Cerebral arterial spasm. 3. In vivo intracisternal production of spasm by serotonin and blood and its reversal by phenoxybenzamine.

@article{Allen1974CerebralAS,
  title={Cerebral arterial spasm. 3. In vivo intracisternal production of spasm by serotonin and blood and its reversal by phenoxybenzamine.},
  author={G. S. Allen and Lawrence H. A. Gold and Shelley N. Chou and Lyle A. French},
  journal={Journal of neurosurgery},
  year={1974},
  volume={40 4},
  pages={
          451-8
        }
}
In vivo experiments in dogs demonstrated that physiological concentrations of serotonin, when injected intracisternally, caused cerebral arterial spasm that lasted for at least 3 hours. Comparable spasm was produced by the injection of blood containing approximately the same amount of serotonin. Phenoxybenzamine reversed both the spasm produced by pure serotonin and that produced by blood. A hypothesis of the etiology of cerebral arterial spasm is proposed based on the experimental results of… 
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Cerebral arterial spasm. 2. In vitro contractile activity of serotonin in human serum and CSF on the canine basilar artery, and its blockage by methylsergide and phenoxybenzamine.
TLDR
The majority of contractile activity in CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin, which was capable of producing a prolonged contraction of the artery depending on its activity.
Cerebral arterial spasm.
  • G. Allen
  • Medicine, Biology
    Clinical neurosurgery
  • 1985
TLDR
In vitro experiments to determine the contractile activity of various vasoactive agents on the canine basilar and middle cerebral arteries concluded that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage.
Effect of Intravenous Ethanol on Cerebral Vasospasm Produced by Subarachnoid Blood
TLDR
In ethanol-treated animals with spasm induced from non-autogenous fresh arterial blood free of ethanol, a reduction in the duration of vasospasm was noted although the initial intensity of spasm was similar to control animals.
Subarachnoid haemorrhage in the rat: effect on the development of cerebral vasospasm of lesions in the central serotoninergic and dopaminergic systems.
TLDR
In the rat an intracisternal injection of blood induces an angiographically demonstrable biphasic cerebral arterial vasospasm and it is suggested that neither serotoninergic and dopaminergic system plays a role in the development of spasm.
Treatment of experiment delayed cerebral arterial spasm with a beta2-adrenergic stimulator and a phosphodiesterase inhibitor.
TLDR
The authors suggest that a combination of beta2-adrenergic stimulation and phosphodiesterase-inhibition might be of value in preventing or treating delayed cerebral arterial pressure.
Cerebral arterial spasm. Part 4: in vitro effects of temperature, serotonin analogues, large nonphysiological concentrations of serotonin, and extracellular calcium and magnesium on serotonin-induced contractions of the canine basilar artery.
TLDR
In vitro experiments were performed using a small volume chamber to study serotonin-induced contractions of the canine basilar artery and extracellular calcium was shown to be an absolute requirement for serotonin- induced contractions.
Cerebral arterial spasm In vitro contractile activity of vasoactive agents on human cortical and temporal arteries
TLDR
Arteries from both locations will be shown to react to a variety of agents including large contractions produced by very small concentrations of vasopressin, which may help explain the marked constriction often seen angiographically during the first few days following a cortical-temporal artery bypass procedure.
Cerebral arterial spasm. Part 5: in vitro contractile activity of vasoactive agents including human CSF on human basilar and anterior cerebral arteries.
TLDR
It was demonstrated that human cerebrospinal fluid, collected up to 17 days after a subarachnoid hemorrhage from patients with clinical and angiographic evidence of cerebral arterial spasm, would cause large, dose-dependent contractions in human anterior cerebral arteries.
Does cerebral vasospasm result from denervation supersensitivity?
TLDR
The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.
Subarachnoid haemorrhage in the rat: effect on the development of vasospasm of selective lesions of the catecholamine systems in the lower brain stem.
TLDR
Lesioning at the level of the mesencephalon of the ascending catecholamine pathways from locus coeruleus in the pons and the A1 and A2 nuclei in the medulla oblongata before cisternal blood injection prevents the development of both acute and late spasm.
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References

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Cerebral arterial spasm. 2. In vitro contractile activity of serotonin in human serum and CSF on the canine basilar artery, and its blockage by methylsergide and phenoxybenzamine.
TLDR
The majority of contractile activity in CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin, which was capable of producing a prolonged contraction of the artery depending on its activity.
Part 2" In vitro contractile activity of serotonin in human serum and CSF on the canine basilar artery, and its blockage by methylsergide and phenoxybenzamine
TLDR
The majority of contractile activity in CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin, which was capable of producing a prolonged contraction of the artery depending on its activity.
Part 1: In vitro contractile activity of vasoactive agents on canine basilar and middle cerebral arteries
TLDR
In vitro experiments performed using a small volume chamber to determine the contractile activity of various vasoactive agents on the canine basilar and middle cerebral arteries concluded that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage.
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