What is the internal elastic lamina?
1.4 Internal Elastic Lamina (IEL) The internal elastic lamina is a fenestrated sheet that forms the boundary between the intimal and medial layers, influencing both its mechanical and mass transport properties. The size and number of these fenestrae vary in the arterial system and change with maturation [100,118].
Which vessel contains internal elastic lamina?
Arterioles contain an internal elastic lamina and one or two layers of smooth muscle cells.
What does outer elastic lamina of artery consist of?
The walls of elastic arteries are composed of three layers: (1) the tunica intima, which is a single-cell layer of endothelial cells adjacent to the arterial lumen; (2) the tunica media, which is composed of concentric layers of collagen and elastic fibers composed of smooth muscle cells and elastin; and (3) the tunica ...
Is there internal elastic lamina in veins?
Veins. An internal elastic membrane is absent. The tunica media is relatively thin. The tunica adventitia is the thickest tunic and there is no external elastic membrane.
Which of the artery types contain the internal and external elastic lamina?
The tunica media of the muscular arteries contains few elastic fibers and large amounts of smooth muscle. The tunica media has a layer of elastic tissue on its internal and external aspects; they are known as the internal elastic lamina and external elastic lamina, respectively.
What is the external elastic lamina?
n. A layer of elastic connective tissue lying immediately outside the smooth muscle of the tunica media of an artery. Also called external elastic layer.
What type of tissue is lamina propria?
loose connective tissueThe lamina propria (LP) is thin and composed of loose connective tissue with sparse collagen.
What is the function of the internal elastic membrane?
The IEL represents a flexible barrier between the endothelium and inner smooth muscle cell layer and may have a role in atherogenesis via its modulation of diffusion across the artery wall (Hutchison & Sanders, 1990; Osborne-Pellegrin, 1986).
What is elastin made of?
What is elastin made of? Amino acids make up proteins. The main amino acids that make up elastin are proline, glycine, desmosine and isodesmosine. They're grouped in short, repeated sequences of three to nine amino acids which create strong, flexible structures.
Why does the aorta have so many elastic lamina?
Elastic arteries are those nearest the heart (aorta and pulmonary arteries) that contain much more elastic tissue in the tunica media than muscular arteries. This feature of the elastic arteries allows them to maintain a relatively constant pressure gradient despite the constant pumping action of the heart.
What is the function of the elastic lamellae?
Microstructural deformation of elastic lamellae plays important roles in maintaining arterial tissue homeostasis and regulating vascular smooth muscle cell fate.
Which is the innermost layer of a blood vessel?
tunica intimaThe innermost layer, the tunica intima (also called tunica interna), is simple squamous epithelium surrounded by a connective tissue basement membrane with elastic fibers. The middle layer, the tunica media, is primarily smooth muscle and is usually the thickest layer.
Does arterioles have internal elastic lamina?
The medial layer in arterioles consists predominantly of vascular smooth muscle cells and an internal elastic lamina.
Do muscular arteries have internal elastic lamina?
In muscular arteries, smooth muscle becomes the predominant constituent of the tunica media. Internal and external elastic laminae are prominent.
Which blood vessel has an external elastic layer?
Muscular Artery Tunica media: - muscle layer, (with some elastin and collagen), sandwiched by an Internal Elastic Layer (IEL), and an External Elastic Layer (EEL). Notice how the tunica media layer is relatively smaller than that for the elastic artery.
Do veins have elastic fibers?
But unlike the arteries, the venous pressure is low. Veins are thin-walled and are less elastic. This feature permits the veins to hold a very high percentage of the blood in circulation.
What is the internal elastic lamina?
The internal elastic lamina is a fenestrated sheet that forms the boundary between the intimal and medial layers, influencing both its mechanical and mass transport properties. The size and number of these fenestrae vary in the arterial system and change with maturation [100,118]. The main function of the fenestrae (or pores) in the IEL, clearly seen in Figs. 8.2b,c and 8.8b, appears to be the enhancement of passage of water, nutrients and electrolytes across the wall. Using a two-dimensional model for macromolecular transport, Tada and Tarbell concluded transport of ATP but not low density lipoproteins is sensitive to IEL pores distribution [288]. Furthermore, three-dimensional models of transmural flow of water through these pores suggest shear stresses on VSMCs adjacent to the IEL could be large enough to influence cell proliferation and migration [286,287]. The density and area fraction of these pores have also indirectly been shown to have a modest influence on the mechanical properties of the IEL [42,43]. Note that the IEL is also conjectured to play a role in preventing direct contact between precursor VSMC and ECs [152]; however, physical contact between ECs protruding through these pores and establishing contact with VSMCs have been reported [238].
How does the intimal cushion form?
The increase in intimal thickening is due (1) to migration of smooth muscle cells from the muscle media into the intima and (2) to proliferation of luminal endothelial cells. The process of intimal cushion formation starts with the accumulation of hyalurona (HA) below the luminal endothelial cells. This is accompanied by the loss of laminin and collagen IV from the basement membrane of the endothelial cells and their subsequent separation from the internal elastic lamina. Laminin and collagen IV ultimately reform under the detached endothelial cells, but HA continues to accumulate in the subendothelial space. The hygroscopic properties of HA cause an influx of water and widening of the subendothelial space; this creates an environment well suited for cell migration. Accompanying the increase in HA is an increase in fibronectin (FN) and chondroitin sulfate (CS) in the neointimal space (de Reeder et al, 1988). The endothelial and smooth muscle cells of the ductus arteriosus differ from those of the adjacent vessels in their ability to form neointimal cushions. Isolated endothelial cells of the ductus arteriosus have an increased rate of HA, FN, and CS accumulation compared with those of the aorta or pulmonary artery (Boudreau et al, 1992). Hyaluron makes ductus smooth muscle cells migrate faster. The potentiating effect of HA on ductus smooth muscle cells is mediated through a hyaluron-binding protein (RHAMM). After delivery, there is a marked increase in ductus arteriosus transforming growth factor (TGF)-β expression, which accentuates the accumulation of HA within the neointima. Prostaglandins, acting through the EP4 receptor, also appear to play a critical role in HA production in the ductus (Yokoyama et al, 2006a). Fibronectin plays an important role in facilitating ductus smooth muscle cell migration. When fibronectin production in the ductus is inhibited, intimal cushion formation is blocked (Mason et al, 1999). CS appears to have no direct effect on ductus smooth muscle cell migration (Boudreau et al, 1990).
How does the intima thicken after delivery?
In the full-term newborn there are progressive intimal thickening and fragmentation of the internal elastic lamina after delivery. As the intima increases in size, it ultimately forms mounds that occlude the already constricted lumen. The increase in intimal thickening is due (1) to migration of smooth muscle cells from the muscle media into the intima and (2) to proliferation of luminal endothelial cells. The process of intimal cushion formation starts with the accumulation of hyaluron (HA) below the luminal endothelial cells. This is accompanied by the loss of laminin and collagen IV from the basement membrane of the endothelial cells and their subsequent separation from the internal elastic lamina. The hygroscopic properties of HA cause an influx of water and widening of the subendothelial space; this creates an environment well-suited for cell migration (Boudreau et al., 1991). The endothelial and smooth muscle cells of the ductus arteriosus differ from those of the adjacent vessels in their ability to form neointimal cushions. Isolated endothelial cells of the ductus arteriosus have an increased rate of HA accumulation compared with those of the aorta or pulmonary artery; this increase appears to be due to transforming growth factor β (Boudreau et al., 1992 ), which is markedly increased in the ductus after birth. PGs, acting through the EP4 receptor, also appear to play a critical role in HA production in the ductus ( Yokoyama et al., 2006). Fibronectin and chondroitin sulfate also play an important role in facilitating ductus smooth muscle cell migration (Boudreau et al., 1991 ).
What are the cracks in the IEL?
8.16. As early as the 1920s, Reuterwall reported ‘tears’ in human IELs. These breaks in the IEL have been termed ‘Reuterwall’s tears’ by Hassler[113]. Such tears, visible as 700–3000 micron long gaps in the IEL, were nearly always found oriented in the circumferential direction (Chapter 5 of [113]), e.g., Fig. 8.16 a. They were most common in larger cerebral vessels such as the basilar and vertebral arteries and generally located away from bifurcations formed by two larger vessels. These tears were uncommon in individuals less than 30 years of age (Chapter 5 of [113] ). Cracks have also been seen in experimental arteriovenous fistulas created between the common carotid artery and jugular vein [39]. In this latter case, no evidence of elastolytic activity was found, so the cause was hypothesized to be due to direct overstressing (acute rupture) or from fatigue-type wear. Histological examination of the IEL from common carotid arteries subjected to longitudinal [39] and circumferential uniaxial loading [118,243] has also shown damage to the IEL in the form of mechanically induced tears, Fig. 8.16 b and c.
Does elastin affect smooth muscle?
The exact relationship between impaired elastin assembly and smooth muscle migration into the neointima is still open for speculation. Impaired assembly of thick elastic laminae might facilitate smooth muscle cell migration by removing a physical barrier. In addition, truncated tropoelastin may act as a chemoattractant for smooth muscle cells (Mecham et al., 1984 ). Conversely, in some genetic forms of PDA, the elastic laminae of the ductus appear abnormally well developed and similar to those in the aorta; when this occurs, intimal cushions fail to develop ( de Reeder et al., 1990; Hsieh et al., 2014; Yokoyama et al., 2014 ).
How long after graft surgery does the elastic lamina lose cells?
Studies using transmission electron microscopyhave reported that between 1 and 4 hours after graft surgery, there is evidence of endothelial damage with cell loss, and the internal elastic lamina is observed as a discontinuous and amorphous line of elastin.
What is the function of the intima?
The intima, as a function of age, consisted of splitting of the internal elastic lamina into two membranes between which smooth muscle fibers were seen, constituting the 'musculoelastic layer'.
Is fibromuscular dysplasia heterogeneous?
Histopathologically, Fibromuscular Dysplasia (FMD) is heterogeneous with various degrees of collagen hyperplasia, internal elastic lamina rupture and disorganization of the tunica media.
Is the MCA the same as the elastic artery?
The MCA is a muscular artery and muscular arteries generally have the same basic composition as elastic arteries but the elastic tissue is reduced to a well-defined, fenestrated elastic sheet, the internal elastic lamina, in the tunica intima, and a diffuse external elastic lamina in the tunica adventitia.
What is the adventitial layer?
The adventitial layer consists of fibroblasts, extracellular matrix, thick bundles of collagen fibers organized along the longitudinal axis of the blood vessel .[3] Evidence suggests that some of the adventitial fibroblasts may consider as a stem mesenchymal progenitor cells.[4] Nonmyelinated free nerve endings are distributed in the adventitial layer approximately 5 µm way from the outermost part of vascular smooth muscle.[5] Recent studies have shown, elastic fibers arranged longitudinally in the outer layer allow arterioles to elongate or recoil in expandable tissues such as skeletal muscle. Arterioles within these expandable tissues usually possess additional external elastic lamina, which is absent in non-expandable tissues like the brain. [6]
What are the smooth muscle cells in the tunica media of the arteriole?
Like other blood vessels, arterioles contain only smooth muscle cells in their middle coat along with other connective tissues, including elastic tissue. Smooth muscle cells are the most abundant component of the tunica media of an arteriole.[34] They are spindle-shaped and transversally arranged to the long axis of the vessel having a luminal side facing toward the internal elastic lamina and abluminal side facing toward the adventitia. The primary function of these smooth muscle cells is to control arteriolar lumen diameter by their contraction or relaxation processes. Although they have the unique ability to detect and respond to mechanical forces under physiological conditions, arteriolar smooth muscle cells display a partial contraction to exert tone. [10][35]
How do endothelial cells control vessel tone?
Functionally, endothelial cells control vessel tone by synthesis and release of vasoactive factors that exert their potential effects on neighboring smooth muscle cells . The functional properties of endothelial cells interlink with their structure. EC has an excellent capacity to sense and transduce mechanical forces and produce vasoactive compounds that can fine-tune the tone of adjacent smooth muscle cells for the appropriate regulation of arteriolar diameter. [2][18][19][20]