Coronary arterial anatomy: Normal, variants, and well-described collaterals
Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead in Cardiovascular Catheterization and Intervention, 2017
The next layer is the tunica media or simply media. It surrounds the internal elastic lamina, and its composition depends on the type of artery. Large arteries have additional circumferential layers of elastic tissue within the media and are referred to as elastic arteries. The epicardial coro- nary arteries are elastic arteries, as are the carotids, cerebral arteries, and the aorta. However, at the point the epicardial arteries turn into the myocardium, usually at a right angle from the parent vessel, they become more muscular arteries with few, if any, elastic fibers.[6] In normal arteries, the vessel lumen diameter can be altered by contraction or relaxation of the medial vascular smooth muscle in response to a variety of systemic signals and locally released factors. The final layer is the tunica adventitia or simply adventitia, which is a layer of loose connective tissue surrounding the media.[6] In elastic arteries, this is demarcated by a layer of elastic fibers termed the external elastic lamina. The adventitia contains a network of small blood vessels (vaso vasorum), which are responsible for nutrition of the outer two-thirds of the artery. The inner third of the artery derives nutrition by diffusion through the endothelium. The adventitia also contains nerves that control the constriction and relaxation of the artery. In various locations within the adventitia, and associated with the outermost elastic layer, are pressure receptors. These pressure or baroreceptors have a phasic discharge rate in harmony with the arterial stretching asso- ciated with the pulse wave. Impulses from the baroreceptors are integrated centrally and when increased or decreased cause appropriate alterations in many vascular beds.
The Cardiovascular System
Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard in Toxicologic Pathology, 2018
This type of injury often involves thickening of vascular intima, endothelial activation/loss, and disruption of internal elastic lamina (Frazier et al. 2015a). Mixed or predominately lymphocytic inflammatory infiltrates may be seen in the vascular wall or surrounding adventitia. There may be mural hypertrophy as opposed to mural degeneration/necrosis which is commonly seen in small molecule-related vascular injury (Frazier et al. 2015a). Intimal hyperplasia is often present, predisposing to thromboemboli which can dislodge and occlude vessels with smaller diameter, ultimately leading to secondary tissue necrosis. Due to relatively long half-lives of biopharmaceuticals, it might take several weeks to months to achieve true exposure free intervals and recovery of vascular alterations. Biopharmaceutical-related morphologic alterations can be distributed widely within the vascular bed, occurring in capillaries, venules, and occasionally larger arteries (Frazier et al. 2015a). They commonly occur in monkeys within small to medium caliber vessels of kidney, heart, pancreas, gall bladder, and gastrointestinal tract (Rojko et al. 2014). Any or both of the following diagnostic terms are preferred to communicate biopharmaceutical-related vascular injury in nonclinical studies: (1) inflammation/inflammatory infiltrate, artery, with mural/perivascular as modifier(s) and (2) hypertrophy/hyperplasia, artery, intima (Frazier et al. 2015a). When degeneration/necrosis of the medial wall is present, they may be captured with mural inflammation or as a separate diagnosis, depending on their incidence and severity. A dose-free interval of 6–12 weeks may be necessary to demonstrate reversal of biopharmaceutical-related morphologic alteration (Frazier et al. 2015a).
Eversion carotid endarterectomy
Sachinder Singh Hans, Alexander D Shepard, Mitchell R Weaver, Paul G Bove, Graham W Long in Endovascular and Open Vascular Reconstruction, 2017
Care must be taken to avoid beginning different planes of dissection for plaque removal. The distal end point of the plaque in the ICA is visualized and disengaged from the underlying media. Demonstration of the plaque shows a feathered end superficial to the internal elastic lamina. This natural transition and termination for plaque allows for a tapered end of the carotid occlusive disease (COD).
Suppression of type 2 diabetes mellitus-induced aortic ultrastructural alterations in rats by insulin: an association of vascular injury biomarkers
Published in Ultrastructural Pathology, 2020
Norah M. Alzamil, Amal F. Dawood, Peter W. Hewett, Ismaeel Bin-Jaliah, Abdullah S. Assiri, Dina H. Abdel Kader, Refaat A. Eid, Mohamed A. Haidara, Bahjat Al-Ani
To test the hypothesis that insulin can ameliorate aortic ultrastructural alterations secondary to T2DM, we investigated the impact of insulin treatment for 8 weeks on the development of T2DM-induced aortic injury using TEM. TEM images of the aortic wall layers, tunica intima and tunica media are shown in Figure 4. As expected normal architecture of endothelium in the tunica intima (Figure 4(a)) and vascular SMC in the tunica media (Figure 4(b)) was present in the control group. These showed the normal appearance of endothelial cells (En) resting on a clear basement membrane (black arrow) adjacent to the lumen (Lu) of the blood vessel. The image of tunica media shown in Figure 4(b) is similar to the one described in detail in Figure 1(b); obtained from the same control group of rats. Whereas, the tunica intima of the aortic wall in T2DM rats (Figure 4(c)) showed a degenerating endothelial cells (En) protruding into lumen (Lu) and resting on an interrupted basement membrane (black arrow). A relatively thickened internal elastic lamina (e) is also seen. The aortic wall layer tunica media shown in Figure 4(d)) is similar to the image described in details in Figure 1(d)); obtained from the same T2DM group of rats.
Berberine alleviates monosodium glutamate induced postnatal metabolic disorders associated vascular endothelial dysfunction in newborn rats: possible role of matrix metalloproteinase-1
Published in Archives of Physiology and Biochemistry, 2022
Abeer A. Abo Zeid, Ibrahim Rowida Raafat, Abeer G. Ahmed
Ultra structural examination of the aorta of a control rats exhibited that the endothelial cells of the intima were flat and regular continues internal elastic lamina. Smooth muscle cells of the media appeared irregular with branched cells (Figure 5(A,B)). However, that of MSG group revealed that the endothelial cells of the intima became atrophic and degenerated with interrupted internal elastic lamina (Figure 6(A)). The smooth muscle cells of the media showed intra-cytoplasmic fatty deposition (Figure 6(B)). The intima was more atrophied with irregular distribution of the endothelial cells. The sub-endothelial region was apparently thickened with interrupted internal elastic lamina. The smooth muscle cell was seen migrating from the media to the sub-endothelial region (Figure 6(C)). The internal elastic lamina was interrupted and fat droplets could be seen in the cytoplasm of the smooth muscle cell (Figure 6(D)). Infiltrating mononuclear cells could be observed in the sub-endothelial region (Figure 6(E)).
Association of CD40 SNPs with Moyamoya in a Chinese children population
Published in British Journal of Neurosurgery, 2019
Wenjun Shen, Yujun Liao, Roxanna Garcia, Kartik Kesavabhotla, Bin Xu, Hao Li
The pathologic process resulting in MMD is through the fibrous eccentric intimal thickening in the proximal internal carotid artery without obvious lipid accumulation. The internal elastic lamina is moderately present but continuous.33 The medial smooth muscle cells have been found to be hypertrophic in the posterior circulation and among coexisting neurofibromatosis type 1 cases.33,34 Masuda et al.35 noted the infiltration of macrophages and T cells in non-stenotic areas. Some have suggested that treating inflammation may play a role in MMD.36 Although, no inflammatory cell infiltration was identified in the stenotic segments.33 One possible explanation is that the chronic inflammation in the vascular wall is the trigger of subsequent stenosis, and macrophages could be activated through the CD40 pathway.37 Endothelial cells, SMCs, and macrophages are target effector cells that are mediated through CD40 ligand and could stimulate proliferation and inflammation in the outbreak and development of MMD. The role between CD40 and the development of MMD remains to be clearly defined and should be an area for future research.
Related Knowledge Centers
- Ageing
- Arteriole
- Basement Membrane
- Elastic Artery
- Giant Cell Arteritis
- Smooth Muscle
- Tunica Intima
- Tunica Media
- Muscular Artery
- Charcot–Bouchard Aneurysm