Thomas C R, al-Rubeai M, Zhang Z
BBSRC Centre for Biochemical Engineering, School of Chemical Engineering, University of Birmingham, Edgbaston, UK.
Cytotechnology. 1994;15(1-3):329-35. doi: 10.1007/BF00762408.
In previous work a model was proposed for estimation of disruption of animal cells in turbulent capillary flows using information about the hydrodynamics, and cell mechanical properties determined by micromanipulation. The model assumed that the capillary flow consists of a laminar sublayer and a homogeneous turbulent region, and within the latter eddies of sizes similar to or smaller than the cells interact with those cells, causing local surface deformations. The proposed mechanism of cell damage was that such deformations result in an increase in membrane tension and surface energy, and that a cell disrupts when its bursting membrane tension and bursting surface energy are exceeded. The surface energy of the cells was estimated from the kinetic energy of appropriate sized eddies. To test the model, cells were disrupted in turbulent flows in capillaries at mean energy dissipation rates ranging from 800 to 2 x 10(4) Wkg-1. The model assumed that the specific lysis rate is almost independent of the number of passes, which was verified by the experimental data. The implication was that despite the damage the cell mechanical properties did not change markedly during multiple recirculations through the capillaries. On average the model underestimated the cell disruption by about 15%. Although the model gave reasonably good predictions, it lacks proper explanation of the independence of the specific lysis rate on the number of passes. In this paper it is shown that this problem can be resolved in principle by consideration of the localisation of the energy dissipation in turbulent capillary flows. The necessity of further modelling of cell-turbulence interactions is demonstrated.
