Most cited article - PubMed ID 24899384
Oral administration of quercetin is unable to protect against isoproterenol cardiotoxicity
Cardiovascular diseases are a leading cause of morbidity and mortality in most developed countries of the world. Pharmaceuticals, illicit drugs, and toxins can significantly contribute to the overall cardiovascular burden and thus deserve attention. The present article is a systematic overview of drugs that may induce distinct cardiovascular toxicity. The compounds are classified into agents that have significant effects on the heart, blood vessels, or both. The mechanism(s) of toxic action are discussed and treatment modalities are briefly mentioned in relevant cases. Due to the large number of clinically relevant compounds discussed, this article could be of interest to a broad audience including pharmacologists and toxicologists, pharmacists, physicians, and medicinal chemists. Particular emphasis is given to clinically relevant topics including the cardiovascular toxicity of illicit sympathomimetic drugs (e.g., cocaine, amphetamines, cathinones), drugs that prolong the QT interval, antidysrhythmic drugs, digoxin and other cardioactive steroids, beta-blockers, calcium channel blockers, female hormones, nonsteroidal anti-inflammatory, and anticancer compounds encompassing anthracyclines and novel targeted therapy interfering with the HER2 or the vascular endothelial growth factor pathway.
- Keywords
- dysrhythmia, heart failure, hypertension, myocardial infarction, stroke,
- MeSH
- Alkaloids adverse effects MeSH
- Amphetamines adverse effects MeSH
- Anti-Arrhythmia Agents adverse effects MeSH
- Anti-Inflammatory Agents, Non-Steroidal adverse effects MeSH
- Adrenergic beta-Antagonists adverse effects MeSH
- Calcium Channel Blockers adverse effects MeSH
- Stroke drug therapy MeSH
- Digoxin adverse effects MeSH
- Hormones adverse effects MeSH
- Cardiovascular Diseases chemically induced drug therapy MeSH
- Cardiovascular System drug effects MeSH
- Cocaine adverse effects MeSH
- Humans MeSH
- Antineoplastic Agents adverse effects MeSH
- Heart Rate drug effects MeSH
- Steroids adverse effects MeSH
- Vascular Endothelial Growth Factor A MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Alkaloids MeSH
- Amphetamines MeSH
- Anti-Arrhythmia Agents MeSH
- Anti-Inflammatory Agents, Non-Steroidal MeSH
- Adrenergic beta-Antagonists MeSH
- Calcium Channel Blockers MeSH
- cathinone MeSH Browser
- Digoxin MeSH
- Hormones MeSH
- Cocaine MeSH
- Antineoplastic Agents MeSH
- Steroids MeSH
- Vascular Endothelial Growth Factor A MeSH
OBJECTIVES: Rutin, quercetin-3-O-rutinoside, a natural flavonol glycoside, has shown various in vitro benefits with potential use treating human diseases, especially cardiovascular system disorders. Antioxidant properties are assumed to underlie the majority of these benefits. Yet rutin pro-oxidant properties have been reported as well. Our research group has recently shown aggravating effects on isoprenaline (ISO)-induced cardiotoxicity in Wistar:Han rats after 24 hours. METHODS: This study was designed to examine in more detail the reasons for the negative effects of rutin (11.5 and 46 mg/kg, i.v.) after administration of ISO (100 mg/kg, s.c.) in rats within 2 hours of continuous experiment and in the H9c2 cardiomyoblast-derived cell line. RESULTS: Like our previous findings, rutin did not (11.5 or 46 mg/kg, i.v.) reduce the ISO-induced mortality within 2 hours although the lower dose significantly reduced cardiac troponin T (cTnT) and partly improved the histological findings. In contrast, the higher dose increased the mortality in comparison with solvent (1.26% w/v sodium bicarbonate). This was not caused by any specific haemodynamic disturbances. It appears to be associated with oxidative stress as rutin enhanced intracellular reactive oxygen species formation in vitro and had the tendency to increase it in vivo. CONCLUSIONS: Rutin, likely due to its pro-oxidative effects, can exacerbate catecholamine cardiotoxicity depending on the dose used.
- Keywords
- Catecholamine, Flavonoid, H9c2 cell line, Isoprenaline, Reactive oxygen species, Rutin, Wistar rat,
- MeSH
- Cell Line MeSH
- Dinoprost analogs & derivatives blood MeSH
- Electrocardiography MeSH
- Glutathione blood MeSH
- Injections, Intravenous MeSH
- Isoproterenol adverse effects MeSH
- Kaplan-Meier Estimate MeSH
- Cardiotoxicity etiology mortality MeSH
- Myocardium pathology MeSH
- Rats, Wistar MeSH
- Reactive Oxygen Species metabolism MeSH
- Rutin administration & dosage adverse effects pharmacokinetics MeSH
- Heart drug effects MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 8-epi-prostaglandin F2alpha MeSH Browser
- Dinoprost MeSH
- Glutathione MeSH
- Isoproterenol MeSH
- Reactive Oxygen Species MeSH
- Rutin MeSH