Erratum to: Effects of adriamycin and candesartan on the collagen and elastin of the aorta in rats
TLDR
After publication of the article, it was discovered that a citation error had occurred, resulting in different citation numbers in the PDF and HTML files, and the correct citation of 20:8 has now been updated in all versions of the manuscript.Abstract:
After publication of the article [1] it was discovered that a citation error had occurred, resulting in different citation numbers in the PDF and HTML files. The correct citation of 20:8 has now been updated in all versions of the manuscript. We apologise for any inconvenience caused by this error.read more
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Effects of adriamycin and candesartan on the collagen and elastin of the aorta in rats
TL;DR: It is suggested that adriamycin has a tendency of decreasing the quantity of elastin fibers and candesartan cannot mitigate the effects of adRIamycin on elast in fibers.
References
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Cardiovascular effects of doxorubicin-induced toxicity in the intact Lou/M Wsl rat and in isolated heart preparations.
TL;DR: Hemodynamic effects were followed in conscious nontumor bearing Lou/M Wsl rats during i.v. administration of doxorubicin (DXR) on 5 consecutive days and then weekly, suggesting compensatory mechanisms were functioning within the DXR-treated rats around day 25 and histological evidence of cardiomyopathy occurring at that time was supported.
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Ultrastructural damage in vascular endothelium in rats treated with paclitaxel and doxorubicin.
TL;DR: Assessment of the damages elicited by the combination use of chemotherapy agents in animal experimental models revealed some clear degenerative findings, notably, administration of a paclitaxel and doxorubicin combinations caused the most dramatic change in ultrastructure, which may disrupt many functions of the endothelium.
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Vascular dysfunction in adriamycin nephrosis: different effects of adriamycin exposure and nephrosis
TL;DR: In vitro vascular function in the isolated thoracic aorta and isolated perfused hearts of rats with adriamycin nephrosis is investigated, finding that nephrotic state reduced the bradykinin-induced increase in coronary flow and enhanced the aortic constrictor response to angiotensin II associated with reduced basal aortIC NO-activity.
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Effect of apoptosis-inducing antitumor agents on endocardial endothelial cells.
Sathish Kumar Maney,Ann Mary Johnson,A. Sampath Kumar,Vineet Nair,T. R. Santhosh Kumar,C C Kartha +5 more
TL;DR: The study revealed that endocardial endothelial cells are relatively resistant to apoptosis induced by doxorubicin, camptothecin, and thapsigargin, and indicates that response to antitumor agents greatly differs depending on the site of origin of endothelium.
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Doxorubicin selectively suppresses mRNA expression and production of endothelin-1 in endothelial cells.
TL;DR: Both the early decrease in endothelial ET-1 production in the presence of DXR and the high plasma level ofDXR during chemotherapy may influence the toxic effects of the drug.