Effect of deferoxamine and sympathectomy on vasospasm following subarachnoid hemorrhage

Utkan T., Sarioglu Y., Kaya T., Akgun M., Goksel M., Solak O.

PHARMACOLOGY, cilt.52, ss.353-361, 1996 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 52
  • Basım Tarihi: 1996
  • Doi Numarası: 10.1159/000139402
  • Dergi Adı: PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.353-361
  • Anahtar Kelimeler: deferoxamine, sympathectomy, subarachnoid hemorrhage, vascular smooth muscle, rabbit, CANINE BASILAR ARTERY, EXPERIMENTAL CEREBRAL VASOSPASM, RABBIT EAR ARTERY, ADRENERGIC-INNERVATION, CEREBROSPINAL-FLUID, SMOOTH-MUSCLE, ENDOTHELIUM, REACTIVITY, SEROTONIN, RECEPTORS
  • Kocaeli Üniversitesi Adresli: Evet

Özet

We examined the effects of subarachnoid hemorrhage (SAH) and treatment with deferoxamine (DFO) or sympathectomy on vascular smooth muscle function, as well as the underlying mechanisms involved, by recording the responses to noradrenaline and serotonin in isolated carotid arteries 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 vasospasm following SAH deferoxamine (DFO) was given to the animals and cervical and periarterial sympathectomy was performed in the other groups of animals. In isolated carotid arteries noradrenaline (10(-8) to 10(-4) mol/l) and serotonin (10(-8) to 10(-4) mol/l) produced concentration-dependent contractions. These contractile responses were significantly enhanced in animals 7 days after SAH compared to controls and did not return to control values in carotid arteries obtained from animals treated with DFO or sympathectomy for 7 days after SAH. These results show that SAH causes supersensitivity in the carotid as well as cerebral arteries during the first week after SAH and could contribute to the development of cerebral vasospasm. Both treatment with DFO and sympathectomy after SAH did not reduce the contractile responses to noradrenaline and serotonin in the carotid arteries. In conclusion, treatment with DFO or sympathectomy during the chronic stage of vasospasm after SAH did not affect the vascular responses of the extradural part of the carotid artery to vasoactive substances.