Cardiovascular toxicity of the first line cancer chemotherapeutic agents: doxorubicin, cyclophosphamide, streptozotocin and bevacizumab.

Objectives: Although the mechanisms responsible for the occurrence of congestive heart failure after anti-cancer therapy are largely unknown, both the formation of free radicals in the myocardium and inflammatory cytokines with resultant production of neurohormones could be operative. The common manifestations of cardiovascular toxicity after anti-cancer therapy may include cardiac ischemia, ST-segment elevation, or depression, serious hypotension and bradyarrhythmias with resultant cardiac depression and congestive heart failure, or hyper-tension, serious ventricular tachycardia, cardiac edema, QT prolongation and thrombo-embolism.

Methods & Results: The mechanisms of cardiotoxicity of four representative anti-cancer agents 1) anthracycline doxorubicin, 2) and 3) alkylating agents cyclophosphamine and streptozotocin and 4) the new humanized monoclonal antibody bevacizumab (directed solely against myocardial and vascular endothelial growth factors), were investigated in chronic experiments on rodents for the occurrence and intensity of early electrocardiographic signs of cardiotoxicity, for late biochemical markers, and for the late production of congestive heart failure.

Participation of reactive oxygen species in diabetes-induced endothelial dysfunction.

Objectives: In the present study, the relationship between diabetes-induced hyperglycemia, reactive oxygen species production and endothelium-mediated arterial function was examined. The effect of antioxidant on the reactive oxygen species induced damage was tested.

Methods: Diabetes was induced by streptozotocin (STZ), 3 x 30 mg/kg i.

Ischaemia/reperfusion-induced organ injury in low dose streptozotocin diabetes.

Objectives: The influence of low dose streptozotocin diabetes on intestinal and vascular injury induced by mesenteric ischaemia/reperfusion (I/R) was studied in rats. The role of reactive oxygen species (ROS) in the exacerbation of ischaemic/postischaemic damage in diabetes was addressed.

Methods: Diabetes was induced by i.

Effect of acetylcholine and ischaemia/reperfusion injury on the heart of rats with STZ-induced experimental diabetes.

Objectives: To investigate the effect of acetylcholine (ACh) and ischaemia/reperfusion injury on functional changes and dysrhythmias of the isolated diabetic rat heart.

Methods And Results: On retrogradely perfused hearts isolated from 10-week-old diabetic rats (streptozotocin 30 mg/kg b.w.