Driessen G, Scheidt H, Inhoffen W, Sobota A, Malotta H, Schmid-Schönbein H
Department of Physiology, Faculty of Medicine, RWTH Aachen, Federal Republic of Germany.
Microvasc Res. 1988 Jan;35(1):73-85. doi: 10.1016/0026-2862(88)90051-9.
The fluidity (the inverse of viscosity) of red blood cell (RBC) suspensions in vivo was estimated by means of microcirculatory measurements such as RBC flow velocity, micropressure in arterioles and venules, and vessel geometry, and by means of simultaneous macrocirculatory measurements such as volume flow and perfusion pressure in the whole organ. These in vivo data were compared to in vitro data obtained by viscometry. The experiments were performed on the isolated rat mesentery perfused with a nonaggregating and an aggregating suspension: Human RBC were either suspended in Ringer's or Ficoll 400 solution. The tissue was perfused at various perfusion pressures and hematocrit values. The microcirculatory perfusion was recorded by means of microscopy using a video TV system. Five major results have been identified: First, microfluidities calculated from velocity data in capillaries of the mesenteric membrane were almost identical to the fluidities calculated from macroflow data (volume flow rates and perfusion pressure in the whole organ). Second, in vivo fluidities of both suspensions decrease with increasing hematocrit value but seem to be independent of driving pressure between 4 and 10 kPa. Third, the fluidity of the Ficoll suspensions is lower than the fluidity of the Ringer's suspensions by the same ratio as the continuous phases. Fourth, the in vivo fluidities of the Ringer's suspensions and the Ficoll suspensions for hematocrit values from 20 to 70% and a range of wall shear stresses from 0.6 to 1 Pa were higher than those measured in vitro. Finally, it has been quantified that an increasing number of vessels became stagnant (that is packed by red blood cells) at high hematocrit values, low perfusion pressure, and increased aggregability of RBC.