| Popis: |
Monitoring and controlling cavitation offer ways of isolating the role of cavitation in lithotripsy‐induced cell damage. Finger cots containing 7 ml of PBS‐diluted blood (3% hematocrit) were treated by 100 lithotripter pulses focused by either a conventional rigid reflector or a pressure‐release reflector. The rigid reflector produced 7% hemolysis at 18 kV. The pressure‐release reflector, which produces an equally strong acoustic pulse but less intense cavitation, produced 1% hemolysis which was indistinguishable from control levels. A passive cavitation detector consisting of two confocal focused transducers operating in coincidence was used to monitor cavitation within each blood sample. With the rigid reflector, each transducer recorded a spike when pre‐existing bubbles were collapsed by the positive portion of the lithotripter pulse and a second spike when the bubbles, caused to grow by the negative portion of the pulse, underwent inertial collapse. The time between spikes was 1.25–1.5 times longer in blood than in water. The results appear to indicate that transient cavitation is an important mechanism in lithotripsy‐induced hemolysis, that lithotripter‐induced cavitation can be monitored in cell samples, and that bubble dynamics in blood and water are not identical. [Work supported by NIH PO1 DK43881, UW STAR, and DARPA/ONR.] |
