Effects of cisplatin on the contractile function of thoracic aorta of Sprague-Dawley rats
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Published on: March 11, 2016
Ying Jiang1, Shigang Shan2, Tieer Gan3
1The First Affiliated Hospital, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China ; Suzhou Biological Technology Co., Ltd., of Centre Testing International Corporation, Kunshan, Jiangsu 215300, P.R. China.
Abstract:
DNA-damaging agents have been reported to be associated with cardiovascular complications, however, the underlying mechanisms remain to be clarified. In the present study, the possible vascular effects of cisplatin was assessed by measuring its effects on the contractile function of thoracic aortic rings dissected from Sprague-Dawley (SD) rats. Contraction of the aortic ring was induced by 60 mM KCl or 10-6 M phenylephrine (PE) in an ex vivo perfusion system. Cisplatin (200 μM) counteracted KCl- and PE-induced contraction by 57.6 and 91.8%, respectively, in endothelium-intact aortic rings. Similar results were obtained in endothelium-denuded aortas. Electromicroscopy analysis revealed severe damage to blood vessel walls in vivo by cisplatin. In addition, cisplatin significantly inhibited adenosine triphosphate (ATP)-induced intracellular Ca2+ concentration ([Ca2+]i) increases in human umbilical vein endothelial cells (HUVECs). These results suggested that the DNA-damaging agent cisplatin can affect the contractile function of thoracic aortas. In addition, in accordance with its DNA-damaging properties, the cardiovascular toxicity of cisplatin may be the result of its direct cytotoxicity.
Insights
Cisplatin, a DNA-damaging agent, impairs thoracic aorta contractile function and damages blood vessel walls. Cardiovascular toxicity may stem from cisplatin
Area of Science:
- Cardiovascular Pharmacology
- Cellular Toxicology
- Biomedical Research
Background:
- DNA-damaging agents are linked to cardiovascular complications.
- Mechanisms underlying these cardiovascular effects require clarification.
Purpose of the Study:
- To investigate the vascular effects of cisplatin on thoracic aorta contractile function.
- To explore the cellular mechanisms of cisplatin-induced cardiovascular toxicity.
Main Methods:
- Ex vivo assessment of thoracic aortic ring contraction in Sprague-Dawley rats.
- Measurement of intracellular calcium ([Ca2+]i) in human umbilical vein endothelial cells (HUVECs).
- Electromicroscopy analysis of blood vessel walls.
Main Results:
- Cisplatin significantly reduced KCl- and phenylephrine-induced contractions in aortic rings.
- Electromicroscopy revealed severe in vivo damage to blood vessel walls.
- Cisplatin inhibited adenosine triphosphate (ATP)-induced intracellular Ca2+ increases in HUVECs.
Conclusions:
- Cisplatin directly impacts the contractile function of thoracic aortas.
- Cardiovascular toxicity of cisplatin may be attributed to its direct cytotoxicity and DNA-damaging properties.
