A morphological study of the long-term repair process in experimentally stretched but unruptured arteries and veins

Mitchell, Geraldine M.; McCann, J.; Rogers, Ian W.; Hickey, Michael J.; Morrison, Wayne A.; OʼBrien, B. M.

doi:10.1016/s0007-1226(96)90184-8

Cited by 35 publications

(32 citation statements)

References 11 publications

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“…8,32 Little attention was given to the adventitia in these studies, but some of the histologic images showed evidence of adventitial damage after axial stretch. 32 In this study, the most frequent type of damage in Protocol 2 was rupture of the IEL and the dense adventitial layer. The fact that broken fibers in the dense adventitial layer were always accompanied by IEL damage indicates that the IEL is more prone to damage under these conditions.…”

Section: Discussionmentioning

confidence: 99%

Sustained Axial Loading Lengthens Arteries in Organ Culture

et al. 2005

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Although it has been recognized for many years that arteries in vivo exist under significant axial strain, studies of the adaptation of arteries to elevated axial strain have only recently been conducted. To determine the effects of sustained elevation of axial loading on arterial structure and function, axial stresses of 250 kPa or greater were applied to porcine common carotid arteries maintained in a perfusion organ culture system for 7 days at physiologic pressure and flow conditions. Our results demonstrated that axial stretch could lead to an increase in unloaded length that was proportional to the axial stretch ratio (stretched length divided by unloaded length) when the axial stretch ratio was above a threshold value of 2.14. Below this threshold, no significant length change occurred. Above this threshold, a significant increase in unloaded length (13 +/- 7%,) and the number of smooth muscle cell nuclei (20 +/- 7%) was observed. Permanent length change was associated with a significant decrease in axial stiffness, and the maximum elongation achieved was limited by rupture of the arterial wall. All tested arteries demonstrated good viability and strong vasomotor responses. These results show that arteries in organ culture can elongate under sustained axial loading.

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Section: Discussionmentioning

confidence: 99%

Sustained Axial Loading Lengthens Arteries in Organ Culture

et al. 2005

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“…13) However, intimal thickening due to atherosclerosis can also lead to IEL defects. In fact, we observed marked intimal thickening at 11 of the 35 sites with IEL defects and usually thin intima at 19 sites.…”

Section: Discussionmentioning

confidence: 99%

Histological Study of the Normal Vertebral Artery-Etiology of Dissecting Aneurysms-

Sato

Sasaki

Suzuki

et al. 2004

Neurol. Med. Chir.(Tokyo)

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Histological evaluation of dissecting aneurysms of the cerebral arteries has suggested that defects in the internal elastic lamina (IEL) induce dissection of the arterial wall. Dissecting aneurysms occur most frequently in the vertebral artery (VA). The present study examined sections of the normal VA to elucidate the mechanisms of arterial dissection. Bilateral VAs (20 vessels) were obtained from 10 patients who died of causes other than intracranial lesions. The VAs were detached from the VA union to the site 10 mm proximal from the point penetrating the dura mater. The VAs were cut at 5-mm intervals, and each segment was observed using modified Masson's trichrome staining for elastic fibers. The thickness of the media and adventitia significantly thinned after the origin of the posterior inferior cerebellar artery (PICA). IEL defects were observed at 35 sites in 11 vessels from six subjects. There was a high incidence of IEL defects in the extradural portion and near the origin of the PICA, areas frequently involved in arterial dissection. There was a high incidence of intimal thinning at areas of IEL defects (19 of 35), and thinning was particularly marked distal to the origin of the PICA. In the absence of intimal thickening, the vascular strength at the site of IEL defects may be reduced, which would promote the occurrence and progression of arterial dissection.

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“…As suggested by Mizutani et al (7), the healing process, including neointimal proliferation, begins one week after the dissection and may not be complete even after one month, depending on the extent of the wall injury. This period of one week may correspond to the usual time for the appearance of the neointima in animal models (8). Clinical data also suggests that the rate of re-bleeding of ruptured dissecting aneurysms decreases one week after SAH.…”

Section: Discussionmentioning

confidence: 81%

Ruptured Dissecting Aneurysm of the Middle Cerebral Artery with Spontaneous Resolution: A Case Report

Ihn

Jung

2011

J Korean Soc Radiol

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Dissecting aneurysms of the middle cerebral artery (MCA) are known to cause cerebral infarcts in younger people and can also cause subarachnoid hemorrhage (SAH) or intracranial hemorrhage. Bleeding caused by an isolated dissecting aneurysm of the MCA is relatively rare. We report the case of a young woman with SAH that occurred subsequent to a ruptured dissecting aneurysm of the MCA which resolved spontaneously as demonstrated by angiography.

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A morphological study of the long-term repair process in experimentally stretched but unruptured arteries and veins

Cited by 35 publications

References 11 publications

Sustained Axial Loading Lengthens Arteries in Organ Culture

Sustained Axial Loading Lengthens Arteries in Organ Culture

Histological Study of the Normal Vertebral Artery-Etiology of Dissecting Aneurysms-

Ruptured Dissecting Aneurysm of the Middle Cerebral Artery with Spontaneous Resolution: A Case Report

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