RESUMO
Tortuous arteries are often associated with aging, hypertension, atherosclerosis, and degenerative vascular diseases, but the mechanisms are poorly understood. Our recent theoretical analysis suggested that mechanical instability (buckling) may lead to tortuous blood vessels. The objectives of this study were to determine the critical pressure of artery buckling and the effects of elastin degradation and surrounding matrix support on the mechanical stability of arteries. The mechanical properties and critical buckling pressures, at which arteries become unstable and deform into tortuous shapes, were determined for a group of five normal arteries using pressurized inflation and buckling tests. Another group of nine porcine arteries were treated with elastase (8 U/ml), and the mechanical stiffness and critical pressure were obtained before and after treatment. The effect of surrounding tissue support was simulated using a gelatin gel. The critical pressures of the five normal arteries were 9.52 kPa (SD 1.53) and 17.10 kPa (SD 5.11) at axial stretch ratios of 1.3 and 1.5, respectively, while model predicted critical pressures were 10.11 kPa (SD 3.12) and 17.86 kPa (SD 5.21), respectively. Elastase treatment significantly reduced the critical buckling pressure (P < 0.01). Arteries with surrounding matrix support buckled into multiple waves at a higher critical pressure. We concluded that artery buckling under luminal pressure can be predicted by a buckling equation. Elastin degradation weakens the arterial wall and reduces the critical pressure, which thus leads to tortuous vessels. These results shed light on the mechanisms of the development of tortuous vessels due to elastin deficiency.
Assuntos
Artérias Carótidas/fisiopatologia , Elastina/metabolismo , Matriz Extracelular/fisiologia , Rigidez Vascular/fisiologia , Animais , Fenômenos Biomecânicos , Artérias Carótidas/efeitos dos fármacos , Artérias Carótidas/metabolismo , Elastina/efeitos dos fármacos , Matriz Extracelular/efeitos dos fármacos , Modelos Animais , Modelos Biológicos , Elastase Pancreática/farmacologia , Estresse Mecânico , Suínos , Rigidez Vascular/efeitos dos fármacosRESUMO
The lock-in amplifier is often used to study the enhancement of the magneto-optical Kerr effect (MOKE) in the presence of plasmon resonances. In the present work we show that it is possible to investigate such effect replacing the lock-in amplifier by a compensator, filter, and differential amplifier. This allows us to extract the full hysteresis loop in and out of the resonance without the need of a lock-in amplifier. Our results demonstrate these two setups are equivalent to study the enhancement of the transversal MOKE (T-MOKE) in magnetoplasmonic systems.
RESUMO
Venous tortuosity is associated with multiple disease states and is often thought to be a consequence of venous hypertension and chronic venous disease. However, the underlying mechanisms of vein tortuosity are unclear. We hypothesized that increased pressure causes vein buckling that leads to a tortuous appearance. The specific aim of this study was to determine the critical buckling pressure of veins. We determined the buckling pressure of porcine jugular veins and measured the mechanical properties of these veins. Our results showed that the veins buckle when the transmural pressure exceeds a critical pressure that is strongly related to the axial stretch ratio in the veins. The critical pressures of the eight veins tested were 14.2 +/- 5.4 and 26.4 +/- 9.0 mmHg at axial stretch ratio 1.5 and 1.7, respectively. In conclusion, veins buckle into a tortuous shape at high lumen pressures or reduced axial stretch ratios. Our results are useful in understanding the development of venous tortuosity associated with varicose veins, venous valvular insufficiency, diabetic retinopathy, and vein grafts.