Does vibration cause poststenotic dilatation in vivo and influence atherogenesis in cholesterol-fed rabbits?

• Published in: Journal of biomechanical engineering Vol. 114; no. 1; p. 20
• Main Authors: Gow, B S, Legg, M J, Yu, W, Kukongviriyapan, U, Lee, L L
• Format: Journal Article
• Language: English
• Published: United States 01.02.1992
• Subjects: Animals; Aorta, Thoracic; Aortic Valve Stenosis - complications; Aortic Valve Stenosis - physiopathology; Arteriosclerosis - etiology; Arteriosclerosis - pathology; Blood Flow Velocity; Cholesterol, Dietary - adverse effects; Dilatation, Pathologic - etiology; Dilatation, Pathologic - physiopathology; Disease Models, Animal; Electromagnetic Phenomena - instrumentation; Electromagnetic Phenomena - methods; Evaluation Studies as Topic; Rabbits; Rheology; Vibration - adverse effects
• ISSN: 0148-0731
• DOI: 10.1115/1.2895443

Arterial post-stenotic dilatation (PSD) is a fusiform swelling immediately down-stream to a stenosis. It is characterized by the presence of turbulent blood flow and wall vibration which has been claimed by others to be causal by producing structural weakening. We tested the hypothesis that vibration causes PSD in vivo by attaching electromagnetic and pneumatic vibrators to the aortic wall in chronic rabbits. We also observed whether mechanical vibration of the aorta in vivo influenced the distribution of oil-red-O lesions during one percent dietary cholesterol feeding. Low mass vibration gauges were developed to measure the vibration. Electromechanical vibrators having a ceramic magnet slug within a coil supplied with 50 Hz were glued to the aorta of chronic rabbits and the vibration maintained for an average of 8 weeks. Despite greater amounts of energy imparted to the wall there was no dilatation or difference in oil-red-O staining from the controls. Five weeks vibration at 100 Hz and an amplitude equal to the normal diameter pulse also produced no dilatation. We conclude that vibration does not cause PSD in vivo and suggest that its cause is likely to involve the vascular muscle stimulated by the effect of turbulent flow on the endothelium.