Abstract
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) |
|---|---|
| Pages (from-to) | 3-11 |
| Number of pages | 9 |
| Journal | Research Communications in Chemical Pathology and Pharmacology |
| Volume | 68 |
| Issue number | 1 |
| State | Published - 1990 |
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ASJC Scopus subject areas
- Toxicology
- Pharmacology
Cite this
Increased DNA synthesis in the heart during acute allylamine cardiotoxicity. / Boor, P. J.; Kretschmer, N.
In: Research Communications in Chemical Pathology and Pharmacology, Vol. 68, No. 1, 1990, p. 3-11.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Increased DNA synthesis in the heart during acute allylamine cardiotoxicity
AU - Boor, P. J.
AU - Kretschmer, N.
PY - 1990
Y1 - 1990
N2 - 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.
AB - 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.
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M3 - Article
C2 - 2345804
AN - SCOPUS:0025240507
VL - 68
SP - 3
EP - 11
JO - Research Communications in Chemical Pathology and Pharmacology
JF - Research Communications in Chemical Pathology and Pharmacology
SN - 0034-5164
IS - 1
ER -