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1 Department of Mechanical Engineering, University of Nevada, Las Vegas, Las Vegas, Nevada, USA; Cancer Institute, University of Nevada, Las Vegas, Las Vegas, Nevada, USA
2 Department of Mechanical Engineering, University of Nevada, Las Vegas, Las Vegas, Nevada, USA
* To whom correspondence should be addressed. E-mail: bmfu{at}nscee.edu.
To investigate the ultrastructural mechanisms of acute microvessel hyperpermeability by vascular endothelial growth factor (VEGF), we combined a mathematical model (Fu et al., J. Biomech. Eng., 116: 502-513, 1994) with the experimental data of VEGF effect on microvessel hydraulic permeability (Lp) and various sized solute permeability (P). The current study examined VEGF effect on microvessel permeability to small solute sodium fluorescein (Stokes radius = 0.45 nm), intermediate-sized solute a-lactalbumin (Stokes radius = 2.01 nm) and large solute albumin (BSA, Stokes radius = 3.5 nm). Exposure to 1 nM VEGF transiently increased apparent permeability Psodium fluorescein to 2.3-fold, P
-lactalbumin to 3.3-fold and PBSA to 6.2-fold of their baseline values within 30 sec, correspondingly, and all returned to control within 2 min. Based on Lp (Bates and Curry, Am. J. Physiol. 40: H2520-2528, 1996) and P data, the prediction from the model suggested that the possible structural changes in the interendothelial cleft by VEGF would be ~ 2.5-fold increase in its opening width and partial degradation of the surface glycocalyx.
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