In vivo oxygen transport in the normal rabbit femoral arterial wall.

Crawford, Donald W.; Back, L. H.; Cole, Mark A.

doi:10.1172/jci109815

Cited by 30 publications

(17 citation statements)

References 26 publications

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“…In each case a curve has been defined, with maximum wall oxygenation immediately adjacent to the vessel lumen, which diminished progressively to a trough level in the middle to outer media and rose progressively again toward the adventitia. This profile was consistent in its overall shape and is similar to profiles obtained in the dog by Heistad and Marcus 10 and in the rabbit by Crawford et al 15 and Crawford and Kramsch.…”

Section: Discussionsupporting

confidence: 89%

Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig.

Barker

Talbert

Cottam

et al. 1993

Arterioscler Thromb

179

108

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Oxygenation of the arterial wall is provided by diffusion of oxygen outward from the main vessel lumen and inward from the adventitial vasa vasorum. In a group of four Yucatan miniature pigs the oxygenation profiles across the superficial femoral arteries were recorded by polarographic oxygen microelectrodes. The profiles obtained suggested a relatively poorly oxygenated media (a trough value of approximately 25% that of the intimal oxygenation) with a progressive rise in oxygenation toward the intimal and adventitial surfaces. In four other survival experiments, occlusion of the adventitial vasa vasorum by flush ligation of the arterial branches that supply them resulted in the production of a focal, intimal hyperplastic lesion that was absent in control vessels (intimal to medial ratios [mean +/- SEM] of 0.053 +/- 0.008, n = 8, p < 0.001 and 0.013 +/- 0.001, n = 8, respectively). By electron microscopy this lesion was seen to be composed mainly of smooth muscle cells. This evidence would support the hypothesis that arterial wall hypoxia may be involved in the initiation of intimal hyperplasia. It is proposed that human atherosclerosis may be initiated by occlusion of the vasa vasorum and concomitant hypoxia.

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Section: Discussionsupporting

confidence: 89%

Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig.

Barker

Talbert

Cottam

et al. 1993

Arterioscler Thromb

179

108

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“…Neointimal thickening 1 mo after angioplasty was found to contribute to only a minor portion ofthe loss in diameter after either BA or LBA, and medial thickness was found to be similar to that reported by others for the normal rabbit femoral artery (41). Several groups of investigators have suggested that visco-elastic recoil frequently contributes to luminal compromise after conventional balloon angioplasty (42,43).…”

Section: Discussionsupporting

confidence: 82%

Modulation by beta-aminopropionitrile of vessel luminal narrowing and structural abnormalities in arterial wall collagen in a rabbit model of conventional balloon angioplasty versus laser balloon angioplasty.

Spears

Zhan²,

Khurana³

et al. 1994

J. Clin. Invest.

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This study was designed to assess the potential relationship between the late loss of angiographic luminal diameter and biochemical abnormalities of arterial wall collagen in rabbits subjected to angioplasty, and to test the hypothesis that a-aminopropionitrile (#APN), an inhibitor of lysyl oxidase, would inhibit such changes when administered orally for 1 mo after angioplasty. Endovascular injury was induced in rabbit iliac arteries by ipsilateral balloon angioplasty (BA) and by contralateral balloon angioplasty accompanied by exposure to continuous wave neodymium: yttrium aluminum garnet laser radiation (LBA). Computer measurement ofangiographic luminal diameter demonstrated significant vessel narrowing at 1 and 6 mo after both procedures. By quantitative histology, the majority of the 1-mo loss in angiographic diameter could not be attributed to neointimal thickening. Analysis of collagen cross-linking by HPLC in collagen obtained from the LBA-injured segments of the arteries 1 mo after angioplasty revealed a significant increase, relative to values from uninjured arteries (P < 0.05), in the difunctional cross-link dihydroxylysinonorleucine (DHLNL). 6 mo after angioplasty, the content of hydroxpyridinium, the trifunctional maturational product of DHLNL, was significantly elevated in both BA-and LBA-treated arteries compared with values from uninjured arteries (P < 0.05). In animals administered ,fAPN, luminal narrowing at 1 mo, compared with controls, was attenuated (P < 0.01) and DHLNL content was decreased (P < 0.05) in arteries subjected to LBA, but not in arteries subjected to BA. The results suggest that lathyrogenic agents may be efficacious in favorably modulating LBA-induced alterations in vessel diameter and mural connective tissue. (J. Clin. Invest. 1984. 93:1543-1553

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“…It is noteworthy that HIF-1␣ and VEGF expression was evident in the outer to middle layers of medial SMCs (Figure 3), which are known to be vulnerable to hypoxia. 9,10 It has been shown that HIF-1␣ protein levels increase markedly as cellular oxygen concentration is reduced and decay rapidly when cells are returned to a nonhypoxic environment. 16 The role of HIF-1␣ in activation of VEGF gene transcription is established in hypoxic cells.…”

Section: Hif-1␣ Induction In Hypertensive Aortamentioning

confidence: 99%

“…8 However, medial thickening may create the hypoxic zone in the media by increasing the distance required for oxygen diffusion from the lumen. 9,10 Because hypertension produces medial thickening, it is conceivable that the AVV plays a role in the maintenance of homeostasis during vascular remodeling in hypertensive arteries. However, there has been little study of the AVV in hypertensive arteries.…”

mentioning

confidence: 99%

Hypoxia-Inducible Factor-1α/Vascular Endothelial Growth Factor Pathway for Adventitial Vasa Vasorum Formation in Hypertensive Rat Aorta

et al. 2002

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Abstract-The roles of adventitial vasa vasorum have been highlighted in vascular wall homeostasis. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor in physiological and pathophysiological conditions. However, little is known regarding the changes in adventitial vasa vasorum and the mechanism of the formation in hypertensive arteries. Accordingly, endothelial cell proliferation, adventitial vasa vasorum count, and expression of VEGF signaling axis proteins were examined in the ascending aorta of hypertensive Wistar rats that underwent suprarenal aortic constriction.Hypertension not only induced medial and adventitial thickening but also significantly increased adventitial vasa vasorum count by day 28. Preceding the medial thickening, BrdU ϩ -proliferative endothelial cells were observed in the adventitia but not in the media and intima after day 3; they peaked at day 7 and remained modestly increased at day 28. The BrdU ϩ endothelial cells showed induction of Ets-1, a transcription factor mediating angiogenic response of VEGF. Furthermore, concomitant expression of VEGF and a hypoxia-inducible transcription factor (HIF-1␣) was observed in the outer layers of medial smooth muscle cells at day 3 and extended to the middle layers of medial smooth muscle cells at day 7, returning to lower levels by day 28. In conclusion, adventitial vasa vasorum formation was induced by hypertension through the HIF-1␣/VEGF/Ets-1 pathway during hypertensive remodeling. There is convincing evidence that disruption of blood flow to the AVV results in medial necrosis 3 and intimal hyperplasia. 4,5 Moreover, it has been demonstrated that in balloon-injured arteries, the arterial wall oxygen supply is impaired after injury but is later compensated for by new AVV formation. 6 Accordingly, the role of AVV has been highlighted in vascular wall homeostasis. Most conduit and muscular arteries have vasa vasorum in the adventitia but not in the media; oxygen and nutrients are supplied by diffusion from the AVV to the outer media and from the main vessel lumen to the inner media. 7 Oxygen requirements of the vessel wall itself are relatively modest. 8 However, medial thickening may create the hypoxic zone in the media by increasing the distance required for oxygen diffusion from the lumen. 9,10 Because hypertension produces medial thickening, it is conceivable that the AVV plays a role in the maintenance of homeostasis during vascular remodeling in hypertensive arteries. However, there has been little study of the AVV in hypertensive arteries.Vascular endothelial growth factor (VEGF) has potent mitogenic and promigratory actions specific for endothelial cells (ECs), intimately linked with new vessel development in physiological and various diseased situations. 11,12 These stimulatory effects on ECs are initiated by the binding of VEGF to its high-affinity tyrosine kinase receptor Flk-1 13 and subsequently result in activation of a transcription factor, Ets-1, leading to conversion of ECs to the angiogenic phenotype. 14,15 A ...

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In vivo oxygen transport in the normal rabbit femoral arterial wall.

Abstract: A B S T R A C T In vivo measuremnents of tissue oxygen tension were malde at 10-,um intervals through functioning itn situ ral)b)it femoral arterial walls, using inhalation anesthesia anid recessed microcathodes with -4-gium external diameters.

Cited by 30 publications

References 26 publications

Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig.

Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig.

Modulation by beta-aminopropionitrile of vessel luminal narrowing and structural abnormalities in arterial wall collagen in a rabbit model of conventional balloon angioplasty versus laser balloon angioplasty.

Hypoxia-Inducible Factor-1α/Vascular Endothelial Growth Factor Pathway for Adventitial Vasa Vasorum Formation in Hypertensive Rat Aorta

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