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Related Experiment Videos

Microcirculatory norepinephrine constrictor response in hemorrhagic shock.

L M Flint, H M Cryer, C J Simpson

    Surgery
    |August 1, 1984
    PubMed
    Summary

    Hemorrhagic shock involves compensation and decompensation. In decompensated shock, small arterioles and venules dilate, contributing to shock progression despite maintained norepinephrine constrictor responses.

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    Area of Science:

    • Physiology
    • Cardiovascular Research
    • Shock Pathophysiology

    Background:

    • Hemorrhagic shock initially triggers compensatory vasoconstriction via catecholamines like norepinephrine (NE) to maintain blood flow.
    • Skeletal muscle microcirculation plays a key role in this compensatory response.
    • Decompensation is marked by arteriolar vasodilation despite ongoing hypovolemia and high NE levels.

    Purpose of the Study:

    • To investigate the constrictor response to norepinephrine (NE) in the skeletal muscle microcirculation during compensated and decompensated hemorrhagic shock.
    • To determine if altered NE responsiveness contributes to decompensation in arterioles and venules.

    Main Methods:

    • Utilized an isolated decerebrate rat cremaster muscle preparation.
    • Measured the constrictor response to a specific tissue concentration of NE (10(-7)M).

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  • Compared responses in compensated and decompensated shock states.

    • Main Results:

    • Larger arterioles (143-152 microns) maintained a constrictor response to NE but with reduced sensitivity.
    • Smaller arterioles (11-22 microns) and all venules exhibited dilation late in shock.
    • Despite dilation, smaller arterioles and venules retained their constrictor responsiveness to NE.

    Conclusions:

    • Arteriolar vasodilation in smaller vessels and venules, not altered NE constrictor response, contributes to decompensation in hemorrhagic shock.
    • The microcirculation's response to NE changes with shock severity, with larger vessels showing reduced sensitivity and smaller vessels dilating.