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Ultrastructural alterations in allylamine cardiovascular toxicity. Late myocardial and vascular lesions
Insights
Chronic allylamine intoxication causes severe damage to rat hearts, leading to myocardial necrosis, scarring, and aneurysm formation. Ultrastructural analysis reveals significant cardiac myocyte and small vessel injury, with endocardial metaplasia also observed.
Area of Science:
- Cardiovascular Toxicology
- Pathology
- Cell Biology
Background:
- Allylamine is a known cardiovascular toxin.
- Previous studies have documented acute effects of allylamine.
Purpose of the Study:
- To investigate the late myocardial and vascular ultrastructural changes in rat hearts after chronic allylamine consumption.
- To characterize the progression of tissue damage and identify specific cellular and extracellular alterations.
Main Methods:
- Rats were administered 0.1% allylamine hydrochloride in drinking water for 10 to 104 days.
- Histopathological and ultrastructural analyses were performed on cardiac tissues at various time points.
- Specific attention was paid to myocardial, vascular, and endocardial changes.
Main Results:
- Early stages (10-21 days) showed acute myocardial necrosis with inflammatory cell infiltration and interstitial cell proliferation.
- Later stages (21-104 days) revealed extensive scarring, left-ventricular aneurysm, and changes resembling endocardial fibroelastosis.
- Ultrastructural examination identified disorganized cardiac myocytes, damaged mitochondria, and smooth muscle cell proliferation in small vessels.
- Focal endocardial metaplasia with chondroid and osseous tissue formation was observed in scarred areas and aneurysms.
- Calcification of the collagen matrix and bone formation within the cardiac tissue were noted.
Conclusions:
- Chronic allylamine intoxication induces severe, progressive injury to the myocardium, small vessels, and endocardium in rats.
- The observed changes include significant fibrosis, aneurysm formation, and metaplasia, highlighting the long-term detrimental effects of this toxin.
- The findings suggest a complex pathological process involving cellular degeneration, inflammation, repair with abnormal matrix deposition, and metaplasia.
Abstract:
The late myocardial and vascular ultrastructural changes in rat hearts following consumption of the cardiovascular toxin allylamine were studied. Rats were given 0.1% allylamine HCl in drinking water for 10-104 days. From 10 to 21 days, there was organization of acute myocardial necrosis by macrophages and scattered polymorphonuclear leukocytes with prominent interstitial-cell proliferation. Alterations at 21-104 days included extensive scarring with formation of dense mature collagen with scattered fibroblasts present, grossly evident left-ventricular aneurysm, and gross and microscopic changes similar to those observed in the secondary form of endocardial fibroelastosis. Areas of scar contained highly cellular foci of smooth-muscle cells, myofibroblasts, and abundant extracellular elastin. Cardiac myocytes frequently showed markedly disorganized myofilaments, bizarrely distorted mitochondria with condensed cristae, and other severe degenerative changes. Small vessels within and adjacent to scar showed proliferation of intimal smooth-muscle cells. Endothelial lesions or recent or organized thrombi were not seen. Focal endocardial metaplasia, consisting of both chondroid and osseous tissue, was found in areas of transmural scarring, or ventricular aneurysm. Chondrocytes had the overall nuclear and cellular morphology, abundant rough endoplasmic reticulum, and surrounding lacunae typical of mature fibrocartilage. In some areas, the collagen matrix was undergoing calcification with the typical cross-banded pattern of calcifying connective tissue. Osteocytes were located in a densely calcified bone matrix and displayed characteristic cellular extensions into surrounding canaliculi. These findings indicate a severe myocardial, small-vessel, and endocardial injury during the course of chronic allylamine intoxication.