Open Access
EffectofDoxorubicin on(w-l-131)Heptadecanoic AcidMyocardial Scintigraphy andEchocardiography inDogs
C. B. Styles,Antoine A. Noujaim,T. K. Shnitka +2 more
- 01 Jan 1983
TL;DR: Findings suggest that the changes leading to analteration of myocardialdynamicImaging with 1-131HA are not the initiatingfactor in doxo rubicincardiotoxicity.
read more
Abstract: Theeffectsof serialtreatmentwithdoxorubicin ondynamicmyocardialscintig raphywith[w-I-131]heptadecanoic acid(1-131HA), andongloballeft-ventricular functiondeterminedechocardiographically, were studiedIn a groupof ninemon greldogs.Totalextractablemyocardiallipidwascomparedpostmortem between a groupof controldogsanddoxorubicin-treated dogs.A significant andthenpro gressivefall in global LV function was obServedat a cumulative doxorubicindose of 4 mg/kg. A significantincreasein the myocardialt112of the 1-131HA was ob servedonlyat a highercumulative dose,10mg/kg.Nosignificant alterationintotal extractablemyocardlallipidswasobservedbetweencontroldogsandthosetreat ed withdoxorubicin. Ourfindings suggest thatthe changesleadingto analteration of myocardialdynamicImagingwith1-131HAare notthe initiatingfactorin doxo rubicincardiotoxicity.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
References
Risk factors for doxorubicin-induced congestive heart failure.
TL;DR: There was a continuum of increasing risk as the cumulative amount of administered drug increased, and a weekly dose schedule of doxorubicin was associated with a significantly lower incidence of congestive heart failure than was the usually employed every 3-week schedule.
2.4K
Adriamycin: the role of lipid peroxidation in cardiac toxicity and tumor response
Charles E. Myers,William McGuire,Robert H. Liss,Ina Ifrim,Karen R. Grotzinger,Robert C. Young +5 more
TL;DR: The results suggest that adriamycin has at least two mechanisms of tissue damage: one, which involves lipid peroxidation, is blocked by tocopherol and results in cardiac toxicity; the other, which consists of binding to DNA, is not antagonized by toCophero and is responsible for tumor response.
1.1K
Uptake and tissue content of fatty acids in dog myocardium under normoxic and ischemic conditions.
TL;DR: Enhanced lipolysis of endogenous lipids or reduced combustion may be held responsible for the accumulation of NEFA in ischemic tissue, since arachidonic and linoleic acids showed the highest relative increase and lipolytic of endogenous phospholipids, rich in these fatty acids, seems to be reasonable.
279
•Journal Article
Cardiac disease induced by chronic adriamycin administration in dogs and an evaluation of vitamin E and selenium as cardioprotectants.
TL;DR: The dog offers a suitable model for studies of chronic ADR cardiotoxicity in man and the lack of cardioprotection from vitamin E and selenium supplementation fails to support the proposed role of lipoperoxidative damage in the development of chronic adriamycin-induced cardiomyopathy.
176
•Journal Article
Comparative Evaluation of Fatty Acids Labeled with C-11, Cl-34m, Br-77, and I-123 for Metabolic Studies of the Myocardium: Concise Communication
H.J. Machulla,Gerhard Stöcklin,Ch. Kupfernagel,Ch. Freundlieb,A. Höck,K. Vyska,Ludwig E. Feinendegen +6 more
TL;DR: Comparative studies of the kinetics of accumulation and clearance from the heart muscle of mice indicate that the extraction of omega-halofatty acids is more efficient than that of alpha-halothermite acids.
150