Nimodipine effects on cerebral microvessels and sciatic nerve in aging rats.

At the ultrastructural level different anomalies of the cerebral microvasculature were encountered in the brains of aged rats. These aberrations can either be attributed to degeneration processes or to the perivascular deposition of, e.g., collagen fibrils and other, unidentified, proteinous debris. We previously reported that chronic treatment with the calcium antagonist nimodipine from 24-30 months especially reduced the incidence of aging-related microvascular deposits in the frontoparietal motor cortex of rats. The same drug treatment did not interfere with the degeneration of pericytes. The reduction of the microvascular depositions was, however, not consistent throughout different cortical layers. We now demonstrate that an earlier onset (16-30 months) of the drug application yields a prominent and consistent reduction of microvascular deposits for all cortical layers studied. The earlier onset of the drug treatment again did not influence the quantity of pericyte degeneration. The effect of long-term nimodipine treatment (16-30 months) was also examined in the sciatic nerve. Compared to young animals the sciatic nerve of aged control rats (30 months) showed a variety of alterations of myelinated fiber (MF) morphometry. Nimodipine treatment from 16-30 months did not significantly change these morphometric aging-related changes. Approximately 6% of the MF in aged rats display morphological myelin irregularities. After nimodipine application the frequency of these alterations was reduced, which was, however, only significant for partial demyelination known as myelin ballooning. These results indicate a consistent influence of nimodipine on cerebral microvessels, while there is only a moderate effect on the morphology of sciatic myelinated fibers during the aging process.