Age-induced changes of cerebral arteries in rats

Kojimahara, Masayasu; Sekiya, Kazuo; Ooneda, Genju

doi:10.1007/bf00543546

Cited by 30 publications

(3 citation statements)

References 8 publications

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“…Medial SMC necrosis of rat cerebral artery was augmented with age 13 and was observed to exist especially in the outer media, as mentioned previously. We found that a loss of SMCs with age was more apparent in the nonhypertensive group than in the hypertensive group.…”

Section: Discussionsupporting

confidence: 59%

Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Masawa

Yoshida

Yamada

et al. 1994

Stroke

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Background and Purpose Medial smooth muscle cell necrosis has been reported as a lesion that may precede angionecrosis, which is a major cause of not only hypertensive brain hemorrhage but also lacunar infarct. We morphometrically studied a loss of smooth muscle cells in the media of cerebral arteries in relation to clinical risk factors.Methods The lateral striate, ie, perforating arteries and the medullary arteries in the subcortical white matter of the temporal lobe (100 to 400 /im in diameter) were histologically investigated in 121 autopsied brains. Medial area was measured quantitatively, and the number of nuclei of smooth muscle cells in the area was calculated in 1210 cross-sectional arteries of histological sections. The influence on the structural (ie, smooth muscle cell) preservation of the tunica media (ratio of number of smooth muscle cell nuclei to medial area [N-MA ratio]) of age, blood pressure, serum lipids, and presence or absence of extracerebral severe atherosclerosis was investigated.Results The N-MA ratio decreased slightly with age in both arteries. A reverse correlation between N-MA ratio and age was seen in groups both with and without hypertension. The mean N-MA ratio in the hypertensive group was significantly lower than that of the nonhypertensive group (P<.001) in all

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Section: Discussionsupporting

confidence: 59%

Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Masawa

Yoshida

Yamada

et al. 1994

Stroke

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“…These were preceded by medial muscle cell necrosis [Su zuki and O oneda, 1972]. The medial muscle cell necrosis in the cerebral arteries was observed not only in hypertensive rats, but also in old normotensive rats [Kojimahara et at., 1973). The causes of the medial muscle cell damage, the earliest lesion of plasmatic arterionecrosis, are hypertension, aging and arterial contraction.…”

Section: Plasmatic a Rterionecrosismentioning

confidence: 99%

Smooth Muscle Cells in the Development of Plasmatic Arterionecrosis, Arteriosclerosis, and Arterial Contraction

et al. 1978

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Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12–24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

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“…Kojimahara and co-workers 22 reported increases in elastin and collagen in the media, and an increase in basement membranelike substances in larger cerebral vessels of rats 10-12 months of age and older. Commercially available rats live approximately 36 months 23 and a 10-12 month-old rat chronologically approximates the third to fourth decade in man.…”

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A histochemical study of cerebral cortical vessels and ganglionic vessels of the caudatoputamen in aging normotensive rats.

Rieke¹,

Cannon²

1985

Stroke

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SUMMARYThe goal was to describe the metabolic profile of ganglionic and cortical arteries and arterioles in aging normotensive male rats. Five enzymes indicative of key metabolic pathways in the vessel walls were semiquantitatively evaluated using bright-field histochemical microscopy. Lactate dehydrogenase showed significant reactivity which increased with vessel diameter in cortical and ganglionic vessels in all age groups tested. Succinate dehydrogenase and cytochrome oxidase showed little reactivity in both cortical and ganglionic vessels, suggesting a reduced role for aerobic metabolic pathways. Myosin ATPase reactivity was high in cortical and ganglionic vessels. Only this enzyme showed an increased reactivity that was correlated with the age and diameter of the vessel. Glucose-6-phosphate dehydrogenase reactivity was more pronounced in cortical than ganglionic vessels, suggesting that the hexose-monophosphate-shunt may be more active in the cortical vessels. There were no regional differences in enzyme reactivity throughout the caudatoputamen. In conclusion, both the cortical and ganglionic vessels are metabollcally active, with significant anaerobic gh/colysis, and reduced, but observable capacity for aerobic metabolism. The decreased myosin ATPase reactivity and the low level of glucose-6-phosphate dehydrogenase reactivity in the ganglionic arterioles of senescent rats may contribute to the susceptibility of these vessels to cerebrovascular accidents. Stroke Vo! 16, No 2. 1985 THE ARTERIAL SUPPLY to the cerebrum and subcortical structures in the rat and man have many similarities, particularly in the pathophysiology of stroke. Terminal branches of the internal carotid arteries, branches from the anastomotic circle, and the posterior cerebral arteries supply the cerebral cortex in rat and man.2 3 All of these vessels provide a dense network of ganglionic arterioles that nourish the basal ganglia, including the caudatoputamen (CPU) and globus pallidus.3 Although the vascular bed of the cerebrum and subcortical structures have been described, little is yet known regarding the metabolism of these vessels.4 " 8 Furthermore, even though age-related structural changes are reported for both cortical and ganglionic vessels in man and other experimental animals, 9 "' 5 virtually nothing is known regarding the effects of aging on cerebral vascular metabolism.The present study utilizes histochemical methodology to semiquantitatively evaluate enzymes of key metabolic pathways in the muscular walls of vessels supplying the neocortex (cortical vessels) and ganglionic vessels in the CPU of aging normotensive male rats. The five enzymes evaluated are indicators of anaerobic glycolysis, the Krebs cycle and respiratory chain (aerobic metabolism), the hexose-monophosphate-shunt, and the availability of myosin ATPase. Our goal was to delineate the metabolic profile of aging stroke-prone ganglionic vessels and of cortical vessels, from which the former arise. Methods Twenty-three male rats (Charles River, COBS CD outbred ...

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Age-induced changes of cerebral arteries in rats

Cited by 30 publications

References 8 publications

Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Smooth Muscle Cells in the Development of Plasmatic Arterionecrosis, Arteriosclerosis, and Arterial Contraction

A histochemical study of cerebral cortical vessels and ganglionic vessels of the caudatoputamen in aging normotensive rats.

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