Abstract
1. Basilar artery vasospasm was induced in cats by mechanical stimulation and application of fresh arterial blood, lysed platelets in saline and blood-CSF mixture incubated at 37°C for 5 to 10 days. Following the observation of sequential changes of the caliber, the basilar arteries were fixed and extirpated, and distributions and conditions of the nerves in the vessel wall were electron-microscopically studied.
2. In the group with fresh arterial blood and lysed platelets in saline, the severity of induced vaso-constriction was light and the duration was short. Mechanical stimulation induced very short-term vaso-constriction. On the other hand, mixture incubated for 5 to 10 days induced severe and prolonged vaso-constriction.
3. In the investigation of nerve endings, small cored vesicles were transformed, decreased and disappeared gradually in the course of time after the development of vasospasm induced with mixture incubated for 5 to 10 days, but these changes were not observed in the group with fresh arterial blood, laysed platelets in saline and mechanical stimulation.
4. In the group with mixture incubated for 5 to 10 days, the relationship between the degree of vasospasm and the nerve distribution was investigated. In the portion with severe vasospasm, the nerve distribution was very rich in the most inner area of the adventitia, within 10 μ from the outer edge of the media. On the contrary, in the same area of the arterial segment with slight vasospasm the nerves were extremely scanty, and they were seen only in the more outer area of the adventitia. This relation was clear in the animals with segmental vasospasm.
5. Basilar artery vasospasm were induced by the blood-CSF mixture incubated for 7 days on the 7th days after the bilateral superior cervical ganglionectomy and perivascular sympathectomy of the cervical carotid arteries. Vasospasm was not suppressed completely but the severity of constriction was definitely lighter and the duration was shorter than the cases without sympathectomy.
6. These findings show that the nerves especially the adrenergic axon in the most inner area of the adventitia may play an important role on the genesis of late vasospasm, and this difference of the nerve distribution may participate in the individual difference in frequency or severity of vasospasm. On the other hand, function of adrenergic nerve is not so important on the genesis of early vasospasm.
