Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mechanisms responsible for coronary vasospasm.

J T Shepherd, P M Vanhoutte

    Journal of the American College of Cardiology
    |July 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    A quantitative study of the response to cold of the circulation through the fingers of normal subjects.

    Clinical science·2014
    Same author

    The average internal temperature of fingers immersed in cold water.

    Clinical science·2014
    Same author

    The effect of acute occlusion of the femoral artery on the blood supply to the calf of the leg before and after release of sympathetic vasomotor tone.

    Clinical science·2014
    Same author

    CONTROL OF BLOOD VESSELS IN HUMAN LIMBS.

    A listing of research in the cardiovascular field·2014
    Same author

    Developmental Disabilities and Long-Term Mental IllnessNew Work Programs.

    Work (Reading, Mass.)·2014
    Same author

    From Belfast to Mayo and beyond: the use and future of plethysmography to study blood flow in human limbs.

    Journal of applied physiology (Bethesda, Md. : 1985)·2001

    Coronary artery vasospasm can be worsened by beta-blockers, which may unmask alpha-receptor constriction. Platelet aggregation and serotonin release contribute to coronary artery spasm and myocardial hypoxia.

    Area of Science:

    • Cardiovascular Physiology
    • Pharmacology

    Background:

    • Coronary arteries possess alpha 1- and beta 1-adrenoceptors, influenced by sympathetic norepinephrine.
    • Beta 1-adrenoceptors dominate, typically mediating vascular smooth muscle relaxation.
    • Platelets release constricting agents like serotonin and thromboxane A2, while the endothelium produces relaxing prostacyclin.

    Purpose of the Study:

    • To investigate the mechanisms underlying coronary artery vasospasm.
    • To understand the role of adrenoceptors and platelet activity in vasospasm.

    Main Methods:

    • Studies on isolated segments of the left circumflex coronary artery of the dog.
    • Analysis of adrenoceptor function (alpha 1, beta 1) and sympathetic nerve activity.
    • Examination of platelet aggregation and endothelial function.

    Related Experiment Videos

    Main Results:

    • Beta 1-adrenoceptor blockade can exacerbate vasospasm by allowing unopposed alpha 1-adrenoceptor-mediated constriction.
    • Platelet aggregation at morphologically altered sites releases serotonin and thromboxane A2, causing arterial constriction.
    • Endothelial prostacyclin normally inhibits platelet aggregation and promotes relaxation, counteracting spasm.

    Conclusions:

    • Coronary artery spasm involves complex interactions between sympathetic stimulation, adrenoceptor activity, and platelet function.
    • Beta-blocker use in patients with coronary spasm may be detrimental due to uninhibited alpha-adrenergic constriction.
    • Endothelial dysfunction and platelet activation are key contributors to coronary artery spasm pathophysiology.