vasa vasorum


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vasa vasorum

[′vā·zə va′sȯr·əm]
(anatomy)
The blood vessels supplying the walls of arteries and veins.
References in periodicals archive ?
To mitigate the effect of hypoxia on hyperplasia, we tried to improve the oxygen supply of vein grafts by promoting vasa vasorum neovascularization.
In conclusion, based on the experimental cases, this study found that promoting vasa vasorum neovascularization of vein grafts extenuated hypoxia of the wall, but did not influence the intimal hyperplasia.
It is the result of hemorrhage within the media from rupture of the vasa vasorum in the absence of an intimomedial tear in the setting of hypertension or trauma.
In terms of capillary plaque bleeding, bleeding and transudation into plaques from thin-walled new vessels originating from vasa vasorum, frequently found at the plaque base, could theoretically increase the intraplaque pressure with resultant cap rupture from the inside (15).
Early studies to elucidate the mechanisms of restenosis focused on intimal de-endothelialization as a primary cause, [sup][3] while more recent studies indicated a potential role for adventitial vasa vasorum (VV) in the initiation and/or progression of atherosclerotic lesions and vessel restenosis.
1, 2) They develop primarily as a consequence of adventitial damage and thrombosis of the vasa vasorum, resulting in damage to the muscular and elastic components of the media and intima with ensuing extravasation of arterial blood, progressive enlargement and eventual rupture.
This is an interesting and plausible explanation that emphasizes the proatherosclerotic properties of periadventitial fat; however, the authors did not address whether the adventitia and vasa vasorum, 2 other anatomic factors that play a role in atherosclerosis, are altered in intra-myocardial arteries.
The cells prevealed the presence of vasa vasorum - capillaries that had developed to nourish the now living implant.
To the Editor: I reviewed the article Quantification of adventitial vasa vasorum (VV) vascularization in double-injury restenotic arteries by Meng et al .
The infectious agent can either travel through the blood stream and harbor in the vasa vasorum of the arterial wall or implant on damaged intima, ulcerated arteriosclerotic plaques, or mural thrombus.
25) Barker et al (26) demonstrated this influence by occluding the adventitial vasa vasorum in pigs and later observing intimal smooth muscle-rich proliferating lesions, which suggested a role for arterial hypoxia in the initiation of intimal hyperplasia.