Examination of the effects of subatmospheric pressure on erythrocytes and the formation of cavitation in blood.

Abstract

It is currently thought that subatmospheric pressure causes hemolysis, resulting in constraints on the design of blood-handling devices and extracorporeal circulation techniques. The work presented in this thesis stems from the hypothesis that subatmospheric pressure is not a hemolytic mechanism, and thus, can be utilized safely. The first portion of the thesis concentrates on the effect of subatmospheric pressure on erythrocytes. A static pressure apparatus is described that prevents bubble formation in blood at pressures below vapor pressure. A second apparatus is presented for the study of erythrocyte damage by pressure induced pipe flow. The plasma free hemoglobin (PFHB) generated by positive pressure induced flow is compared to that generated by subatmospheric pressure induced flow. The results from these experiments show that subatmospheric pressure is not a hemolytic mechanism. The second portion of the thesis investigates cavitation in blood. To study cavitation inception in blood, a Cavitation Susceptibility Meter (CSM) and a syringe-pump flow apparatus were designed. The CSM and flow apparatus were used in a sheep model to measure the nuclei content of in vivo blood. At tensions $\le$120 kPa, the nuclei content of arterial blood was determined to be $\le$2.7 per liter of plasma, with venous blood having $\le$0.5 per liter of plasma. From bubble stability theory, the nucleus radii were calculated to be 0.3 $\mu$m. It was also shown that a tension of 120 kPa ($-$127 kPa, gauge) does not cause erythrocyte lysis, further validating that subatmospheric pressure is not hemolytic. To study the hemolytic potential of cavitation, an analytical model was formulated based on the Rayleigh-Plesset equation, and the assumption that erythrocyte lysis is caused by the straining flow generated by a cavitating bubble. To validate the model, in vitro experiments with the CSM and flow apparatus were performed. At cavitation event rates up to 9 events/sec (270 nuclei per liter of plasma), the increase in PFHb was only 1 mg/dl, as predicted by the analytical model. Higher event rates could not be achieved without flow separation. Recirculating studies with the CSM showed that an increase in PFHb correlated with the formation of attached cavitation.