[Sites of arterial occlusion in the brain of cerebral infarct].
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Biomedical subjects
Publications and source records attributed to J Ogata.
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The relationship of the vascular changes to the cerebral lesions has been studied using serial sections of the brains from five cases of the stroke-prone spontaneously hypertensive rats. Infarction was observed in a form of microinfarct related to single or plural occluded arterioles in the brain and subarachnoid space. Though most arterioles with fibrinoid necrosis of the wall were occluded with thrombus, infarct, which was obviously related to the occluded arterioles, was verified only in a few occasions. It was proved that infarction did not develop in all the areas irrigated by the occluded arterioles, and the regional circulation was assumed to have been maintained by the collateral circulation. There was rarefaction of the neutrophil with preservation of the neurons in the cortex around the vascular changes, such as fibrinoid necrosis of the wall. Widespread rarefaction and cyst formation were observed in the subjacent white matter, which were more marked in the vicinity of the vascular changes in the cortex. These histological changes were interpreted to be the tissue degeneration secondary to edema.
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Changes of the internal (d) and external diameter (D) of cerebral arteries in response to the various levels of arterial pCO2 were studied in anesthetized rats, of which brains were frozen in situ with isopentane cooled in liquid nitrogen. The parietal cortex was fixed with osmium tetroxide and stained with toluidine blue for morphometry of the cerebral arteries. In comparison with control animals (pCO2 = 41.2 mm Hg), the d/D ratio in animals with hypercapnia (pCO2 = 69.9 mm Hg) was increased by 11.7% in the pial arteries and 7.9% in the cortical arteries, indicating vasodilatation. In contrast, the d/D ratio in those with hypocapnia (pCO2 = 27.7 mm Hg) was decreased by 6.2% and 13.0%, respectively, indicating vasoconstriction. There was a significant linear correlation existing between the d/D ratio of either pial or cortical arteries and pCO2. It is concluded that the cortical arteries respond to changes of arterial pCO2 in a similar manner to the pial arteries.
A pathological study of the brain of the stroke-prone spontaneously hypertensive (SHRSP) rats revealed development of fibrinoid necrosis of the wall of the intracerebral arterioles. These arterioles were frequently accompanied by occlusion of the lumen, and occasionally intracerebral hemorrhages and mincroinfarcts. The predominant tissue alteration consisted of rarefaction and cyst formation in the white matter, and rarefaction of the neuropil and preserved neurons in the neocortex at the paramedian region of the cerebral hemispheres. Edema fluid was present in and around the lesions. The tissue degeneration can be interpreted to be the sequela of brain edema. Microinfarcts or hemorrhages are only focal lesions, and are assumed to have minor contribution to the brain swelling. Widespread expansion of the extracellular space is assumed to be responsible for the brain swelling. Overall vascular changes of the brain, kidney, and other organs were consistent with those found in malignant hypertension.
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A new method for pelvic arteriography using a disposable elastic vein needle is presented. The technique is carried out by percutaneous transfemoral artery puncture and contrast medium is injected by a power air-driven injector which makes bilateral pelvic arteriography possible. Neither a radioopaque long catheter nor a guide wire are necessary in the present method. No major complications have been observed in a series of 162 cases. The present method is advantageous due to its simplicity and safety compared with ordinary Seldinger's method which is not always free of complications.
An uptake of fluorescein isothiocyanate labeled neocarzinostatin into normal and cancerous epithelial cells from bladder was investigated. Results showed that neocarzinostatin traversed the cell membrane into cytosol and nuclei, and it appeared to have a preferential cytotoxicity for the cancer cell.
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The effects of antihypertensive treatment on brain metabolism after bilateral carotid occlusion were studied in spontaneously hypertensive rats. The results indicate that an increase in metabolites of ischaemic brain such as lactate and the lactate/pyruvate ratio after carotid occlusion in spontaneously hypertensive rats is apparently suppressed by treating hypertension. This suggests that hypertension may play an important role in susceptibility to cerebral ischaemia.
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A 41-year-old Japanese male with a new type of primary familial amyloidosis was reported. The patient developed vitreous opacities, and later, disturbances in the gastrointestinal and nervous systems. At autopsy, amyloid was observed in the vitreous and the retinal vessels. There were extensive cerebral infarcts and heavy meningo-vascular amyloid deposition. Although the postmortem study revealed slight peripheral nerve degeneration in the lower extremities secondary to amyloid deposition, there was no clinical evidence of polyneuropathy.
An unusual case of fungus ball formation of Aspergillus in the bladder without any evidence of disseminated and renal aspergillosis is presented. A 49-year-old man whose chief complaint was progressively worsening dysuria after a stomach operation was admitted. Cystoscopy revealed many ball-like masses on the retrotrigone and left wall. Histological studies showed that these masses were composed of many Aspergilli. The uniqueness of the case and the route of infection are discussed.
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The injection of clinical doses of neocarzinostatin (NCS) in guinea pigs did not result in antibody formation as judged by immunoelectrosyneresis, micro-Ouchterlony agar diffusion, fluorescence polarization, and passive cutaneous anaphylaxis reaction. This confirmed previous work on passive hemagglutination and passive cutaneous anaphylaxis reaction in a heterocytotropic system in guinea pigs. Forty-eight serum samples from 28 patients who were previously treated with NCS alone (8--161 mg) for a period of 8-85 days did not show any sign of antibody formation as revealed by immunoelectrosyneresis, micro-Ouchterlony agar diffusion, and fluorescence polarization techniques. In a homocytotropic system, the passive cutaneous anaphylaxis reaction was carried out with sera of sensitized guinea pigs and test guinea pigs which revealed that no IgE and IgA antibody to NCS was present in the sensitized sera. Those patients with bladder cancer who did not respond to NCS therapy or exhibit any side effects even after 21 mg were found to have proteolytic activity in their sera which degraded NCS very rapidly as revealed by the fluorescence polarization technique.
Peripheral neuropathy was not found even six to ten years after the onset of visual symptoms in a family with primary amyloidosis, except in the propositus at the terminal stage. The propositus had mainly ocular and CNS involvement. An ocular manifestation, the vitreous opacity, was the only involvement in the family members, in spite of the long clinical course. This family may have a different type of familial primary amyloidosis from that previously reported.
The effects of bilateral common carotid artery occlusion on brain metabolism and arterial acid-base balance were studied in normotensive and experimental renovascular hypertensive rats. One hour after carotid occlusion in hypertensive rats, supratentorial lactate increased to 383% and lactate-pyruvate ratio to 280% of the controls, while adenosine triphosphate (ATP) decreased to 69%. These metabolic changes were thought to be due to cerebral ischemia. Arterial pCO2 was lowered and the pH was raised in the hypertensive animals due to cerebral ischemia induced hyperventilation. In the normotensive rats, carotid occlusion had minimal effects on cerebral metabolism and arterial acid-base balance. These results suggest that hypertensive rats are more susceptible to cerebral ischemia caused by carotid occlusion than normotensive rats. Increased cerebrovascular resistance in hypertension is discussed as a causal factor in cerebral ischemia.
An ultrastructural study of cerebral infarcts in spontaneously hypertensive rats 1--5 h after bilateral carotid artery occlusion was performed. The alteration of the neocortex consisted of shrinkage of the neurons surrounded by swollen astrocytic processes. Distension of the rough endoplasmic reticulum of the neuronal cytoplasm appeared early, while changes of the mitochondria were slight. Though there appeared slight to moderate perivascular astrocytic swelling, endothelial swelling was rare and there was no severe narrowing of the capillary lumen. There were no filling defects of colloidal carbon injected to the blood vessels of the ischemic brains. Ischemic neuronal alterations were proved to develop in the absence of severe morphological changes of the microvasculature in the developing cerebral infarcts in the present experimental model.