Arteries stress relaxation

Blood and lymphatic vessels are soft tissues with densities which exhibit nonlinear stress-strain relationships [1]. The walls of blood and lymphatic vessels show not only elastic [2, 3] or pseudoelastic [4] behavior, but also possess distinctive inelastic character [5, 6] as well, including viscosity, creep, stress relaxation and pressure-diameter hysteresis. The mechanical properties of these vessels depend largely on the constituents of their walls, especially the collagen, elastin, and vascular smooth muscle content. In general, the walls of blood and lymphatic vessels are anisotropic. Moreover, their properties are affected by age and disease state. This section presents the data concerning the characteristic dimensions of arterial tree and venous system the constituents and mechanical properties of the vessel walls. Water permeability or hydraulic conductivity of blood vessel walls have been also included, because this transport property of blood vessel wall is believed to be important both in nourishing the vessel walls and in affecting development of atherosclerosis [7-9]. 

When a subject is suddenly strained and then the strain is maintained constant afterward, the corresponding stresses induced in the subject decrease with time, this phenomenon is called stress relaxation. If the subject is suddenly stressed and then the stress is maintained afterwards, the subject continues to deform, this phenomenon is called creep. Creep and stress relaxation are another two important phenomena in the arterial viscoelasiticity. Langewouters et al [46] studied the creep responses of human thoracic and abdominal aortic segments. The pressure in the... 

Stress relaxation relations for human arteries are not available however, Tanaka and Fung [48] studied the stress relaxation spectrum of the canine aorta. They expressed the stress history with respect to a step change in strain in the form ... 

The authors discuss the mechanical behavior of arteries and the mathematical method required for quantification of such data. The discussion is entirely concerned with the elastic or pseudoelastic behavior of blood vessels. It should be emphasized that the arterial wall also exhibits inelastic properties, such as viscosity, creep, stress relaxation and pressure-diameter hysteresis. Very few data on mechanical properties of blood vessels are presented. 

How does laughter work Maybe it counters the ill effects of stress hormones such as adrenaline and cortisol on blood vessel function. Or perhaps it boosts the body s production of nitric oxide, which relaxes the arterial lining and allows for more efficient blood flow. Both modes of action would in turn lower blood pressure. I think it works in a number of ways, those two and others as well. 

The nitrates act by releasing nitric oxide, which relaxes vascular smooth muscle. The discovery that endothelium-derived relaxing factor (EDRF) is nitric oxide (1) stimulated new interest in these drugs, as nitric oxide not only controls local vessel wall tension in response to shear stress, but also plays a role in regulating the interaction of platelets with blood vessel walls. The release of nitric oxide from the walls of atheromatous arteries is reduced, because of malfunctioning or absent endothelium. Atheromatous arteries behave differently from healthy arteries, in that these vessels vasoconstrict rather than vasodilate when stimulated by acetylcholine. This impairment of the acetylcholine vasomotor response appears to be related to serum cholesterol concentration (2). 

FIGURE 2 Inhibition of shear stress-induced release of nitric oxide in isolated endothelial cells by S-nitroso-N-acetylpenicillamine (SNAP). Relaxant responses of the first arterial strip in a three-tissue cascade are illustrated. The flow rate through the column of endothelial cells was varied from 0.3 to 3 ml/min. Three sets of control responses were obtained at 15-min intervals before the addition of SNAP. After the third set of control responses, 1 /rmol/liter SNAP was perfused through the column for 15 min (positioned away from the target arterial strips), following which the column was perfused with plain Krebs bicarbonate solution for a further 15 min. The perfusate was then directed over the target strips, and responses to shear stress were obtained. Data represent the means se from at least four separate experiments. 

A mechanism for the pathophysiology of high-flow priapism is described by Bastuba et al. (1994). Unlike a traditional arteriovenous fistula, the condition is described as an arterial-lacunar fistula where the helicine arteries are bypassed, and the blood passes directly into the lacunar spaces. The high-flow in the lacunar space creates shear stress in adjacent areas, leading to increased nitric oxide release, activation of the cGMP pathway, smooth muscle relaxation and trabecular dilatation. These authors also postulate that the delay in onset of high-flow priapism may be secondary to a delay in the complete necrosis of the arterial wall after the initial trauma or secondary to clot formation at the site of injury followed by the normal lytic pathway, which progresses in a few days. 

In rabbits, vascular ACE activity was significantly increased by atherogenic diet with significant correlation between vascular ACE activity and plaque area, however, contractile responses of the femoral arteries to AI and All in the atherogenic diet-fed animals were not different from those of the normal diet-fed animals (273). ACE inhibition improves vascular compliance, NO production, vascular relaxation, plasma markers of relaxation, oxidative stress, and thrombosis (reviewed in ref. 274). On the other hand, hypercholesterolemia in rabbits resulted in atherosclerosis, loss of endothelium-dependent relaxation, increased ATI in aortic tissues with enhanced constrictor response to All (275). 

Another proposed mechanism is the release of vasoactive substances by the shear stress that results from mechanical compression of vessel walls. Animal studies have demonstrated increased endothelial-derived relaxing factor (EDRF) production in response to compression of arterial segments (86). Others have shown that short periods of shear-stress application result in an increase in mRNA production for nitric oxide (NO) synthase (87). It has also been shown that the vasodilatation response is attenuated if NO production is halted by the administration of drugs that inhibit NO synthase (88). Other studies show that limb compression leads to systemic vasodilatation in a manner that is dependent on shear stress (89). To produce adequate shear stress on the vessel wall, compression must be prompt rather than gradual. 

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