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Medial necrosis and acute alterations in aortic distensibility following removal of the vasa vasorum of canine ascending aorta.

OBJECTIVE: It is known that the outer layers of the thoracic aorta receive substantial blood flow through vasa vasorum. This study was undertaken to test the hypothesis that removal of vasa vasorum flow will alter the elastic properties of the ascending aorta. METHODS: Distensibility of the ascending aorta was determined before and 30 min after careful removal of the periaortic fat network which contains the vasa vasorum in 10 acutely instrumented dogs (experimental group) and the results were compared with those obtained from six weight matched sham operated control dogs. Aortic distensibility was measured using the formula: distensibility = 2 x pulsatile changes in aortic diameter divided by (diastolic aortic diameter x pulse pressure). Aortic pressures were measured directly from the ascending aorta by a pressure gauge. Aortic diameters were simultaneously determined by an elastic air filled ring connected to a transducer. The efficacy of the technique for the interruption of vasa vasorum blood supply to the aortic wall was proved in six additional animals by histology of transverse blocks of aortic wall from the area of interest. Histology was performed before vasa vasorum removal in two animals, 30 min after vasa vasorum removal in another two, and 15 d after vasa vasorum removal in the remainder. RESULTS: At baseline, there was no difference in the measured variables between the two groups. Aortic distensibility decreased significantly in the experimental group after vasa vasorum removal by 0.90(SEM 0.17) 10(-6).cm2.dyn-1 (p < 0.001), while it remained unchanged in the control group during the experiment. Complete removal of vasa vasorum of the ascending aorta was found in experimental group animals which were killed 30 min after operation, while ischaemic medial necrosis was observed in those killed 15 d after operation. CONCLUSIONS: Vasa vasorum removal led to an acute decrease in the distensibility of the ascending aorta. Lack of blood supply to the outer part of the aortic wall is most likely to have accounted for these findings.

Animals↗

Re-endothelialization of isolated segments of the canine carotid artery with reference to the possible role of the adventitial vasa vasorum.

This study was designed to determine if the adventitial vasa vasorum contribute to re-endothelialization of the canine carotid artery after removal of the endothelial flow surface. Casting studies demonstrated that vasa vasorum are present only in the adventitia of the canine carotid artery. Ninety autograft segments of the carotid artery from which the endothelium had been removed were implanted in both carotid arteries of 45 dogs. Glutaraldehyde-processed canine carotid allografts were positioned at each end to prevent pannus ingrowth and a Gore-Tex wrap to prevent periarterial tissue growth was placed into the outer wall. Three methods were used, with observations at 4 and 8 weeks. In method 1 the test segment was treated with superficial endarterectomy. In method 2 a balloon catheter was used to remove the endothelium. In method 3 balloon catheter denudation of the flow surface was also employed and, in addition, the adventitia was removed surgically as completely as possible, although a few vasa vasorum were shown to remain in some grafts. In method 1 all the patent endarterectomized arteries were partially re-endothelialized at both the 4- and 8-week intervals. In method 2, 72% of the balloon-denuded patent arteries with intact adventitial vasa vasorum were partially re-endothelialized at 4 weeks and 84% at 8 weeks. However, in method 3 the flow surfaces had no endothelium at 4 weeks and 83% still had none at 8 weeks. These findings suggest that, in the absence of pannus ingrowth, re-endothelialization of the canine carotid artery depends on not only the presence but also the number of adventitial vasa vasorum.

Animals↗

Experimental hypercholesterolemia differentially affects adventitial vasa vasorum and vessel structure of the left internal thoracic and coronary arteries.

OBJECTIVE: Atherosclerosis is a chronic and diffuse disease that affects all vascular beds. However, some vascular beds are more prone to atherosclerosis than others. Recent evidence suggests a role for the vasa vasorum in the atherosclerotic process. We hypothesized that there is a difference in adventitial vasa vasorum structure between the left internal thoracic artery and the coronary artery. Hence the current study was designed to characterize and compare the structure of the adventitial vasa vasorum in the left internal thoracic and coronary arteries. METHODS: Samples of vessels were obtained from female crossbred domestic pigs maintained on a normal (n = 6) or high-cholesterol (n = 6) diet for 12 weeks. The samples were scanned with micro-computed tomography, and the tomographic images were reconstructed and analyzed to obtain lumen area, vessel wall area, vasa vasorum count, vasa vasorum density, mean diameter of first- and second-order vasa vasorum, and second-order/first-order vasa vasorum ratio. RESULTS: Vasa vasorum density was significantly higher in the coronary arteries versus that seen in the left internal thoracic arteries in the normal group, as well as in the high-cholesterol group. The higher vasa vasorum density in the high-cholesterol group versus that in the normal group was significant for both vessels, being more pronounced in the left internal thoracic artery. Lumen area and second-order/first-order vasa vasorum ratio were higher in the high-cholesterol group than in the normal group only in the left internal thoracic artery. CONCLUSION: This study demonstrated that low vasa vasorum spatial density and higher lumen area observed in the left internal thoracic artery compared with that seen in the native coronary artery can be the structural background for the low incidence of atherosclerosis in this vessel.

Animals↗

Immunohistochemical detection of intracranial vasa vasorum: a human autopsy study.

The existence of intracranial vasa vasorum supplying the larger vessels of the circle of Willis has long been debated. Much of this debate results from contradictory findings of microanatomic studies in a variety of nonprimate species. Recently, however, a growing body of evidence seems to suggest that in certain pathological situations, such as human intracranial atherosclerosis, vasa vasorum are present. In an effort to determine whether intracranial vasa vasorum are present in humans without clinical evidence of intracranial vascular disease, we studied the circle of Willis in five autopsy specimens using immunohistochemistry. Antiserum to the endothelial-specific antigen, Factor VIII, revealed staining of 10- to 20-microns vascular channels in the outer media and adventitial layers. Staining was present in the proximal carotid, middle cerebral (M1), and anterior cerebral (A1) arteries but could not be detected in M2 or A2 segments. Hematoxylin and eosin staining was additionally helpful in identifying the nuclear morphology of the endothelial cells lining these channels, as well as the presence of erythrocytes within them. We conclude that in nonpathological settings, endothelial-lined channels exist in the proximal intracranial vessels of humans. These vessels might represent intracranial vasa vasorum, which in turn might play a role in pathological conditions, such as atheroma formation, intracranial dissection, and vasospasm.

Adolescent↗

Vasa vasorum growth in the coronary arteries of newborn pigs.

Experimental studies have shown that a "plexus" of vasa vasorum already exists in fetal arteries. In this study we examine the further development of vasa vasorum in the newborn. Hearts from 1- and 6-month-old pigs were harvested and infused with Microfil via the aortic ostia of the coronary arteries at physiological pressure (100 mmHg). Coronary arteries (RCA, LAD, and LCX) were then isolated and scanned intact with micro-CT (20 microm cubic voxel size). Using Analyze 5.0 software we digitally isolated individual vasa vasorum trees (eight from 1-month-old and eight from 6-month-old pigs) and measured geometrical data such as interbranch segmental diameters, lengths, and branching angles as well as mother-daughter branch relationships for all segments of each vasa vasorum tree structure. Also, we determined the volume of vessel wall perfused by individual vasa vasorum trees. Our results show that the vasa vasorum architecture in newborn pigs is already tree-like, and this structure as well as the volume of vessel wall perfused by it expand in concert with the growth of the host coronary artery. We give quantitative details of this growth of vasa vasorum in terms of its branching architecture and hemodynamic capacity, based on direct measurements from 3D images of this microvasculature.

Animals↗

Intracranial cerebrovascular vasa vasorum associated with atherosclerosis and large thick-walled aneurysms.

Atherosclerotic plaques that develop in the extracranial circulation are usually extensively vascularized by vasa vasorum. However, human vasa vasorum associated with intracranial atherosclerosis has not been adequately addressed. Anterior and posterior circulation specimens from fresh autopsy material were studied under the magnification of a dissecting microscope and proliferative vasa vasorum was found to be frequently associated with intrinsic atheromatous plaques. Vasa vasorum associated with an incidental large aneurysm supports the radiological literature demonstrating that many large and giant thick-walled aneurysms exhibit vascularized walls on contrast computed tomography scans. This information may aid in the preoperative assessment and possible repair of these aneurysms.

Adolescent↗

Three-dimensional arrangement of the vasa vasorum in explanted segments of the aged human great saphenous vein: scanning electron microscopy and three-dimensional morphometry of vascular corrosion casts.

The vasa vasorum of skeletonized and nonskeletonized segments of five human great saphenous veins (GSVs), harvested during coronary bypass grafting, were cannulated, rinsed, and injected (casted) with the polymerizing resin Mercox-Cl-2B. After removal of the dry vascular tissue, the casts were examined using scanning electron microscopy. Stereopaired images (tilt angle, 6 degrees ) were taken, imported into a 3D morphometry system, and the 3D architecture of the vasa vasorum (arterial and venous vasa as well as capillaries) was studied qualitatively and quantitatively in terms of vasa diameters, intervascular and interbranching distances, and branching angles. Diameters of parent (d(0)) and large (d(1)) and small (d(2)) daughter vessels of arterial and venous bifurcations served to calculate asymmetry ratios (alpha) and area ratios (beta). Additionally, deviations of bifurcations and branching angles from optimal branches were calculated for selected arterial vasa. The arrangement of the vasa vasorum closely followed the longitudinally oriented connective tissue fibers in the adventitia and the circularly arranged smooth muscle cell layers within the outer layers of the media. Venous vasa by far outnumbered arterial vasa. Vasa vasorum changed their course several times in acute angles and revealed numerous circular constrictions, kinks, and outpouchings. Due to their spatial arrangement, the vasa vasorum are prone to tolerate vessel wall distension generated by acute increases in blood pressure or stretching of the vessel without severe impact on vessel functions. Preliminary comparisons of data from the bifurcations of cast arterial vasa vasorum, with calculated optimal bifurcations, do not yet give clear insights into the optimality principle(s) governing the design of arterial vasa vasorum bifurcations of the human GSVs.

Aged↗

Coronary vasa vasorum neovascularization precedes epicardial endothelial dysfunction in experimental hypercholesterolemia.

OBJECTIVE: Experimental hypercholesterolemia is associated with vasa vasorum neovascularization, unknown to occur before or after initial lesion formation. Thus, this study was performed to determine the temporal course of neovascularization of coronary vasa vasorum in relation to endothelial dysfunction, a hallmark of early atherosclerosis. METHODS: Female domestic pigs were fed a normal diet (Group 1), a hypercholesterolemic diet for 2 and 4 weeks (Group 2), or a hypercholesterolemic diet for 6 and 12 weeks (Group 3). In vitro analysis of relaxation response to bradykinin served as an index for epicardial endothelial function. Spatial pattern and density of coronary vasa vasorum were assessed by three-dimensional microscopic computed tomography. RESULTS: Relaxation response of coronary arteries to bradykinin was normal in both Group 1 (93+/-6%) and Group 2 (89+/-7%) but impaired in Group 3 (71+/-11%; P<0.05 vs. Group 1 and 2). In contrast, density of coronary vasa vasorum was significantly higher in both Group 2 (4.88+/-2.45 per-mm(2)) and Group 3 (4.50+/-1.37 per-mm(2)) compared to Group 1 (2.97+/-1.37 per-mm(2); P<0.05 vs. Group 2 and 3). CONCLUSION: This study demonstrates that coronary vasa vasorum neovascularization occurs within the first weeks of experimental hypercholesterolemia and prior to the development of endothelial dysfunction of the host vessel, suggesting a role for vasa vasorum neovascularization in the initial stage of atherosclerotic vascular disease.

Analysis of Variance↗

Vasa vasorum visualised by power-Doppler in normal and arteriosclerotic carotid arteries.

Vasa vasorum and the perfusion of the carotid wall in normal arteries and in arteries with arteriosclerotic plaques was evaluated in-vivo using power-Doppler. Two types of arteries were studied using high-resolution ultrasound. These were arteries with a normal wall (intima, media and adventitia clearly separated) and arteries with intima-media thickening and plaques without calcification. In 10 normal subjects and in 10 patients with early plaques vasa vasorum were visualised. On power-Doppler they appeared as distinct, glomerular-like perfusion units, regularly placed along the course of normal arteries and at similar distance (2 to 4 mm from the lumen-wall interface, within the adventitia and periadventitia layers). In arteriosclerotic vessels the distribution of vasa vasorum units was more irregular, often concentrated in one spot with some perfusion units more distant from the lumen (between 2.5 and 5 mm) and their pulsatility was reduced. Flow velocity complex in most vasa vasorum was comparable, in lower scale to the pattern observed in the carotid lumen without significant differences between normal and arteriosclerotic arteries. The average peak systolic flow velocity was 15: +/-4 cm/sec and the average diastolic velocity was 6 +/- 4 in normal arteries with a median pulsatility index of 1.8 (range 2.2-1.05); in arteriosclerotic arteries velocities were 13 +/- 4 (peak systolic) and 3 +/- 2 (end diastolic) with a median pulsatility index of 1.71 (range 2.1-1.1). In conclusion a different, apparent distribution of vasa vasorum was observed in normal carotids and in carotids with arteriosclerotic lesions.

Adult↗

Role of vasa vasorum in nourishment of the aorta.

The media of arteries is virtually avascular. Thus, oxygen and nutrients must reach the cells of the media by diffusion from the lumen of the vessel and from adventitial vessels. The thickness of the thoracic aorta of man and dog exceeds the effective diffusion distance of oxygen, but nutrition is supplemented by vasa vasorum which enter into the outer layers of the media. Occlusion of vasa vasorum in dogs produces medial necrosis, which indicates that these vessels are essential for the nourishment of the aorta. Recently the microsphere method has been used to provide the first measurements of blood flow through vasa vasorum. There is substantial flow to the outer layers of media of the thoracic aorta in dogs, with virtually no blood flow in the inner layers. The vessels are very responsive to physiological stimuli: they dilate during infusion of adenosine and constrict during stimulation of sympathetic nerves. During acute increases in arterial pressure, blood flow to the media decreases probably from distortion of vasa vasorum. Vasa vasorum may play role in disease states. Insufficient blood flow through vasa vasorum may contribute to medial necrosis of the aorta and to aortic atherosclerosis. A role of vasa vasorum in aortic changes in hypertension and other vascular diseases merits further study.

Animals↗

The effect of balloon angioplasty on vasa vasorum blood flow in canine coronary arteries.

To assess the effects of balloon dilatation on vasa vasorum flow, we performed percutaneous transluminal coronary angioplasty on the circumflex arteries of 12 dogs. Left anterior descending and circumflex coronary vasa vasorum flows were measured with radioactive microspheres at baseline, during, and 10 minutes after a 3-minute, 8 atm balloon inflation. With inflation, vasa vasorum flow at the balloon dilatation site profoundly decreased (from 0.25 +/- 0.08 to 0.03 +/- 0.01 ml/min/gm). The flow returned to normal within 10 minutes after deflation. This effect was not mediated by hemodynamic deterioration during coronary occlusion and did not occur in the contralateral coronary artery. Endomyocardial flow in the distribution of the dilated artery decreased markedly during balloon inflation (from 1.14 +/- 1.9 to 0.08 +/- 0.04 ml/min/gm), which confirmed coronary occlusion. We conclude that a prolonged decrease in vasa vasorum flow is not produced by experimental balloon angioplasty, which makes it unlikely that a sustained vasa vasorum flow reduction plays a role in the maintenance of patency or the induction of restenosis.

Angioplasty, Balloon↗

Chronic endothelin receptor antagonism prevents coronary vasa vasorum neovascularization in experimental hypercholesterolemia.

OBJECTIVES: The purpose of this study was to test the hypothesis that endothelin (ET) receptor antagonism reduces coronary vasa vasorum neovascularization in experimental hypercholesterolemia. BACKGROUND: Experimental hypercholesterolemia is associated with increased expression of ET-1, an endothelium-derived peptide with vasoconstricting, mitogenic and angiogenic properties, in the coronary arterial wall as well as with vasa vasorum neovascularization. A pathomechanistic role of the endogenous ET system in vasa vasorum neovascularization in hypercholesterolemia has, however, remained uncertain so far. METHODS: Female domestic pigs were placed on a normal diet (N; n = 7) or on a hypercholesterolemic diet without (HC; n = 6) or with ET-A receptor antagonism (ABT-627, 4 mg/kg/day; HC + ET-A; n = 6). After 12 weeks, coronary vasa vasorum structure was assessed by three-dimensional microscopic computed tomography, expression of vascular endothelial growth factor (VEGF) within the coronary arterial wall by Western blotting and immunostaining. RESULTS: Compared with the N group, plasma concentrations of low-density lipoprotein cholesterol were higher in both the HC and HC + ET-A groups (36 +/- 3 mg/dl vs. 312 +/- 153 mg/dl and 303 +/- 113 mg/dl, p < 0.01). Vasa vasorum density was higher in the HC group compared with the N group (4.7 +/- 1.8 per mm(2) vs. 2.5 +/- 1.5 per mm(2); p < 0.05) and was preserved in the HC + ET-A group (3.2 +/- 0.7 per mm(2)). In parallel, increase in VEGF expression in the coronary arterial wall in the HC group was preserved in the HC + ET-A group. CONCLUSIONS: The current study demonstrates that chronic endothelin receptor antagonism prevents the increase in VEGF expression and vasa vasorum density of coronary arteries in experimental hypercholesterolemia. These findings support a role for the endogenous ET system in vasa vasorum neovascularization in early coronary atherosclerosis.

Animals↗

Effects of neural stimuli on blood flow through vasa vasorum in dogs.

The purpose of this study was to determine whether neural stimuli alter blood flow through vasa vasorum in the thoracic aorta. We measured flow with microspheres in anesthetized dogs and observed responses to sympathetic stimulation and baroreceptor stimulation. 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. Electrical stimulation of the stellate ganglion at 10 Hz reduced blood flow to vasa vasorum in the thoracic aorta from 11 +/- 1.6 (mean +/- SE to 6.8 +/- 1.1 ml/min per 100 g (p less than 0.05). Aortic diameter, measured with a sonomicrometer technique, did not change during sympathetic stimulation. Thus, the reduction in blood flow through vasa vasorum during sympathetic stimulation appears to be a direct effect, and not the result of constriction of the aorta and compression of vasa. To determine effects of physiological alterations in neurogenic vasoconstrictor activity, we examined responses to stimulation of carotid baroreceptors. When pressure in isolated, perfused carotid sinus baroreceptors was raised from 81 +/- 3 to 198 +/- 2 mm Hg, blood flow to vasa vasorum of the thoracic aorta increased from 3.7 +/- 0.6 to 10 +/- 2.2 ml/min per 100 g (P less than 0.05). We conclude that vasa vasorum are responsive to neural stimuli, since they constrict during sympathetic stimulation and dilate in response to baroreceptor stimulation.

Animals↗

Adventitial vasa vasorum in balloon-injured coronary arteries: visualization and quantitation by a microscopic three-dimensional computed tomography technique.

OBJECTIVES: The objective of this study was to examine the quantitative response of the adventitial vasa vasorum to balloon-induced coronary injury. BACKGROUND: Recent attention has focused on the role of vasa vasorum in atherosclerotic and restenotic coronary artery disease. However, the three-dimensional anatomy of these complex vessels is largely unknown, especially after angioplasty injury. The purpose of this study was to visualize and quantitate three-dimensional spatial patterns of vasa vasorum in normal and balloon injured porcine coronary arteries. We also studied the spatial growth of vasa vasorum in regions of neointimal formation. A novel imaging technique, microscopic computed tomography, was used for these studies. METHODS: Four pigs were killed 28 d after coronary balloon injury, and four pigs with uninjured coronary arteries served as normal controls. The coronary arteries were injected with a low-viscosity, radiopaque liquid polymer compound. Normal and injured coronary segments were scanned using a microscopic computed tomography technique. Three-dimensional reconstructed maximum intensity projection and voxel gradient shading images were displayed at different angles and voxel threshold values, using image analysis software. For quantitation, seven to 10 cross-sectional images (40 normal and 32 balloon injured cross-sections) were captured from each specimen at a voxel size of 21 microm. RESULTS: Normal vasa vasorum originated from the coronary artery lumen, principally at large branch points. Two different types of vasa were found and classified as first-order or second-order according to location and direction. In balloon-injured coronary arteries, adventitial vasa vasorum density was increased (3.16+/-0.17/mm2 vs. 1.90+/-0.06/mm2, p = 0.0001; respectively), suggesting neovascularization by 28 d after vessel injury. Also, in these injured arteries, the vasa spatial distribution was disrupted compared with normal vessels, with proportionally more second-order vasa vasorum. The diameters of first-order and second-order vasa were smaller in normal compared with balloon-treated coronary arteries (p = 0.012 first-order; p < 0.001, second-order; respectively). The density of newly formed vasa vasorum was proportional to vessel stenosis (r = 0.81, p = 0.0001). Although the total number of vasa was increased after injury, the total vascular area comprised of vasa was significantly reduced in injured vessels compared with normals (3.83+/-0.20% to 5.42+/-0.56%, p = 0.0185). CONCLUSIONS: Adventitial neovascularization occurs after balloon injury. The number of new vessels is proportional to vessel stenosis. These findings may hold substantial implications for the therapy of vascular disease and restenosis.

Angioplasty, Balloon, Coronary↗

Vasa vasorum of blood and lymph vessels in the broad ligament of the sheep uterus analyzed by scanning electron microscopy.

The morphology of vasa vasorum of the blood and lymph vessels in the broad ligament of the uterus was examined in 12 adult ewes. The technique of vascular corrosion casts with the usage of Mercox resin allows multiple surveys of a three-dimensional organization of vascular networks under a scanning electron microscope (SEM). The study was appended by tissue pieces dried by the critical point method for SEM and semi-thin sections stained with toluidyne blue for light microscopy. Vasa vasorum surrounded both the larger vessels and the lymph vessels emanating from the ovary and the uterus. Significant differences in location and intensity of vasa vasorum in blood vessels were observed. They were less developed in the first part of the ovarian and the uterine arteries than in their smaller branches. Significantly large, two- or even three-layer vasa vasorum surrounded the ovarian and the uterine branches of the ovarian artery as well as the ovarian veins in the area of mesovarium. In the other areas of the broad ligament of the uterus, arterial vessels of similar sizes usually had a single-layer vasa vasorum. The lymph vessels leaving the ovary and uterus were surrounded by dense, although usually single-layed, microvascular network. The presence of vasa vasorum on relatively small blood and lymph vessels of the broad ligament of uterus indicates their particular functions that are probably connected with the estrous cycle or pregnancy and changes of blood flow rate entering the ovary and uterus. However, the presence of significantly developed, multi-layer vasa vasorum networks on only some of the blood vessels indicates that it is probably one of the vessels morphological adaptations to serve the counter-current transfer of biologically-active regulators in the area of the broad ligament of the sheep's uterus.

Animals↗

Vasa vasorum in atherosclerotic coronary arteries: responses to vasoactive stimuli and regression of atherosclerosis.

The goals of this study were to determine whether vasa vasorum in atherosclerotic coronary arteries respond to vasoactive stimuli and to examine effects of regression of atherosclerosis on blood flow through vasa vasorum in coronary arteries. We studied three groups of monkeys: normal, atherosclerotic, and regression. Blood flow to vasa vasorum was measured with microspheres. Blood flow to intima-media (ml/min x 100 g) was 5 +/- 1 (mean +/- SEM) in normal and 47 +/- 7 in atherosclerotic monkeys (p less than 0.05). Infusion of phenylephrine or serotonin did not alter flow through vasa in normal monkeys. In atherosclerotic monkeys, phenylephrine decreased flow through vasa vasorum in intima-media of coronary arteries to 24 +/- 4 (p less than 0.05), and serotonin decreased flow to 27 +/- 5 (p less than 0.05). In regression monkeys, blood flow to intima-media was sixfold less (7 +/- 2 ml/min x 100 g) than in atherosclerotic monkeys (p less than 0.05). During infusion of adenosine, blood flow to vasa was fourfold greater in atherosclerotic monkeys than after regression of atherosclerosis. This finding suggests that loss of vessels, not constriction of existing vessels, accounts for the decrease in flow through vasa in intima-media after regression of atherosclerosis. We conclude that vasa vasorum in atherosclerotic coronary arteries respond to vasoconstrictor stimuli and that there is loss of vasa vasorum and a large decrease in blood flow through vasa to intima-media of coronary arteries after regression of atherosclerosis.

Animals↗

Arterial vasa vasorum: a quantitative study in the rat.

This study was designed to quantitate the vasa vasorum of common iliac arteries in 20 rats. The number of vasa vasorum per mm2 of arterial wall was extremely variable - from 0 to 124, the mean being 33 . 95 +/- 29 . 86 (S.D.). There was no significant difference in the vasa vasorum vascularity between the right and left common iliac arteries. The mean wall thickness of these arteries was 0 . 085 +/- 0 . 015 (S.D.) mm and 60 +/- 8% (S.D.) of this was made up by the tunica media. Arterial tissue in this study was shown to have approximately 10% of the vascularity of muscle tissue. By relating these data to the 'critical depth' hypothesis, on the nutritional supply of large arteries, it was concluded that the vasa vasorum in the common iliac arteries in rat (major arteries in small animals) probably play an insignificant role in the nutrition of the arterial wall.

Animals↗

Effects of aortic pressure and vasoactive agents on the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

1. We have developed a new preparation for continuously measuring changes in vascular resistance of the vasa vasorum of the canine isolated thoracic aorta perfused at a constant flow rate with Krebs-bicarbonate solution. 2. An increase of more than 150 mmHg in aortic pressure caused a significant increase in the vascular resistance of the vasa vasorum. 3. 5-Hydroxytryptamine (5-HT), noradrenaline (NA), adrenaline and dopamine caused dose-dependent increases in the vascular resistance of the vasa vasorum. The decreasing order of potency in the vasoconstrictor responses was as follows: 5-HT >> NA = adrenaline >> dopamine. The 5-HT- and adrenaline-induced vasoconstrictor responses were inhibited by methysergide and by phentolamine plus propranolol, respectively. 4. Acetylcholine (ACh), isoprenaline (ISP), histamine (His), ATP, ADP and adenosine produced dose-related decreases in the vascular resistance of aortic vasa vasorum perfused with the Krebs solution containing 10(-5) M-NA. The decreasing order of potency in the response was as follows: ACh = ISP > His >> adenosine = ATP = ADP. The ACh-, ISP- and His-induced vasodilator responses were antagonized by atropine, propranolol and famotidine, respectively. 5. The results suggest that the preparation described is useful for studying the regulation of vascular resistance of aortic vasa vasorum and that aortic pressure and vasoactive compounds may directly regulate the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

Animals↗