Release of endothelium-derived relaxing factor after subarachnoid hemorrhage.

@article{Kim1989ReleaseOE,
  title={Release of endothelium-derived relaxing factor after subarachnoid hemorrhage.},
  author={Phyo Kim and Robert R. Lorenz and Thoralf M. Sundt and Paul Michel Vanhoutte},
  journal={Journal of neurosurgery},
  year={1989},
  volume={70 1},
  pages={
          108-14
        }
}
The purpose of this study was to determine the cause of the loss of endothelium-dependent relaxation observed in chronic cerebral vasospasm. A bioassay system was developed to measure the release of endothelium-derived relaxing factor (EDRF) from canine basilar arteries. Subarachnoid hemorrhage (SAH) was induced in dogs by two injections of autologous blood into the cisterna magna. Angiograms were performed on the 7th day after SAH to check the presence of chronic vasospasm. The animals were… 
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Reduced production of cGMP underlies the loss of endothelium-dependent relaxations in the canine basilar artery after subarachnoid hemorrhage.
TLDR
The data indicate that the altered endothelium-mediated relaxations of the smooth muscle after subarachnoid hemorrhage is due, at least in part, to an impaired activation of soluble guanylate cyclase leading to a reduced production of cGMP in the Smooth muscle.
The effect of chronic subarachnoid hemorrhage on basal endothelium-derived relaxing factor activity in intrathecal cerebral arteries.
TLDR
The findings support the view that adventitially applied hemoglobin can inhibit basal EDRF activity and that in vivo adventitial exposure to whole blood leads to a reduction in basal cGMP levels in association with vasoconstriction of intrathecal arteries.
Effects of deferoxamine and sympathectomy on endothelin-1-induced contraction and acetylcholine-induced relaxation following subarachnoid hemorrhage in carotid artery.
Attenuation of experimental subarachnoid hemorrhage--induced cerebral vasospasm by the adenosine A2A receptor agonist CGS 21680.
TLDR
This is the first evidence that adenosine A2A receptor agonism is effective in preventing SAH-induced vasospasm without significant complications.
Pharmacological studies on relaxation of spastic primate cerebral arteries in subarachnoid hemorrhage.
TLDR
It seems that histamine mediates relaxation of intact MCA's mostly by an H1-receptor-mediated release of endothelium-derived relaxing factor (EDRF).
Pharmacological studies on relaxation of spastic primate cerebral arteries in subarachnoid hemorrhage
TLDR
It seems that histamine mediates relaxation of intact MCA's mostly by an H-receptor-mediated release of endotheliumderived relaxing factor (EDRF), which influences both the generation of EDRF and the constriction of affected arteries.
Subarachnoid Hemorrhage and Endothelial L‐Arginine Pathway in Small Brain Stem Arteries in Dogs
TLDR
It is suggested that in small arteries of the brain stem vasopressin causes relaxations by activation of the endothelial L-arginine pathway, which is selectively inhibited by subarachnoid hemorrhage.
Nitric oxide synthase and guanylate cyclase levels in canine basilar artery after subarachnoid hemorrhage.
TLDR
The reduced expression of soluble guanylate cyclase may be related to the impairment of endothelium-dependent vasodilation in vasospasm following subarachnoid hemorrhage.
Modulatory role of endothelial and nonendothelial nitric oxide in 5-hydroxytryptamine-induced contraction in cerebral arteries after subarachnoid hemorrhage.
TLDR
The results suggest that cerebral arteries after SAH exhibit hyperreactivity to 5-HT via a mechanism that involves the absence of the modulatory role of endothelial NO, that SAH does not modify the modulation role of nonendothelial No, and that impairment of themodulatory action of endothelium NO on vascular responses to 4-hydroxytryptamine could contribute to the pathogenesis of cerebral vasospasm afterSAH.
Cerebrovascular effects of substance P after experimental subarachnoid haemorrhage
TLDR
The vasoactive effects of substance P (SP), as well as the content of cyclic guanine monophosphate (cGMP), were determined in the rabbit basilar artery after subarachnoid haemorrhage (SAH), suggesting a link between impaired vaso active response to SP and decreased production of cGMP after SAH.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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