Presence Of Vasa Vasorum Research Articles

Morphological and ultrasonographic characterization of the three zones of supratesticular region of testicular artery in Assaf rams

To fully understand the histological, morphometrical and heamodynamic variations of different supratesticular artery regions, 20 mature and healthy Assaf rams were examined through ultrasound and morphological studies. The testicular artery images of the spermatic cord as shown by B-mode analysis indicated a tortuous pattern along its course toward the testis, although it tends to be less tortuous close to the inguinal ring. Doppler velocimetric values showed a progressive decline in flow velocity, in addition to pulsatility and vessel resistivity when entering the testis, where there were significant differences in the Doppler indices and velocities among the different regions. The peak systolic velocity, pulsatility index and resistive index were higher in the proximal supratesticular artery region, followed by middle and distal ones, while the end diastolic velocity was higher in the distal supratesticular region. The total arterial blood flow and total arterial blood flow rate reported a progressive and significant increase along the testicular cord until entering the testis. Histological examination revealed presence of vasa vasorum in the tunica adventitia, with their diameter is higher in the proximal supratesticular zone than middle and distal ones. Morphometrically, the thickness of the supratesticular artery wall showed a significant decline downward toward the testis; meanwhile, the outer arterial diameter and inner luminal diameter displayed a significant increase distally. The expression of alpha smooth muscle actin and vimentin was higher in the tunica media of the proximal supratesticular artery zone than in middle and distal ones.

Presence of vasa vasorum in human intracranial aneurysms.

Vasa vasorum is associated with the pathogenesis of various cerebrovascular diseases, but its presence in intracranial aneurysms (IA) and its ability to act as a predicting factor of IA rupture remain unrevealed. Histological investigation was performed for 3 middle meningeal arteries and 25 human IAs that were sequentially collected from 2017 to 2019. Relevant medical information was collected from the hospital information and imaging system. Fisher's exact tests and Student's t tests were performed to identify the histological and clinical differences between aneurysms with and without vasa vasorum. Vasa vasorum were present in 14/25 (56%) aneurysm samples. They were detected at a similar frequency in male patients (4/9, 44.4%) and (10/16, 62.5%) female patients. Patients with vasa vasorum present aneurysms (47.07 ± 3.668years, n = 14) or vasa vasorum absent aneurysms (50.27 ± 2.289years, n = 11) did not differ in age (p = 0.49). True aneurysms and pseudoaneurysms also shared a similar rate of vasa vasorum presence (10/16, 62.5% in true aneurysms vs 4/9, 44.4% in pseudoaneurysms). The average size of aneurysms with vasa vasorum varied from 21.70 to 3.00mm, and no statistical difference in size was detected when comparing aneurysms with and without vasa vasorum (p = 0.71). The vasa vasorum in almost all IAs had uniform vascular trajectory with occasional exceptions. The presence of vasa vasorum appears to be tightly associated with important histopathological changes of myointimal hyperplasia and increased immune cell infiltration in IAs (both p value < 0.05), though it does not appear to be indicative of IA rupture or other rupture-related histological degenerations (all p values > 0.05). The presence of vasa vasorum is common in IAs. While it is associated with aneurysm wall remodeling and robust inflammatory cell infiltration, our results indicate that it is not a single specific marker of rupture-prone aneurysms.

The Bilateral Ovariectomy in a Female Animal Exacerbates the Pathogenesis of an Intracranial Aneurysm

Considering the poor outcome of subarachnoid hemorrhage (SAH) due to the rupture of intracranial aneurysms (IA), mechanisms underlying the pathogenesis of IAs, especially the rupture of lesions, should be clarified. In the present study, a rat model of IAs in which induced lesions spontaneously ruptured resulting in SAH was used. In this model, the combination of the female sex and the bilateral ovariectomy increased the incidence of SAH, similar to epidemiological evidence in human cases. Importantly, unruptured IA lesions induced in female animals with bilateral ovariectomy were histopathologically similar to ruptured ones in the presence of vasa vasorum and the accumulation of abundant inflammatory cells, suggesting the exacerbation of the disease. The post-stenotic dilatation of the carotid artery was disturbed by the bilateral ovariectomy in female rats, which was restored by hormone replacement therapy. The in vivo study thus suggested the protective effect of estrogen from the ovary on endothelial cells loaded by wall shear stress. β-estradiol or dihydrotestosterone also suppressed the lipopolysaccharide-induced expression of pro-inflammatory genes in cultured macrophages and neutrophils. The results of the present study have thus provided new insights about the process regulating the progression of the disease.

Immune cells and vasa vasorum in the tunica media of atherosclerotic coronary arteries.

In coronary artery disease (CAD), the disruption of the tunica media immune privilege manifests as increased leukocyte infiltration and the formation of vasa vasorum. We aimed to characterize the immune privilege status of the tunica media in human coronary arteries (CAs) with atherosclerotic plaques, by comparing the abundance and composition of immune-cell infiltrates within the individual arterial-wall layers, and by evaluating vasa vasorum neovascularization of the tunica media. The tissue samples were obtained from 36 symptomatic patients with diffuse CAD (aged 60-72 years) who underwent coronary endarterectomy. T and B cells, macrophages and endothelial cells in the CAs were detected by immunohistochemistry. Morphological analysis of CAs showed significant atherosclerotic changes in all specimens. In the media, we observed damage and loss of smooth muscle cells, destruction of the extracellular matrix architecture, and fibrosis. There were 43.3% of immune cells in the intima, 50% in the adventitia, and 6.7% in the media. In the media, 51.1% of the immune cells were T cells (p ˂ 0.001 compared to B cells and macrophages; ANOVA, Scheffe post hoc analysis), 23.5% were B cells, and 25.4% were macrophages. The number of vasa vasorum in the media was 1 in 38.9% of CAs, 2-3 in 36.1%, and ≥4 in 25% of CAs. Our results indicate that, in atherosclerotic CAs, the immune privilege of the media is disrupted by the infiltration of T and B cells, macrophages, and the presence of vasa vasorum.

Vessel Wall Enhancement in Unruptured Intracranial Aneurysms: An Indicator for Higher Risk of Rupture? High-Resolution MR Imaging and Correlated Histologic Findings.

Recent studies have suggested that wall enhancement of unruptured intracranial aneurysms in high-resolution MR imaging might serve as an imaging biomarker for higher risk of rupture. Histologic studies have revealed a possible association among inflammatory processes, degeneration, and destabilization of the aneurysm wall preceding rupture. Understanding the histologic condition underlying aneurysm wall enhancement could be an important step toward assessing the value of this method for risk stratification. We present our observations of aneurysm wall enhancement in MR vessel wall imaging and underlying histologic changes. We reviewed records of patients with an unruptured middle cerebral artery aneurysm who underwent MR vessel wall imaging before aneurysm clipping. Contrast enhancement of the aneurysm wall was dichotomized into either none/faint or strong. Histologic analysis included myeloperoxidase stain for detection of inflammatory cell invasion and CD34 stain for assessment of neovascularization and vasa vasorum. Thirteen aneurysms were included. Five aneurysms showed strong wall enhancement. Among these, myeloperoxidase staining revealed inflammatory cell infiltration in 4. Three showed neovascularization. In 2 aneurysms, vasa vasorum were present. Seven aneurysms did not show wall enhancement; 1 had only mild enhancement. None of these bore evidence of inflammatory cell invasion or neovascularization, and they all lacked vasa vasorum. Wall enhancement in MR vessel wall imaging is associated with inflammatory cell invasion, neovascularization, and the presence of vasa vasorum. Enhancement does not occur when histologic signs of inflammation are absent. Our results support the hypothesis that MR vessel wall imaging could provide valuable information for risk stratification.

Endothelium and Fibrinolysis in Hypertension

Despite the blood vessels in hypertension being exposed to high pressure, the main complications of hypertension (ie, heart attacks and stroke) are paradoxically thrombotic in nature rather than hemorrhagic. Increasing clinical and laboratory evidence is consistent with the concept that hypertension, per se, may confer a prothrombotic or hypercoagulable state, with abnormalities of coagulation, platelets, and the endothelium.1 Indeed, it has long been suggested that the latter organ, with roles in hemostasis and in regulating the NO/endothelin-mediated relaxation and contraction of the blood vessel wall, may be both a target and/or promoter of hypertension and a promoter of thrombosis and, thus, atherosclerosis.2 Other evidence linking the endothelium to atherogenesis is the presence of vasa vasorum in the adventitia and media at a higher density in atherosclerotic tissue, as well as neovascularization and collateral growth bypassing stenotic vascular disease. Such neovascularization reflects the process of angiogenesis, and given these close links, it is no surprise that angiogenesis is yet another important aspect of the pathophysiology of vascular disease, intimately linked with both thrombogenesis and atherogenesis, in a new “vascular triad.”3 For example, the major angiogenic growth factor, vascular endothelial growth factor, is linked with both NO and with a major proinflammatory cytokine, interleukin-6.3 However, skeptics would argue that the clinical (ie, human) evidence does not conclusively show evidence of overt angiogenesis, per se, in conditions such as hypertension, despite (eg) the …