearing ethylnitrosourea induced glioma of various size was investigated with 14C-antipyrine autoradiography. In the small tumors (less than 2 mm in diameter), blood flow was uniformly reduced when compared to the adjacent brain. Even in tiny tumors (0.3-0.4 mm in diameter), reduction in blood flow was evident. In the medium (2-4 mm in diameter) and large (greater than 4 mm in diameter) tumors, the blood flow increased in the viable center of the tumor and decreased in the necrosis and peripheral edge. High blood flow in the viable center may be attributable to the neovascularization of the tumor. Blood flow in the brain tissue adjacent to medium and large tumors was lower than control brain tissue probably due to local edema. This reduction in blood flow may be partly attributable to the appearances of the focal neurologic deficits. The result obtained may provide some information about growth regulation of glioma and also pharmacokinetic delivery of chemotherapeutic drugs to the malignant brain tumors.

Animals↗