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.