Cerebrovascular responses to subarachnoid blood and serotonin in the monkey.

@article{Boisvert1977CerebrovascularRT,
  title={Cerebrovascular responses to subarachnoid blood and serotonin in the monkey.},
  author={Donald P. J. Boisvert and Bryce K. A. Weir and Thomas R. Overton and R. J. Reiffenstein and Michael Grace},
  journal={Acta neurologica Scandinavica. Supplementum},
  year={1977},
  volume={64},
  pages={
          322-3
        }
}
✓ Preliminary in vitro experiments were performed to determine the serum concentration of serotonin in the monkey, and the ability of cyproheptadine to block serotonin and serum-induced contractions in monkey cerebral arteries. Thirty-four cynomolgus monkeys were subsequently used to study changes in regional cerebral blood flow (CBF) obtained by the intracarotid 133Xe technique, and in the angiographic cerebral arterial caliber resulting from subarachnoid injection of artificial cerebrospinal… 
Subarachnoid hemorrhage-induced upregulation of the 5-HT1B receptor in cerebral arteries in rats.
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Insight into the mechanism of upregulation may provide new targets for developing specific treatment against cerebral vasospasm and changes in the receptor phenotype in favor of contractile receptors may well represent the end stage in a sequence of events leading from SAH to the actual development of cerebral Vasospasm.
Effect of diltiazem on experimental chronic cerebral vasospasm in the monkey.
TLDR
It is demonstrated that vascular narrowing and neurological deficit can be markedly attenuated by diltiazem pretreatment.
The role of platelets in the development of cerebral vasospasm
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.
Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em.
TLDR
The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls, and this depolarization was present as early as 30 min post ictus.
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TLDR
The hydrogen clearance method was used to measure local and total cerebral blood flow in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage, suggesting that vasoactive agents in fresh whole blood and the arterial spasm they produce when added to cerebrospinal fluid play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.
Effect of Topically Applied Serotonin on Local Cerebral Blood Flow
TLDR
Although 5HT is a potent vasoconstrictor, under physiologic conditions it apparently is unable to effect hemodynamically significant constriction of the peripheral cerebral vasculature of the anesthetized monkey brain.
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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.
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.
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.
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TLDR
Cerebral blood flow recordings and vessel caliber measurements should complement experiments in cerebral vasospasm to ascertain whether the spasm is producing significant ischemia and to assess the efficacy of subsequent treatment techniques.
Part 3: In vivo intracisternal production of spasm by serotonin and blood and its reversal by phenoxybenzamine
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
Noradrenergic Mediation of Experimental Cerebrovascular Spasm
TLDR
The data suggest that cerebral vasospasm is produced by substances acting at the alpha adrenergic receptor of the vessel wall, and that blood contains a vasoconstrictor substance capable ofacting at the receptor site.
Responsiveness of Isolated Cerebral and Peripheral Arteries to Serotonin, Norepinephrine, and Transmural Electrical Stimulation
TLDR
These studies demonstrate that a gradual transition occurs from characteristic responses seen in mesenteric arteries to those seen in cerebral arteries (high sensitivity to serotonin, low sensitivity to norepinephrine), which appears that sympathetic nerves cannot play an important role in the regulation of vascular tone in large cerebral arteries.
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The study of irrigation fluids for use on the exposed brain, which forms the subject of the present report, is a part of a series of investigations on the general problem of the reaction of the brain to exposure which is being carried out under the direction of Professor Wilder Penfield.
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