Arterial elastance

Diseases. Liquid crystals have been impHcated in a number of disease conditions in the human body. A complex cholesterol—phosphoHpid—Hpoprotein Hquid crystal phase has been identified in the initiation and maintenance of atheromatous deposits on the aortic intima in dissected human and rabbit arteries (40). The paracrystalHne nature of this precursor to plaque buildup with the resultant loss of arterial elasticity... 

Westhoff TH, Schmidt S, Glander P, Liefeld L, et al. 2007. The impact of FTY720 (fingolimod) on vasodilatory function and arterial elasticity in renal transplant patients. Nephrol Dial Transplant. 22 2354-2358. 

The viscoelasticity of blood vessels affects the hemodynamics of arterial flow. The primary function of arterial elasticity is to store blood during systole so that forward flow continues when the aortic valve is closed. Elasticity also causes a finite wave propagation velocity, which is given approximately by the Moens-Korteweg relationship... 

In addition to intimal thickening, the arterial wall properties also change with age. Most measurements suggest that arterial elastic modulus increases with age (hardening of the arteries) however, in some cases arteries to become more compliant (inverse of elasticity) [Learoyd and Taylor, 1966]. Local weakening of the wall may also occur, particularly in the descending aorta, giving rise to an aneurysm, which, if ruptures, can cause sudden death. 

Figure 3. Schematic illustration of the dependence of the amount of the external mechanical work (shown by shaded area) that a ventricle performs at a constant preload and under a constant contractility (i.e., a fixed slope of end-systolic pressure-volume relationship) on afterloaded arterial elastance E . Note that the shaded area becomes maximum when equals E .

In Apo E-KO mice. All treatment accelerated atherosclerosis in the carotid artery, increased blood pressure, increased arterial stiffening, increased pulse wave velocity, and decreased arterial elasticity. These functional changes were correlated with morphological and biochemical changes as demonstrated by an increase in collagen content, a decrease in elastin content, and breaks in the internal elastic lamina in the aortic wall. In addition, endothelium-independent vasorelaxation to sodium nitroprusside was impaired (265). 

Studies using pathology-related intermediate markers, e.g., arterial thickening or reduced arterial elasticity precancerous polyposis, etc. 

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