The vasa vasorum and angioplasty.

Abstract

Interruption of flow in the vasa vasorum may lead to medial necrosis and aneurysm formation. The purpose of this study was to determine whether angioplasty produces significant alterations in the morphology or blood flow of the vasa vasorum of the dilated artery. The morphology of the canine vasa vasorum was studied before and after angioplasty; in a separate experiment vessel wall blood flow (VWBF) in canine carotid arteries was measured after angioplasty to determine whether physiologic regulation of the blood flow was disrupted by arterial dilation. No morphologic changes could be demonstrated in the vasa vasorum of the dilated artery; however, VWBF was increased by 1194 +/- 215% (mean +/- standard error, p less than 0.01) between 90 and 120 minutes after angioplasty. VWBF in the adjacent nondilated arterial segment was also increased (720 +/- 177% between 10-30 minutes, p less than 0.01) but returned toward normal after 60 minutes. Adenosine caused a "paradoxical" decrease in VWBF (p less than 0.05) of the dilated arterial segment while causing increased VWBF (p less than 0.05) in the thoracic aorta. Angioplasty appears to produce persistent hyperemia in the dilated arterial wall. A paradoxical response to adenosine suggests that vasa vasorum in the dilated arterial segment are maximally vasodilated. This may be due to mechanical disruption of vasomotor tone or to release of vasoactive substances.

The implication of vasa vasorum in surgical diseases of the aorta

“…A network of capillaries/venules is then laid down around the outer media, and the vasa vasorum veins empty into the veins in close proximity to the arteries [9]. Interest in the vasa vasorum has lasted for more than a century [10], first because of their attribute to supply blood to the walls of host vessels, and, second, because of their possible participation in certain cardiovascular diseases, such as atherosclerosis [7,[11][12][13][14][15][16], coronary interventions [17][18][19], diet-induced hypercholesterolemia [20][21][22][23], and hypertension [24][25][26]. It is remarkable that removal of periaortic fat containing the vasa vasorum [27] or occlusion of the vasa vasorum surrounding the abdominal aorta of dogs [11] causes extensive medial necrosis and changes aortic reactivity in vivo.…”

Scanning Electron Microscopic Studies of the Vasa vasorum of Thoracic Aortas

“…One school claims there is none below the abdominal aortas limiting the critical depth to a certain number of lamel lar units [Ramsey, 1936;Wolinsky and Glagov, 1967: Geiringer, 19511. whereas another group shows the pres ence of vasa vasorum even in the common iliac arteries of the rat [McGeachie et al, 1982], canine carotid ar teries [Cragg et al, 1983], and human femoral arteries [Train et al, 1982], Because of this discrepancy, and because of possible diffusion from the luminal side of blood into the tunica media of the aortic wall [Schlicter, 1946], it has commonly been accepted that the first 0.5 mm thickness at the internal elastic lamina (I EL) is avascular [Geiringer, 1951;Heistad et al, 1978], Thus, classically the vasa vasorum have been consi dered to exist mainly in the adventitia and enter the media of large arteries, in the zone where the arterial wall is unable to obtain adequate amounts of oxygen and nutrients from the arterial lumen because of the long diffusion distance. In 1967.…”

Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E −/− /Low-Density Lipoprotein −/− Double Knockout Mice

“…[1][2][3][4][5][6] Acute and chronic inflammation of large blood vessels, as seen in atherosclerosis, is associated with proliferation of VV and is one of the predominant vascular responses that may function to sustain by perfusing the vessel wall beyond diffusion limits from the artery lumen. 6 VV may also facilitate monocyte/macrophage entry into the lesion and cause intraplaque hemorrhage.…”