PD 0332991 doxorubicin is used for treating a wide spectrum of malignancies, and hence serves as a prototype in our study. Cardiotoxicity, the most characterized deleterious effect of doxorubicin toxicity, is cumulative dose-related. It has been formerly implied that endothelial damage may contribute to this pathogenesis; in acute cases, the patient may suffer from hypotension, tachycardia and arrhythmia, while an increased cumulative dose of doxorubicin can cause congestive heart failure. It has already been documented that doxorubicin-treated rats develop marked ascites and that the in vitro permeability to albumin of bovine pulmonary artery endothelial cells monolayer, 24 hours after exposure to clinically relevant concentrations of doxorubicin, was 10 fold higher than that of control cells. Several studies have confirmed that doxorubicin induces oxidative stress, a condition known to be toxic to endothelial cells, leading to loss of their barrier trait. Few ex vivo studies have explored the effect of doxorubicin on tissues excised from doxorubicin-injected animals. An impaired endothelial-dependent vasodilatory response to acetylcholine or adenosine was observed in rabbit and rat models with doxorubicin–induced cardiomyopathy. Brachial artery reactivity, a marker for endothelial vasodilatation function, detected by high-resolution ultrasound, was decreased in human patients that received at least 300 mg/m2 of doxorubicin compared to control patients. Furthermore, brachial artery flow-mediated dilation in patients undergoing doxorubicin based chemotherapy was markedly attenuated after a single dose of doxorubicin. Recently, it has been shown by phase-contrast cardiovascular magnetic resonance measurements of PW velocity and aortic distensibility that anthracyclins induce a significant increase in thoracic aorta stiffness in patients receiving anthracyclins compared to age and sex-matched controls. We have previously studied the effect of doxorubicin on mice ovaries, manifested by reduced ovulation rate and ovarian size, as observed by high resolution MRI. Our results indicated an acute insult to the ovary, reflected by the presence of peri-ovarian edema, encouraged us to further investigate the potential acute vascular effect induced by doxorubicin administration. In the current study, ovarian blood volume was visualized by measuring the baseline concentration of injected microbubbles at the designated blood vessels and the concentration throughout the chemotherapeutic treatment.