Disease relevance of Vasa Vasorum

• Medial fibrosis occurred to the same extent as in control grafts, as did the early appearance of platelet factor VIII and fibronectin and the lack of vasa vasorum at 3 days followed by reappearance at 7 days [1].

High impact information on Vasa Vasorum

• The results support the hypothesis that basic FGF may be contributing to the growth and maintenance of the vasa vasorum and of vascular smooth muscle cells [2].
• During these interventions, changes in arterial pressure were prevented with propranolol or an arterial reservoir, to minimize indirect effects on vasa vasorum mediated through changes in aortic wall tension [3].
• 3. 5-Hydroxytryptamine (5-HT), noradrenaline (NA), adrenaline and dopamine caused dose-dependent increases in the vascular resistance of the vasa vasorum [4].
• During maximal dilatation induced by iv adenosine (4.7 mumol . kg-1 per min) flow delivered via vasa vasorum increased by 100% in both hypertensive and normotensive dogs [5].
• RESULTS: Oxygen tensions were significantly decreased in the outer artery wall immediately after the creation of the anastomosis and showed a further decrease in oxygen tensions at days 7 and 14, which correlated with the absence of a vasa vasorum [6].

Biological context of Vasa Vasorum

• In utero remodeling of the fetal lamb ductus arteriosus: the role of antenatal indomethacin and avascular zone thickness on vasa vasorum proliferation, neointima formation, and cell death [7].

Anatomical context of Vasa Vasorum

• Whereas saline infusion increases the mean number of vasa vasorum to 2.73 +/- 0.011 capillaries/field (p less than 0.01), basic FGF (1 ng/microliter/hr) increases the capillary number to 13.4 +/- 0.67 capillaries/field [2].
• After delivery, there was an increase in TGF-beta immunoreactivity in the smooth muscle cell layers of the vasa vasorum without any concurrent mRNA expression [8].
• There is evidence suggesting that this effect is not unique to noradrenaline and that the effect of any agonist stimulating a blood vessel through its lumenal surface may be reversed following its release from vasa vasorum [9].
• The main form, the beta-CGRP, is produced by the enteric nervous system and perivascular nerves of the vasa-vasorum [10].

Associations of Vasa Vasorum with chemical compounds

• A paradoxical response to adenosine suggests that vasa vasorum in the dilated arterial segment are maximally vasodilated [11].
• Luminal diameter and vasa vasorum response to stent dilation in the rabbit aorta [12].
• Lack of sumatriptan-induced aortic contraction or relaxation: 5-HT1B receptor protein detected in endothelium and smooth muscle of vasa vasorum but not aorta [13].
• Oxygen tension changes in the outer vascular wall supplied by vasa vasorum following adenosine and epinephrine [14].
• The response to noradrenaline administered topically through the vasa vasorum was augmented by administration of cocaine (2 X 10(-5) M) through the same route, while that to acetylcholine was not [15].

Gene context of Vasa Vasorum

• VEGF administration produced a significant (P < 0.05) increase in vasa vasorum ingrowth and neointima formation [16].
• In contrast to the pattern described above, the appearance of TGF-beta protein differed from that of mRNA in the vasa vasorum of the ductus wall [8].
• Thus, the 5-HT1B receptor mRNA detected in tissue extracts of the rat aorta most likely reflects 5-HT1B receptor expression in the arterioles of the vasa vasorum [13].
• In higher vertebrates SMC of vasa vasorum were both V- and D-positive and showed high enzyme activity [17].

Analytical, diagnostic and therapeutic context of Vasa Vasorum

• RATIONALE AND OBJECTIVES: We examined the changes in luminal diameter and vasa vasorum after stent dilation of the aorta of nonatherosclerotic rabbits [12].

References