Do fish acclimated to low temperature improve microcirculatory perfusion by adapting red cell rheology?
We have measured the rheological properties of individual red blood cells from fishes inhabiting different thermal environments and have also investigated the effects on red cells of acute in vitro temperature changes. The membrane shear elastic modulus (rigidity) increased markedly with decreasing temperature, and the dependence was similar if temperature was varied acutely in vitro or if cells were measured at normal body temperatures. Red cells from trout and Notothenia coriiceps had almost equal membrane rigidity at comparable temperatures and showed similar temperature-sensitivity in acute experiments. Entry times of trout cells into narrow (approximately 4 microm diameter) micropipettes also increased during in vitro reduction of temperature, and this could be explained largely by the temperature-dependence expected of aqueous solutions. Perhaps surprisingly, entry times did not vary when trout living at different temperatures were tested at these temperatures. Transit times of individual cells through somewhat larger pores (5 microm) in oligopore filters again increased with decreasing temperature in vitro (partly due to increasing fluid viscosity), but such transit times did show a similar temperature-dependence for cells from trout living at different temperatures. Thus, the temperature-dependence of cellular flow resistance appears to arise from variations in membrane rigidity and in the viscosity of fluid components, along with unquantified variations in components such as microtubular structures (which we found did not influence membrane rigidity but did affect pore entry time) and the cell nucleus. Thermal acclimation did not involve adaptation to compensate for increased membrane rigidity or a large pore transit time, with, at most, minor compensation in entry times into smaller pores. We conclude that impaired cellular rheology is not a major factor influencing circulation in fish at low temperature.
Lecklin
T
T
Department of Physiology, The Medical School, The University of Birmingham, Birmingham B15 2TT, UK.
Nash
G
G
Egginton
S
S