Role of neuron density of the stellate ganglion on regulation of the basilar artery volume in subarachnoid hemorrhage: An experimental study

The purpose of this study was to test whether endothelium-dependent relaxation is decreased during acute vasospasm following subarachnoid hemorrhage (SAH) and the mechanism underlying the decrease. Basilar artery in situ was 35% constricted 3 days following injection of autologous arterial blood into the rabbit cisterna magna compared with vessels from control rabbits. In situ suffusion with the endothelium-dependent relaxant, acetylcholine (ACh; 10 microM), relaxed resting and serotonin (5-HT)-contracted control vessels but not vasospastic and 5-HT-contracted vasospastic vessels. In contrast, the relaxant potency and efficacy of ACh was similar in control and vasospastic vessels contracted with 5-HT in vitro. In situ suffusion with the ETA-receptor antagonist, BQ-123 (1 microM), reversed the vasospasm by 51% and restored the magnitude of ACh relaxation of vasospastic and 5-HT-contracted vasospastic vessels to that of controls. ACh in situ and in vitro relaxed endothelin-1 (ET-1)-contracted control vessels to a smaller magnitude than 5-HT-contracted control vessels. These results suggest, in contrast to previous studies, that endothelium-dependent relaxation is decreased during acute vasospasm following SAH. The decreased endothelium-dependent relaxation is secondary to the underlying ET-1-mediated spasm. The inhibition of endothelium-dependent relaxation observed in situ following SAH cannot be demonstrated in vitro, presumably due to loss of the ET-1-mediated vasospasm.

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Brainstem hypoperfusion in severe symptomatic vasospasm following aneurysmal subarachnoid hemorrhage: role of basilar artery vasospasm

Acta Neurochirurgica ◽

10.1007/s00701-006-0802-9 ◽

2006 ◽

Vol 148 (9) ◽

pp. 929-935 ◽

Cited By ~ 3

Author(s):

G. E. Sviri ◽

G. W. Britz ◽

D. H. Lewis ◽

B. Ghodke ◽

A. H. Mesiwala ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Basilar Artery ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Symptomatic Vasospasm

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Role of Protein Kinase C in the Pathogenesis of Cerebral Vasospasm after Subarachnoid Hemorrhage

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1993.30 ◽

1993 ◽

Vol 13 (2) ◽

pp. 247-254 ◽

Cited By ~ 46

Author(s):

Masaharu Sako ◽

Jun Nishihara ◽

Shinsuke Ohta ◽

Jinze Wang ◽

Saburo Sakaki

Keyword(s):

Protein Kinase C ◽

Subarachnoid Hemorrhage ◽

Protein Kinase ◽

Cerebral Vasospasm ◽

Basilar Artery ◽

Sustained Contraction ◽

Kinase C ◽

Intracisternal Injection ◽

Membrane Bound

This study investigated the role of protein kinase C (PKC) in the pathogenesis of vasospasm after experimental subarachnoid hemorrhage (SAH). PKC activation by intracisternal injection of a phorbol ester [12- O-tetradecanoylphorbol-13-acetate (TP)] induced dose-dependent, slowly developing, severe contraction of the basilar artery. A single intracisternal injection of TP (5 × 10−9 M in the CSF) induced sustained contraction lasting over 3 days, which almost paralleled the changes of membrane-bound PKC activity in the basilar arterial wall. In a two-hemorrhage SAH model, membrane-bound PKC activity in the basilar artery increased up to day 4 and returned to the control level by day 14, whereas angiographic contraction reached a maximum on day 7 and still persisted at a moderate level on day 14. Thus, there was a discrepancy between arterial PKC activity and arterial contraction. Multiple intracisternal injections of TP produced 30–40% sustained contraction of the basilar artery lasting for more than 10 days along with sustained activation of PKC to levels compatible with that observed in the SAH model. However, TP injection caused considerably milder histological changes in the basilar artery than those noted in the SAH model. We concluded that cerebral vasospasm after SAH cannot be explained solely on the basis of activation of the PKC pathway.

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