Medical Journals

Large Negative Stress Phase Angle (Spa) Attenuates Nitric Oxide Production in Bovine Aortic Endothelial Cells.

Authors:
  • Dancu Michael B
  • Tarbell John M

From: Biomolecular Transport Dynamics Laboratory, Department of Bioengineering, The Pennsylvania State University, University Park, PA 16802, USA. mbd131@psu.edu

Journal of biomechanical engineering

  • Publish Date: Jun 2006
  • ISSN: 0148-0731
  • Volume: 128
  • Issue: 3
  • Pages: 329-34
  • Medium: Print
  • Language: English
  • Citation (JAMA): Dancu Michael B, Tarbell John M, et al. Large Negative Stress Phase Angle (Spa) Attenuates Nitric Oxide Production in Bovine Aortic Endothelial Cells.. Jun 2006;128:329-34

Abstract

Hemodynamics plays an important role in cardiovascular physiology and pathology. Pulsatile flow (Q), pressure (P), and diameter (D) waveforms exert wall shear stress (WSS), normal stress, and circumferential strain (CS) on blood vessels. Most in vitro studies to date have focused on either WSS or CS but not their interaction. Recently, we have shown that concomitant WSS and CS affect EC biochemical response modulated by the temporal phase angle between WSS and CS (stress phase angle, SPA). Large negative SPA has been shown to occur in regions of the circulation where atherosclerosis and intimal hyperplasia are prevalent. Here, we report that nitric oxide (NO) biochemical secretion was significantly decreased in response to a large negative SPA of -180 deg with respect to an SPA of 0 degrees in bovine aortic endothelial cells (BAEC) at 5 h. A new hemodynamic simulator for the study of the physiologic SPA was used to provide the hemodynamic conditions of pro-atherogenic (SPA = -180 deg) and normopathic (SPA = 0 deg) states. The role of complex hemodynamics in vascular remodeling, homeostasis, and pathogenesis can be advanced by further assessment of the hypothesis that a large negative SPA is pro-atherogenic.

Mesh Headings (Keywords): Animals, Anisotropy, Aorta, Blood Pressure, Cattle, Cells, Cultured, Computer Simulation, Endothelial Cells, Mechanotransduction, Cellular, Models, Cardiovascular, Nitric Oxide, Physical Stimulation, Shear Strength, Stress, Mechanical


Check for Full Text / PubMed Unique Identifier (PMID): 16706582


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