No abstract

Alkaline phosphatase activity of capillary endothelial cells in the heart of Wistar and Sprague-Dawley rats was studied sequentially after single doses of 10, 15, 20, or 25 Gy. Following irradiation capillary density and alkaline phosphatase activity were focally lost before myocardial degeneration or clinical symptoms of heart disease developed. Recovery from both changes took place after doses of 10 or 15 Gy. The decrease in capillary density and enzyme activity showed the same strain difference in latency times and in the extent of the lesions as previously described for pathological and clinical signs of heart disease.

Radiation-induced myocardial degeneration in the rat is preceded by changes in capillary structure and function, which may be a major factor in the pathogenesis of radiation-induced heart disease. In order to investigate the mechanism of capillary damage we studied endothelial cell proliferation in untreated control rats and in rats at different times following local heart irradiation with 20 Gy using [3H]thymidine autoradiography. Since the latency times of myocardial degeneration as well as capillary damage are about twice as long in Sprague-Dawley rats as in Wistar rats, endothelial cell proliferation was studied in both strains. The percentage of labelled nuclei (LI) after repeated labelling over a period of 12 h was 0.32 +/- 0.06 in control animals of both strains. Therefore the turnover time of endothelial cells was estimated to be between 115 and 400 days. Following irradiation the LI increased above control levels. In both strains this was concurrent with the time of onset of capillary depletion and alkaline phosphatase loss, which occurred at around 23 days post-irradiation in Wistar rats and 58-74 days in Sprague-Dawley rats. In both strains the increase in LI was confined to alkaline-phosphatase-negative areas. In phosphatase-positive areas endothelial cell proliferation was unchanged in spite of the reduction in capillary density. Since, in general, the latency to post-irradiation death of a cell is closely related to its normal turnover time, the decrease in capillary density is not due to mitotic death of proliferating cells as is commonly seen in other tissues.

No abstract

No abstract