These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.
    Author: Nakagomi T, Kassell NF, Sasaki T, Fujiwara S, Lehman RM, Torner JC.
    Journal: Stroke; 1987; 18(2):482-9. PubMed ID: 3564107.
    Abstract:
    The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.
    [Abstract] [Full Text] [Related] [New Search]