Chemotherapeutic drugs used to combat solid tumors sometimes have severe side effects. They include weight loss, nausea, destruction of intestinal lining and bone marrow. The dosage and frequency of drug therapy is often determined by the patient's ability to tolerate side effects. It would be desirable to reduce the dosage or frequency of drug treatment by enhancing the effectiveness of drugs at the site of the tumor.Results presented here demonstrate that ultrasound may be used to promote the reactivity, or activate, chemotherapeutic agents. As a non-invasive modality for cancer therapy, ultrasound has the attractive ability to penetrate deeply into tissues while maintaining well-localized power deposition patterns. The ability to localize ultrasound suggests the possible use of the ultrasound-drug interaction for providing locally intense chemotherapy while maintaining minimal damage peripheral to the target volume.Demonstration of ultrasound-drug interaction suggests that ultrasound may interact with or affect the activity of molecular compounds, or the drugs may increase cell susceptibility to ultrasound-induced damage. Ultrasound may interact mechanically or chemically via acoustic cavitation, broadly defined as the interaction between a stabilized gas pocket, or microbubble, and an applied acoustic field. Results presented in this dissertation indicate that acoustic cavitation is the primary mechanism of activation of anticancer drugs, and the results suggest that some ultrasound-drug interactions in the literature are due to the effects of acoustic cavitation. |