Search PubMed⌕ Search

Biomedical subjects

H Haebara

Publications and source records attributed to H Haebara.

At least 37 records · Page 2Linked to original sources
PubMed1981

Aicardi's syndrome - report of an autopsy case.

A Japanese girl aged 19 months had generalized convulsions, agenesis of the corpus callosum, peculiar chorioretinopathy, scoliosis and marked retardation of psychomotor development. Pathological investigation revealed polymicrogyria, cortical heterotopias, disorganization of the cerebellar cortex. In ocular histopathology, lacunae were composed of hypo- or depigmented zones of the retinal pigment epithelium accompanied with dispersion of pigments into the rod and cone layer. Coloboma of the optic nerve was also evident. There was no evidence of inflammation or pathogenic organisms.

Agenesis of Corpus Callosum↗
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↗
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

Effects of central and peripheral angiotensin blockade in hypertensive rats.

The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.

Angiotensin II↗
PubMed1978

What makes the renin-angiotensin system a pathogenic factor?

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.

Angiotensin II↗
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↗
PubMed1976

Does the renin-angiotensin system contribute to the vascular lesions in renal hypertensive rats?

1. Renal hypertensive rats with a normal or suppressed activity of the renin-angiotensin system develop vascular lesions which are similar to those observed in spontaneously hypertensive rats on high sodium diet. 2. Exposure of a vascular bed to high blood pressure results in a rapid damage of the vascular wall, irrespective of the state of the renin-angiotensin system.

Angiotensin II↗
PubMed1976

Tissue iso-renins.

1. Several extrarenal tissues contain enzymes which are similar to kidney renin: they hydrolyse angiotensinogen to form angiotensin I; they have characteristic substrate specificity; the physicochemical properties of kidney renin and of extrarenal tissue iso-renin are similar. 2. Results indicate that tissue iso-renins are part of a complex enzyme system with mainly local function. A possible biological role has been demonstrated in brain, adrenal gland and tissue culture.

Adrenal Glands↗
PubMed1975

Pathogenesis and prevention of stroke in spontaneously hypertensive rats.

1. A colony of stroke-prone spontaneously hypertensive rats has been developed by selective breeding. 2. These animals developed severe hypertension early in life, the magnitude of the hypertension being closely related to the incidence of stroke. 3. No evidence was obtained of any humoral factor responsible for strokes. 4. Local factors predisposing to stroke were a scanty arterial supply with characteristic recurrent branching of long and large arteries, together with increased vascular permeability, angio-necrosis, and formation of microaneurysms. 5. Strokes could be prevented by adequate antihypertensive therapy from an early age.

Animals↗
PubMed1975

Changes in vascular permeability in stroke-prone spontaneously hypertensive rats studied with peroxidase as a tracer.

Cerebrovascular permeability in stroke-prone spontaneously hypertensive rats (SHR) at various ages was histologically studied using horseradish peroxidase as a tracer and such was related to the cerebrovascular lesions in the animals. An increase in permeability was demonstrated in the brain of SHR, particularly in those animals with an extremely high blood pressure. Increased cerebrovascular permeability occurred in some animals without any organic vascular change or severe parenchymal changes, although edema was present. Histologically, the SHR brain with an increase in permeability showed mild focal edema, rarefaction of tissue and necrosis with cyst formation. Thus a transitional progress was evident. Localization of the increase in permeability corresponded well with the predilection sites of cerebrovascular lesions in SHR. Constrictions and dilatations of intracerebral arterioles and small arteries were also demonstrated by the peroxidase method, and the dilated arterial walls did reveal a darker staining. From these results it is strongly suggested that certain cerebrovascular lesions, especially necrosis with cyst formation in SHR are sequelae of the increased cerebrovascular permeability caused by a chronic hypertensive state.

Animals↗