An analytical study of the low frequency structural responses of a submerged hull

This paper studies the low frequency vibrational behaviour of a submerged hull. The submerged hull is modelled as a finite fluid-loaded cylindrical shell closed at each end by circular plates. The external pressure acting on the hull due to the fluid loading is analytically calculated using an infinite model. Three excitation cases of the hull are considered. In the first model, an axial point force is applied at the centre of one end plate, giving rise to an axisymmetric case in which only the zeroth circumferential shell modes are excited. In the second model, an axial point force is applied at the edge of the end plate. In the third model, a radial point force is applied also at the edge of the end plate. In the second and third load cases, all cylindrical shell circumferential modes are excited. The effects of fluid loading and different excitation locations are studied. A more complex hull model including stiffeners and bulkheads is then examined. A smeared approach is used to analytically model the ring stiffeners. All load cases are again considered and the effects of the various influencing factors on the low frequency responses are described.

Changes in biomechanical properties of the coronary artery wall contribute to maintained contractile responses to endothelin-1 in atherosclerosis.

AIMS: Our aim was to determine whether alterations in biomechanical properties of human diseased compared to normal coronary artery contribute to changes in artery responsiveness to endothelin-1 in atherosclerosis. MAIN METHODS: Concentration-response curves were constructed to endothelin-1 in normal and diseased coronary artery. The passive mechanical properties of arteries were determined using tensile ring tests from which finite element models of passive mechanical properties of both groups were created. Finite element modelling of artery endothelin-1 responses was then performed. KEY FINDINGS: Maximum responses to endothelin-1 were significantly attenuated in diseased (27±3 mN, n=55) compared to normal (38±2 mN, n=68) artery, although this remained over 70% of control. There was no difference in potency (pD2 control=8.03±0.06; pD2 diseased=7.98±0.06). Finite element modelling of tensile ring tests resulted in hyperelastic shear modulus μ=2004±410 Pa and hardening exponent α=22.8±2.2 for normal wall and μ=2464±1075 Pa and α=38.3±6.7 for plaque tissue and distensibility of diseased vessels was decreased. Finite element modelling of active properties of both groups resulted in higher muscle contractile strain (represented by thermal reactivity) of the atherosclerotic artery model than the normal artery model. The models suggest that a change in muscle response to endothelin-1 occurs in atherosclerotic artery to increase its distensibility towards that seen in normal artery. SIGNIFICANCE: Our data suggest that an adaptation occurs in medial smooth muscle of atherosclerotic coronary artery to maintain distensibility of the vessel wall in the presence of endothelin-1. This may contribute to the vasospastic effect of locally increased endothelin-1 production that is reported in this condition.