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Biomedical subjects

F Hazama

Publications and source records attributed to F Hazama.

At least 109 records · Page 6Linked to original sources
PubMed1980

Experimentally induced cerebral aneurysms in rats: Part V. Relation of hemodynamics in the circle of Willis to formation of aneurysms.

All the rats were made hypertensive and fed beta-aminopropionitrile. Among them, cerebral aneurysms were never found in rats without carotid ligation. In rats with ligation of one or both common carotid arteries, cerebral aneurysms developed on the vessels where hemodynamic stresses were apparently increased. The relationship of hemodynamics in the circle of Willis to the development of cerebral aneurysms is discussed, being compared with findings in spontaneous lesions in man.

Aminopropionitrile↗
PubMed1980

General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations.

Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.

Child↗
PubMed1979

Acid phosphatase activity of the brain in SHR-- the first report of enzyme histochemical studies of spontaneously hypertensive rat brain.

Changes in acid phosphatase activity in the cerebrovascular system and brain parenchyma in SHR were investigated histochemically. An increased activity of the enzyme was demonstrated in the SHR endothelial and medial smooth muscle cells of the cerebral arterial system as compared to the control. The pericytes of intraparenchymal blood vessels also showed an intensified enzyme activity. The enzyme activity increased with advancing age. In SHR brain parenchyma, the enzyme activity was decreased in the cortical nerve cells. Glial cells with the enzyme activity were increased in number and showed an intensified activity. Causative factors of changes in acid phosphatase activity in SHR cerebral arteries and parenchyma were discussed.

Acid Phosphatase↗
PubMed1979

Pathology of Kawasaki disease: I. Pathology and morphogenesis of the vascular changes.

Histopathological investigation of the vascular changes in Kawasaki disease was carried out on thirty-seven autopsied Japanese patients. Arterial lesions could be classified into following five stages from the view point of morphogenesis of arteritis; 1) endothelial degeneration and increased vascular permeability, 2) edema and degeneration of the media, 3) necrotizing panarteritis, 4) granulation formation, and 5) scarformation. Aneurysm with thrombus was observed mainly in the coronary artery in most patients. It is considered that the initial changes begins in the endothelial cells with increased vascular permeability. Platelet aggregation in the damaged endothelial cells seems to play an important role in the further development of the arteritic changes. Vascular lesions were observed not only in the arterial system but also in the venous system, therefore Kawasaki disease is a systemic vasculitis rather than a systemic arteritis.

Aneurysm↗
PubMed1979

Pathology of Kawasaki disease: II. Distribution and incidence of the vascular lesions.

Histopathology, distribution and incidence of vascular changes were studied in tissues obtained at autopsy on thirty-seven children. Elastic and musculoelastic arteries showed a high incidence of arteritic changes, however the degree of the lesions was in general mild to moderate with the exception of the iliac artery, which revealed severe changes and a necrotizing panarteritis which was often accompanied with an aneurysm formation. A high incidence of arteritic changes, of which main histological feature was necrotizing panarteritis, was seen in extravisceral middle sized arteries. The coronary artery in particular was involved in each case and most had an accompanying aneurysm, some of which had ruptured. Intravisceral small sized arteries showed a relatively low incidence of arteritic changes and the degree of inflamation was in general mild. Phlebitis was present in over half the number of patients. The degree of lesions was mild in the small veins and mild to moderate in the large veins. Vascular lesions in Kawasaki disease should be termed systemic vasculitis rather than a systemic arteritis. There was a correlation between the caliber of involved vessels and the degree of vascular lesions. According to the histopathology, distribution and incidence of angitis, Kawasaki disease does resemble infantile periarteritis nodosa with the exception of the different manner of the coronary and iliac involvement.

Aorta↗
PubMed1979

Experimentally induced cerebral aneurysms in rats: Part III. Pathology.

Experimentally induced cerebral aneurysms in rats treated with unilateral ligation of the common carotid artery, deoxycorticosterone and salt hypertension, and beta-aminopropionitrile, were studied macroscopically and with light-microscopy. The material consisted of 13 aneurysms located on the anterior cerebral-anterior communicating arterial complex and one on the posterior cerebral artery. The findings were generally in accordance with that of spontaneous lesions in man. The results show the validity of these experimental aneurysms as a model for saccular cerebral aneurysms in man.

Aminopropionitrile↗
PubMed1979

Experimentally induced cerebral aneurysms in rats: part II.

An experimental condition that permits easy inducement of cerebral aneurysms in rats is reported. Previously, we demonstrated that saccular cerebral aneurysms were inducible in experimental animals and suggested that adult rats might be more preferable for inducing the lesion. Therefore, a longer-term study was performed intending to increase the incidence of cerebral aneurysms, using only adult rats. Adult rats were treated with ligation of one common carotid arter, deoxycorticosterone and salt hypertension, and beta-aminopropionitrile. Cerebral aneurysms developed in eleven of 30 rats which died 11-21 weeks after the start of the beta-aminopropionitrile feeding. All aneurysms were located on the anterior cerebral-anterior communicating arterial complex. Contributory mechanisms are discussed.

Aminopropionitrile↗
PubMed1978

Ectopic ACTH-MSH producing carcinoid tumor with multiple endocrine hyperplasia in a child.

An autopsy case of a 9-year-old Japanese girl revealed a carcinoid tumor originating in the duodenum and hyperplasia of the multiple endocrine organs as manifested by ectopic ACTH syndrome, carcinoid syndrome and giantism. The tumor cells were positive for histochemical argyrophile reaction and two types of secretory granules were identified by electron microscopy. Biochemical assay revealed the production of ACTH and beta-MSH by the tumor cells. Other changes of multiple endocrine organs included acidophil dominant hyperplasia of the pituitary, diffuse hyperplasia of the thyroid, chief cell hyperplasia of the parathyroid, hyperplasia of the islets of Langerhans and the adrenal cortex. This case was considered to be a type of multiple endocrine adenomatosis including carcinoid tumor. The relationship between the carcinoid tumor and multiple endocrine adenomatosis was discussed.

Adenoma↗
PubMed1978

Enzymatic histo and cytochemical investigation on the cardiovascular system in spontaneously hypertensive rats.

The functional abnormalities of the cells in the cardiovascular system in SHR were revealed by enzyme histo-cytochemical study. The enzymatic activity was usually increased in the area where the arteries branched and in proliferating cells in the thickened wall. Such was more remarkable in the distorted arteries with aging. Functional roles of these 4 enzymes were discussed.

Acid Phosphatase↗
PubMed1978

Experimentally induced cerebral aneurysms in rats.

Saccular cerebral aneurysms were successfully induced in rats treated with beta-aminopropionitrile, deoxycorticosterone and salt hypertension and ligation of unilateral common carotid artery. This experiment was performed on the hypothesis that if hemodynamic stresses were increased on the fragile, cerebral arterial wall of beta-aminopropionitrile-fed animals, cerebral aneurysms might be produced. Although the incidence of cerebral aneurysms was low and the contributory mechanisms of these procedures must be more clearly elucidated, the present results show that saccular cerebral aneurysms are really inducible in experimental animals.

Aminopropionitrile↗
PubMed1977

Autoradiographic investigation of cell proliferation in the brain of spontaneously hypertensive rats.

Cell proliferation in the brain of spontaneously hypertensive rats (SHR) and control Wistar rats of various ages was autoradiographically investigated using [3H]thymidine. The brain of SHR showed an increase in labeled cells. The increase of labeled cells was seen in the early stage of the development of hypertension when there were still no definite morphological changes in the cerebral vessel walls or brain parenchyma. The labeled cells tended to increase in number with the age of the animals. The distribution of these cells corresponded with areas of increased vascular permeability and cerebrovascular lesions, that is, water-shed regions. The labeled cells consisted of endothelial and adventitial cells of the intracerebral arterioles and pial arteries as well as glial cells. Arachnoid cells, subarachnoid cells, medial smooth muscle cells of the pial arteries were also labeled, though less intensely. The significance of labeled endothelial cells in the development of cerebrovascular changes and sequential parenchymal changes is discussed.

Animals↗
PubMed1977

Left atrial infarction with saddle embolism.

Left atrial and left ventricular infarction with various atrial arrhythmias, multiple systemic arterial thromboembolism, and a large mural thrombus over the left atrial infarction is reported. In ischemic heart disease, systemic arterial thromboembolism may develop due to atrial infarction which is often overlooked in antemortem as well as in postmortem examinations. When a clinical diagnosis of atrial infarction is made, the possibility of a Stokes-Adams syndrome, thromboembolism, and rupture of the atrium should also be investigated.

Electrocardiography↗