Myocardial fibrosis and smooth muscle cell hyperplasia in coronary arteries of allylamine-fed rats.
Immature female Long-Evans rats were fed 2 g of allylamine-HCl kg of commercial diet for periods of 84-281 days. Coronary arteries and myocardium were examined in 16 control and 23 test rats. Cellular alterations in the arterial tributaries were found principally proximal to or within the areas of myocardial fibrosis. Whereas intimal smooth muscle cell (SMC) hyperplasia was prominent in vessels of smaller caliber, medial hyalinosis was seen frequently in arteries with diameters greater than 200 mu. Intimal hyperplasia developed in the peripheral coronary branches without any evidence of leukocytic infiltration or thrombus formation. It appeared that SMC hyperplasia in the intima contributed more often to a reduction of luminal patency than medial hyalinosis in allylamine-fed rats. On the basis of alterations in the coronary arteries and the localization of fibrosis, we believe that hypoxia is the cause of myocardial necrosis.
D000475:Alkenes / Q000633:toxicity*; D000498:Allyl Compounds / Q000633:toxicity; D000818:Animals; D001835:Body Weight; D003331:Coronary Vessels / Q000473:pathology*; D004719:Endomyocardial Fibrosis / Q000139:chemically induced* / Q000473:pathology; D005260:Female; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects; D006965:Hyperplasia; D008854:Microscopy, Electron; D009130:Muscle, Smooth / Q000187:drug effects / Q000473:pathology*; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D009929:Organ Size; D051381:Rats
D000475:Alkenes; D000498:Allyl Compounds