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Monocytes and radiation-induced atheromatosis in rabbits
Virchows Archiv. B, Cell Pathology Including Molecular Pathology
|January 1, 1984
Summary
Radiation-induced atheromatosis in rabbits was partially prevented by prednisolone but fully inhibited by VP-16 (Vepesid). Monocytes play a crucial role in this plaque formation, more so than lymphocytes.
Area of Science:
- Cardiovascular Research
- Immunology
- Radiation Biology
Background:
- Local irradiation of carotid arteries in hypercholesterolemic rabbits induces atheromatosis.
- The process involves monocyte adherence, subendothelial migration, and foam cell formation.
Purpose of the Study:
- To investigate the efficacy of prednisolone and VP-16 (Vepesid) in preventing radiation-induced atheromatosis.
- To determine the roles of lymphocytes and monocytes in the pathogenesis of this condition.
Main Methods:
- Hypercholesterolemic rabbits underwent local carotid artery irradiation.
- Animals were treated with either prednisolone or VP-16 (Vepesid).
- Differential blood cell counts were performed to assess treatment effects.
Main Results:
- Prednisolone partially prevented plaque formation and caused relative lymphocytopenia.
- VP-16 (Vepesid) fully inhibited plaque development and induced severe monocytopenia.
- Monocyte reduction correlated with plaque inhibition.
Conclusions:
- Monocytes play a critical role in radiation-induced atheromatosis pathogenesis.
- While lymphocytes may have a role, monocytes are more significant in this process.
- VP-16 (Vepesid) is a potent inhibitor, highlighting the monocyte's importance.