EFFECT OF DEFEROXAMINE AND SYMPATHECTOMY ON VASOSPASM FOLLOWING SUBARACHNOID HEMORRHAGE

Citation
T. Utkan et al., EFFECT OF DEFEROXAMINE AND SYMPATHECTOMY ON VASOSPASM FOLLOWING SUBARACHNOID HEMORRHAGE, Pharmacology, 52(6), 1996, pp. 353-361
Citations number
44
Categorie Soggetti
Pharmacology & Pharmacy
Journal title
ISSN journal
00317012
Volume
52
Issue
6
Year of publication
1996
Pages
353 - 361
Database
ISI
SICI code
0031-7012(1996)52:6<353:EODASO>2.0.ZU;2-1
Abstract
We examined the effects of subarachnoid hemorrhage (SAH) and treatment with deferoxamine (DFO) or sympathectomy on vascular smooth muscle fu nction, as well as the underlying mechanisms involved, by recording th e responses to noradrenaline and serotonin in isolated carotid arterie s in vitro, All studies were performed before and 7 days after SAH. An experimental subarachnoid hemorrhage model was created in rabbits by injecting autologous arterial blood into the subarachnoid space of the rabbits via cisterna magna punction. During the chronic stage of vaso spasm following SAH deferoxamine (DFO) was given to the animals and ce rvical and periarterial sympathectomy was performed in the other group s of animals. In isolated carotid arteries noradrenaline (10(-8) to 10 (-4) mol/l) and serotonin (10(-8) to 10(-4) mol/l) produced concentrat ion-dependent contractions. These contractile responses were significa ntly enhanced in animals 7 days after SAH compared to controls and did not return to control values in carotid arteries obtained from animal s treated with DFO or sympathectomy for 7 days after SAH. These result s show that SAH causes supersensitivity in the carotid as well as cere bral arteries during the first week after SAH and could contribute to the development of cerebral vasospasm. Both treatment with DFO and sym pathectomy after SAH did not reduce the contractile responses to norad renaline and serotonin in the carotid arteries. In conclusion, treatme nt with DFO or sympathectomy during the chronic stage of vasospasm aft er SAH did not affect the vascular responses of the extradural part of the carotid artery to vasoactive substances.