Roles of subarachnoid blood clots and norepinephrine in cerebral vasospasm.
The content of norepinephrine (NE) in the ventricular, basal cisternal and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms. The cisternal CSF in patients with vasospasm contained a significantly higher level of NE (0.246 +/- 0.0490 ng/ml) compared with those without vasospasm (0.075 +/- 0.001 ng/ml) (p less than 0.001). However, this increase is not considered to be high enough to constrict cerebral arteries, unless there is an increased NE-sensitivity in subarachnoid haemorrhage. Vascular responses to NE in vivo were then studied after reversing blood-induced prolonged vasospasm of the rabbit's basilar artery through a transclival approach as well as a newly developed basal cisternal irrigation model. However, NE in molar concentrations between 1 x 10(-10) and 10(-2) failed to produce further contraction of the artery. In conclusion, the increase in NE with vasospasm might be only a secondary phenomenon, and not a causative factor of vasospasm. Early removal of subarachnoid blood clots seemed to prevent the development of vasospasm.
D000818:Animals; D006406:Hematoma / Q000503:physiopathology*; D006801:Humans; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008954:Models, Biological; D009638:Norepinephrine / Q000502:physiology*; D011817:Rabbits; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*
D009638:Norepinephrine