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Biomedical subjects

F Hazama

Publications and source records attributed to F Hazama.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1975

Vascular lesions in the various substrains of spontaneously hypertensive rats and the effects of chronic salt ingestion.

Among different races, countries and districts there are definite differences in incidence of hypertensive vascular diseases, for example cerebral bleeding. Hereditary and dietary factors presumably play significant roles. Experimental studies under controlled conditions and utilizint suitable animals are indispensable for analysis of the related factors. For confirmation, hypertensive vascular changes in the spontaneously hypertensive rats were histopathologically studied and related to the difference of substrains. Dietary effects of sodium chloride on these vascular changes were investigated by providing the animals with 1% saline for drinking.

Animals↗
PubMedDate not supplied

Animal model of cerebral aneurysms: pathology and pathogenesis of induced cerebral aneurysms in rats.

Saccular cerebral aneurysms are induced in rats treated with ligation of one or both of the common carotid arteries, experimental hypertension, and beta-aminopropionitrile feeding. Combination of ligation of the carotid artery and experimental hypertension is the minimal requirement for inducing aneurysms within a few months. beta-aminopropionitrile makes the arterial wall fragile, increasing the incidence of aneurysmal development. Induced aneurysms are strongly related to haemodynamic stresses. They are located on the large arteries at the base of the brain. Some of them apparently originate from the apex of bifurcation. The macroscopic and microscopic findings are generally in accordance with those of spontaneous lesions in man. The results of electron microscope and histochemical studies indicate the participation of leukocytes and their lysosomal enzymes in the development and growth of aneurysms. Adventitial cells are also suggested to be responsible for the growth of aneurysms.

Aminopropionitrile↗
PubMedDate not supplied

Neurotoxicity of vincristine after the osmotic opening of the blood-brain barrier.

The direct effect of intravascularly injected vincristine on the rat brain was investigated after the osmotic opening of the blood-brain barrier. This was opened unilaterally by injecting 2.5 ml of 1.4 molal mannitol solution into the right carotid artery through a cannula inserted in the external carotid artery in retrograde fashion. Vincristine (0.75 mg/kg) was then injected into either the carotid artery or into a vein. Animals, thus treated, developed left hemiparesis and choreo-athetoid head motion within several days. Microscopical analysis revealed 1 intracytoplasmic eosinophilic inclusions at an early period, 2 neuronal argyrophilic change and axonal thickening with spheroid formation at later times, and 3 glial mitotic arrest, a finding not reported in the previous studies with intrathecal injection of vincristine. Neuronal changes were usually confined to the selected area in the midbrain, whereas glial mitotic figures were seen in the hippocampus, midbrain and cerebellum. These changes are thought to be direct effects of the vincristine binding with cellular microtubules, including mitotic spindle tubules and neurotubules. The transient opening of the blood-brain barrier seems to be a useful technique for studying the experimental neurotoxicology of drugs to which the blood-brain barrier is impermeable.

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