Allylamine cardiotoxicity. II. Histopathology and histochemistry

P. J. Boor, T. J. Nelson, P. Chieco

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The progression of cardiac lesions induced in the rat by allylamine administration (0.1% in drinking water) was studied histopathologically. 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 tissue. 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.

Original languageEnglish (US)
Pages (from-to)739-764
Number of pages26
JournalAmerican Journal of Pathology
Volume100
Issue number3
StatePublished - 1980

Fingerprint

Allylamine
Monoamine Oxidase
Necrosis
Blood Vessels
Thrombosis
Arteries
Metaplasia
Drinking Water
Muscle Cells
Catecholamines
Smooth Muscle
Cardiotoxicity
Fibrosis
Coloring Agents
Cell Proliferation
Staining and Labeling
Wounds and Injuries

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Boor, P. J., Nelson, T. J., & Chieco, P. (1980). Allylamine cardiotoxicity. II. Histopathology and histochemistry. American Journal of Pathology, 100(3), 739-764.

Allylamine cardiotoxicity. II. Histopathology and histochemistry. / Boor, P. J.; Nelson, T. J.; Chieco, P.

In: American Journal of Pathology, Vol. 100, No. 3, 1980, p. 739-764.

Research output: Contribution to journalArticle

Boor, PJ, Nelson, TJ & Chieco, P 1980, 'Allylamine cardiotoxicity. II. Histopathology and histochemistry', American Journal of Pathology, vol. 100, no. 3, pp. 739-764.
Boor, P. J. ; Nelson, T. J. ; Chieco, P. / Allylamine cardiotoxicity. II. Histopathology and histochemistry. In: American Journal of Pathology. 1980 ; Vol. 100, No. 3. pp. 739-764.
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