Trauma to the blood in prosthetic heart devices is a major concern to the health of patients. Significant study has shown that much damage is caused by high stresses involved in the flow through the mechanical device and the onset of turbulence in the system. The short-term objective of this investigation is to develop experimental procedures and perform the initial characterization of a device which measures the damage of the cells due to the effects of turbulence. The device chosen is a stirred tank reactor with a 6-blade Rushton impeller. Damage to the cells is measured by assay techniques for free hemoglobin released by ruptured cells over the length of an experiment. The rate of damage to the cells can then be determined. During the development of the experimental procedure, several experimental considerations were realized including length of blood storage and significant pig-to-pig variation in blood characteristics. In addition, the rate of damage to the cells increased with increased power input to the reactor system.
A longer-term objective of the work is to understand the mechanism by which turbulence inflicts damage to the cells. Several theories of the disruption mechanism are presented through out this investigation. In addition, a second area of focus involves the addition of blood additives to increase the viscosity of the solution. Preliminary data is presented that is consistent with the evidence that has demonstrated that damage to the cells can be redced by increasing the viscosity. An initial investigation into the viscosity considerations is presented using the additive Dextran 40.
Further experimentation (Aziz, Honors Thesis 2000) determined that this investigation was performed in a hypotonic solution. This conclusion implies that a significant proportion of the weaker cell population could have been damaged due to osmotic pressure changes during the resuspension of the red blood cells. Therefore, the damage rates presented could be lower than the actual damage rate because a significant portion of the weaker cells were already damaged. Also, the remaining cells are likely to be more susceptible to damage as a result of being in a hypotonic environment during exposure to turbulence.