Electron Microscopic Study on the Middle Cerebral Artery Lesions in Hypertensive Rats

Kojimahara, Masayasu; Ooneda, Genju

doi:10.1111/j.1440-1827.1970.tb00097.x

Cited by 12 publications

(3 citation statements)

References 8 publications

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“…They have de scribed dense necrotic cells, fragmentation of cellular parts with condensed granular and filamentous content and a variety of lyso somal bodies occurring in human and exper imental atherosclerosis and arteriosclerosis and as a response to stress influences [Takebayashi, 1970;Shiraishi et al, 1983]. Similar findings were made in the cerebral arteries of renal hypertensive rats [Kojimahara and Ooneda, 1978] and in the epicardial arteries of spontaneously hypertensive rats [Saer et al, 1981].…”

Section: Discussionsupporting

confidence: 69%

Progressive Involution and Physiological Death of Smooth Muscle Cells of Rat Incisal Arterioles

Thorball¹,

Moe²,

Winther-Nielsen³

1985

J Vasc Res

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The sequential morphology of vascular smooth muscle cell involution and physiological cell death was studied by electron microscopy on rat incisors. Concurrently with changes in the pulp of the continuously growing incisor, its arterioles pass through a cycle of growth, remodeling, regression and decay. During the cycle, smooth muscle cells of the arterioles were observed to involute by segregation of cytoplasmic components, formation of autophagic and digestive vacuoles and shedding of cell fragments. Phagocytic vacuoles were found in neighbouring muscle cells and in adventitious macrophages. Concomitant with the involution in some cells, physiological death was observed among other smooth muscle cells. This appears as an apoptosis with sequential transformations of polyribosomes into monoribosomes, nuclear and cytoplasmic condensation, and finally fragmentation followed by phagocytosis mainly by adventitious macrophages. Knowledge of the features of physiological involution and cell death of the vascular smooth muscle cells may be of importance not only in studies of functional remodeling and adaption, but also in the interpretation of vascular lesions.

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Section: Discussionsupporting

confidence: 69%

Progressive Involution and Physiological Death of Smooth Muscle Cells of Rat Incisal Arterioles

Thorball¹,

Moe²,

Winther-Nielsen³

1985

J Vasc Res

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“…Smooth muscle cell proliferation continued above control levels in muscular arteries after 21 days following the con striction of the aorta, even though the blood pressure was relatively stable. Apart from obvious cell necrosis, electron microscopy of the arterial wall has demonstrated focal cytoplasmic degradation of VSM cells in hypertension [23,34], This may be associated with increased turnover of VSM cells. It is not known whether there is actual hyper trophy of individual VSM cells.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have been made of the pathological changes in the blood vessels in human and experimental hypertension both by light [12,15,26,27,30,32,37] and electron microscopy [13,18,23,28,32,34], The rat has dominated the literature as an experimental animal. The in vestigation of hypertensive states, both spontaneous and those induced by renal abnormalities, steroid and salt treatment, adrenal regeneration, aortic stenosis, and drugs, in this species has furnished data elucidating mechanisms of this disease.…”

Section: Introductionmentioning

confidence: 99%

An Autoradiographic and Pathological Study of Cellular Proliferation in Rabbit Arteries Correlated with an Increase in Arterial Pressure

Bevan¹

1976

J Vasc Res

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Following partial constriction of the abdominal aorta, the increase in arterial pressure in vessels proximal to the ligature at 3, 6, 14, 21 and 28 days was correlated with pathological changes and with proliferation of cells in the arterial wall measured by ³H-thymidine labeling indices and mitotic counts. The time course of arterial pressure rise and vascular smooth muscle cell proliferation were similar. Patterns of proliferation of cells of the artery wall varied in distribution with time, the presence or absence of traumatic changes seen by light microscopy, and the histological structure of the vessel. Arteries not subject to hypertension did not differ from sham-operated animals.

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Studies on intra-arterial cushions

Gorgas

Böck

1976

Anat. Embryol.

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The distribution of horseradish peroxidase (HRP) in intraarterial cushions at the origins of intercostal arteries was studied in mice 30 min after intravenous injection of the tracer. HRP is found to be evenly distributed in the extracellular space of the entire arterial wall. Basal lamina material is penetrated by the tracer protein. This is not the case with collagenic fibrils, elastic material and intercellular granular deposits which occur regularly in cushions of adult mice but not in those of newborn animals (granules 300 to 800 A in diameter, probably cell debris). However, the elastic sheets do not act as diffusion barriers. HRP is not phagocytized in significant amounts by ramified smooth muscle cells within the time intervals tested. It is therefore assumed that granular deposits are also not phagocytized by smooth muscle cells.

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Electron Microscopic Study on the Middle Cerebral Artery Lesions in Hypertensive Rats

Cited by 12 publications

References 8 publications

Progressive Involution and Physiological Death of Smooth Muscle Cells of Rat Incisal Arterioles

Progressive Involution and Physiological Death of Smooth Muscle Cells of Rat Incisal Arterioles

An Autoradiographic and Pathological Study of Cellular Proliferation in Rabbit Arteries Correlated with an Increase in Arterial Pressure

Studies on intra-arterial cushions

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