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Journal ArticleDOI

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.

George S. Allen, +3 more
- 01 May 1976 - 
- Vol. 44, Iss: 5, pp 585-593
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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.
Abstract
In vitro experiments were performed using a small volume chamber to study serotonin-induced contractions of the canine basilar artery. Temperature was found to have a profound effect on the artery's response to serotonin. Raising the temperature to 40 degrees C (104 degrees F) increased the maximum response by 20% and lowering the temperature by 10 degrees C caused a 40% reduction in the maximum contraction. Cumulative log-dose response curves for analogues of serotonin demonstrated a high degree of specificity for the serotonin receptor and large nonphysiological concentrations of serotonin caused relaxation of the contracted artery. Extracellular calcium was shown to be an absolute requirement for serotonin-induced contractions. Extracellular magnesium, in contrast, was shown to inhibit serotonin-induced contractions.

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Journal ArticleDOI

Cerebral Arterial Spasm – A Controlled Trial of Nimodipine in Patients with Subarachnoid Hemorrhage

TL;DR: It is concluded that nimodipine should be given to patients who are neurologically normal after subarachnoid hemorrhage in order to reduce the occurrence of severe neurologic deficits due to cerebral arterial spasm.
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Migraine and Magnesium: Eleven Neglected Connections

TL;DR: This essay will focus on certain failures of intercluster communication in scientific articles.
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Prevention of vasospasm in subarachnoid haemorrhage. A controlled study with nimodipine

TL;DR: This study confims the effectiveness of Nimodipine in reducing the occurrence of neurological deficit due to vasospasm, even if this action is not observed in all cases.
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Pharmacological analysis of 5-hydroxytryptamine receptors in isolated intracranial and extracranial vessels of cat and man.

TL;DR: The mode of inhibition by the β-antagonists suggests that the dilator effect of 5-HT is mediated by a receptor that may be the same as, or closely related to, the adrenergic fireceptor.
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Effect of nimodipine on intracellular brain pH, cortical blood flow, and EEG in experimental focal cerebral ischemia.

TL;DR: It is hypothesized that nimodipine exerts its effects through reversal of ischemia-induced secondary vasoconstriction, and that this drug may be an important adjunctive treatment for patients with focal cerebral ischemIA.
References
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Journal ArticleDOI

Excitation-Contraction Coupling in Rabbit Aorta Studied by the Lanthanum Method for Measuring Cellular Calcium Influx

TL;DR: Using La3+ to eliminate extracellular bound Ca2+ from calcium-influx measurements showed that depolarization by high K+, Na+ replacement, and high pH activate smooth muscle contraction by stimulating Ca2- influx.
Journal ArticleDOI

Cerebral arterial spasm.

TL;DR: In this article, the authors used a small volume chamber to determine the contractile activity of various vasoactive agents on the basilar and middle cerebral arteries, and concluded from these curves, and the known concentrations in blood, that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage.
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Vascular Smooth Muscle Updated

TL;DR: A brief review of the rapidly developing research on vascular smooth muscle presents the state of the art as I see it from within my own frame of reference.
Journal ArticleDOI

A beta-adrenergic receptor of the turkey erythrocyte. I. Binding of catecholamine and relationship to adenylate cyclase activity.

TL;DR: It was concluded that in addition to catechol-specific binding, a further interaction between plasma membrane and hormone is necessary for activation of adenylate cyclase, and this further interaction appears to involve a site specific for the ethanolamine portion of thecatecholamine molecule.
Journal ArticleDOI

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

TL;DR: 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 that was comparable to that produced by the injection of blood containing approximately the same amount of serotonin.
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