The cardiotoxin allylamine causes acute myocellular degeneration and necrosis; in a previous ultrastructural study we observed marked mitotic activity in endothelial cells following allylamine. In the present study, we assessed proliferative activity in the heart: groups of male rats were given either a single dose (100 mg/kg) of allylamine, or two doses on successive days; all rats were killed 24 hours after the last dose. Three hours before killing, rats were given 0.37 mCi/kg (SA 6.7 mCi/mMole) H3-Thymidine, iv. Under ether anesthesia rats were killed by cardiac perfusion with formalin; the entire heart was sectioned at 4 μm for autoradiography. Multiple adjacent fields were viewed and labeled endothelial and interstitial cell nuclei were counted across the interventricular septum (IVS), right ventricular free wall (RV), and left ventricular free wall (LV). Endothelial nuclear labeling was markedly increased in IVS after 2 doses (9.7 ± 2.2 mitoses/mm2 vs 1.6 ± .2 in control; P < .05), whereas LV and RV showed their most pronounced increases at 24 hours after the first dose. Increased endothelial and interstitial cell labelling correlated with histopathologic lesions, although increased labelling after 1 dose was also seen in the absence of lesions. Prominent endothelial cell proliferation and interstitial cell activation occur rapidly in acute allylamine myocardial damage.
|Original language||English (US)|
|Number of pages||9|
|Journal||Research Communications in Chemical Pathology and Pharmacology|
|State||Published - May 15 1990|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)