The nature of latent cerebral irradiation damage and its modification by hypertension

The cerebral hemispheres of normotensive and hypertensive rats were irradiated using exposures from 1,000 R to 4,000 R. Hypertension was shown to shorten the latent period between irradiation and death for exposures of 2,000 and 3,000 R and to lower the threshold for radiation damage to 1,000 R. Following an exposure of 4,000 R no differential shortening of the latent period occurred, normotensive and hypertensive animals dying after similar lengths of time.

The hypothesis is put forward that with low exposures of X rays (2,000–3,000 R) radiation death is due to sudden vascular damage while with high values of exposure (3,000–4,000 R) death is due to white matter necrosis which follows glial depletion and subependymal stem cell damage respectively.

Hypertension only accelerates vascular radiation damage and reduces the effective threshold dose of radiation.

The latent period and both modes of damage are explained on the basis of the known slow mitotic replacement of vascular and glial cells in the central nervous system.