| Allylamine cardiotoxicity: II. Histopathology and histochemistry. | |
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MedLine Citation:
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PMID: 6448005 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The progression of cardiac lesions induced in the rat by allylamine administration (0.1% in drinking water) was studied histopathologically and histochemically. Early changes (4-8 days) consisted of piecemeal acute apical and subendocardial myocardial necrosis with morphologic features of coagulation necrosis and myocytolysis. These early lesions progressed and coalesced; resolution of the subendocardial necrosis was associated with remarkably proliferative fibroblastic tissus. Late lesions (21 days to 3 months) consisted of extensive dense fibrous tissue with adjacent continuing focal necrosis and organization. Although vascular alterations were not present during the early course of injury, after 21 days an exuberant proliferation of cells, predominantly within the intima of intramyocardial smaller arteries and not associated with total occlusion or thrombosis, became evident. Other late lesions included rare intraventricular mural thrombi and cartilagenous metaplasia of trabeculae carnae. Early histochemical alterations (3 days) included focal myocardial cell "calcification," demonstrated by the alizarin red S stain, and increased monoamine oxidase (MAO) staining in apical subendocardium and periarterial myocytes. As necrosis continued and fibrosis developed (7-21 days) MAO dramatically increased in pericicatricial and periarterial cells. Biochemical measurement of myocardial MAO showed an initial drop in activity, followed by a steady rise to high activity (21 days), especially toward a Type "B" MAO substrate. Although there are many similarities between allylamine-induced myocardial necrosis and ischemic or catecholamine-induced myocardial damage, other unusual findings-especially the early histochemical and chemical MAO alterations and the proliferative late vascular and cicatricial lesions-suggest that the primary pathophysiologic effect of allylamine, mediated through the MAO system, is on the medial smooth muscle of intramyocardial arteries. |
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Authors:
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P J Boor; T J Nelson; P Chieco |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of pathology Volume: 100 ISSN: 0002-9440 ISO Abbreviation: Am. J. Pathol. Publication Date: 1980 Sep |
Date Detail:
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Created Date: 1980-11-25 Completed Date: 1980-11-25 Revised Date: 2010-06-22 |
Medline Journal Info:
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Nlm Unique ID: 0370502 Medline TA: Am J Pathol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 739-64 Citation Subset: AIM; IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Allylamine
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toxicity* Amines / toxicity* Animals Calcium / metabolism Calcium-Transporting ATPases / metabolism Cardiomyopathies / chemically induced*, enzymology, pathology Histocytochemistry Male Monoamine Oxidase / metabolism Myocardium / enzymology, pathology* Rats Succinate Dehydrogenase / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL-07066/HL/NHLBI NIH HHS; HL-21327/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Amines; 107-11-9/Allylamine; 7440-70-2/Calcium; EC 1.3.99.1/Succinate Dehydrogenase; EC 1.4.3.4/Monoamine Oxidase; EC 3.6.1.8/Calcium-Transporting ATPases |
| Comments/Corrections | |
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