Role of shear stress and stretch in vascular mechanobiology

Lu, Dongsi; Kassab, Ghassan S.

doi:10.1098/rsif.2011.0177

Cited by 273 publications

(212 citation statements)

References 74 publications

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“…Stehbens et al [10] in their histological study of human UVs observed cell debris in the walls of umbilical vessels that could be attributed to hemodynamic stress of the fetoplacental circulation resembling early events of atherogenesis. Lu and Kassab, [15] stated that the vascular walls are subjected to three hemodynamic forces; the blood pressure created by cardiac contraction, the circumferential stretch of the vessel with the cardiac cycle, and the shear stress. Shear stress is the frictional force of the viscous blood on the endothelial surface.…”

Section: Histomorphometric Resultsmentioning

confidence: 99%

“…There was no external elastic lamina, adventitia, or vasa vasorum. Endothelial cells of intima showed vacuolations in H&E preparations whereas, it demonstrated positive adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1) and monocyte chemotactic protein 1 (MCP1) [15,17,19] . Recent studies indicate that disturbed blood flow and associated low and reciprocating shear stress induce a sustained activation of some atherogenic genes in endothelial cells like monocyte chemotactic protein-1 (MCP-1) that induces monocyte infiltration into the arterial wall [18] .…”

Section: Discussionmentioning

confidence: 99%

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Development of Human Umbilical Vessels in The Second Trimester of Pregnancy: Histological, Immunohistochemical and Morphometric Study

EI-Nefiawy

2017

Egyptian Journal of Histology

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Introduction: There are many publications describing structure of full term umbilical vessels, however, few studies in early gestation. Aim: To elucidate changes in microstructure of developing umbilical vessels in the second trimester of pregnancy. Material and Methods: Twelve specimens of human umbilical cords were obtained from legal termination of uncomplicated pregnancies at gestational weeks 13, 16, and 20. Two centimeter segments of the cords were cut near the placenta. Specimens were processed for paraffin blocks, sectioned, and stained with haematoxylin & eosin, Masson Trichrome, Orcein, and Periodic Acid Schiff. Immunohistochemistry for alpha smooth muscle actin & laminin antibodies was performed. Morphometry and image analysis for vascular wall thickness & diameter of lumen, and diameter of umbilical cord were done. Results: Umbilical cord sections revealed two arteries (UA) and one vein (UV) embedded in Wharton's jelly and covered with amniotic epithelium formed of flat then cuboidal epithelium. Umbilical vessels composed of inner intima and outer media. Endothelium demonstrated areas of damage and adhesion of inflammatory cells. Internal elastic lamina was thin, interrupted initially, double layered, and well-developed finally. Smooth muscle cells (SMCs) migrated from vascular lumen or from media by a process of mesenchymal-endothelial transition to replace injured endothelium. The media was composed of immature SMCs initially (thin (morphometry), non-contractile, non-secretory as proved by different stains and collagen content. Wharton's jelly spindle shaped mesenchymal cells close to vessels revealed positive staining for alpha smooth muscle actin and contributed to the media to compensate for SMC migration. UAs showed thicker wall, narrower lumen than veins and cord diameter increased significantly at the 20 week. Conclusion: Development of umbilical vessels was the result of a continuous remodeling process initiated by secreted endothelial factors from damaged endothelium that influenced; SMCs of media, stem cells of cord blood and Wharton's jelly simulating early events of atherosclerosis.

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Section: Histomorphometric Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Development of Human Umbilical Vessels in The Second Trimester of Pregnancy: Histological, Immunohistochemical and Morphometric Study

EI-Nefiawy

2017

Egyptian Journal of Histology

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“…Multiple other structures or molecules (e.g., caveolae and G proteins) may also serve as mechanosensors in SMC. 76,80,97,98 Considerably more work remains before we learn enough to allow the stretch response to be selectively manipulated toward investigative and therapeutic ends.…”

Section: Myogenic Vasoconstrictionmentioning

confidence: 99%

“…Finally, increased wall stress causes pathologic remodeling in systemic arteries. [73][74][75][76][77] Note that intravascular pressure is not the only plausible relevant mechanical force. The cross-sectional area of the pulmonary vascular bed is presumably reduced with PVHincreased PVR, implying (absent lower flow) that shear stress is increased.…”

Section: Wall Stress and Pvh-phmentioning

confidence: 99%

Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

Kulik

2014

Pulm. circ.

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The effect of pulmonary venous hypertension (PVH) on the pulmonary circulation is extraordinarily variable, ranging from no impact on pulmonary vascular resistance (PVR) to a marked increase. The reasons for this are unknown. Both acutely reversible pulmonary vasoconstriction and pathological remodeling (especially medial hypertrophy and intimal hyperplasia) account for increased PVR when present. The mechanisms involved in vasoconstriction and remodeling are not clearly defined, but increased wall stress, especially in small pulmonary arteries, presumably plays an important role. Myogenic contraction may account for increased vascular tone and also indirectly stimulate remodeling of the vessel wall. Increased wall stress may also directly cause smooth muscle growth, migration, and intimal hyperplasia. Even long-standing and severe pulmonary hypertension (PH) usually abates with elimination of PVH, but PVH-PH is an important clinical problem, especially because PVH due to left ventricular noncompliance lacks definitive therapy. The role of targeted PH therapy in patients with PVH-PH is unclear at this time. Most prospective studies indicate that these medications are not helpful or worse, but there is ample reason to think that a subset of patients with PVH-PH may benefit from phosphodiesterase inhibitors or other agents. A different approach to evaluating possible pharmacologic therapy for PVH-PH may be required to better define its possible utility.Keywords: pulmonary hypertension, pulmonary venous hypertension. As a perfect example of how clinical imperative can drive basic physiological investigation, studies of the effect of pulmonary venous hypertension (PVH) on the lung's circulation were in full swing by the very early 1950s, 1 close on the heels of the development of surgical relief of mitral valve stenosis. Cardiac catheterization of patients with mitral valve disease has characterized the physiology of PVH, and histological investigations demonstrated the microvascular changes provoked by PVH. Just as important, the effect of relief of left atrial (LA) hypertension on the circulation has been extensively reported, usually for patients who have had mitral valve intervention. We have learned that the circulatory alterations provoked by PVH share some characteristics with other forms of pulmonary hypertension (PH), such as the idiopathic variety, PH due to chronic alveolar hypoxia, and PH secondary to congenital cardiac shunting lesions. For example, acute "reactivity" to vasodilators may be observed, and there is overlap in the microarchitectural abnormalities seen. On the other hand, the "natural history" of PVH-PH is very different than that of the idiopathic variety or that seen with shunting defects: in the former (as demonstrated with mitral valve disease), PH is likely to largely or completely resolve if PVH is relieved, even with long-standing and severely increased pulmonary vascular resistance (PVR), 2,3 while in the latter two, PH is more likely to inexorably increase. PVH-PH is ther...

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“…In fact, it is well known that blood vessels are under constant mechanical loading from flowing blood which cause internal stresses, known as endothelial shear stress (caused by flow) and circumferential stretch (caused by pressure). These mechanical forces not only cause morphological changes of endothelium and blood vessel wall, but also trigger a myriad of intracellular events in endothelial cells and activate biochemical and biological events (Lu & Kassab, 2011). The triggering of endothelial signaling by mechanic forces seems to be mostly determined by the cytoskeleton, which represents a highly dynamic network that constantly assembles and disassembles, playing an active role in responding to mechanical stimuli (Wong et al, 1983).…”

Section: Effects Of Aging On Vascular Functionmentioning

confidence: 99%