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Progressive vasomotor changes in ischaemic myocardium.

M W Gorman, R D Wangler, D F DeWitt

    Acta Medica Scandinavica. Supplementum
    |January 1, 1985
    PubMed
    Summary

    During myocardial ischemia, increased vascular resistance is partly due to reduced vasodilator release, not vasoconstrictors. This creates a feedback cycle worsening heart function and blood flow.

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    Area of Science:

    • Cardiovascular Physiology
    • Myocardial Ischemia Research

    Background:

    • Coronary artery stenosis can lead to increased vascular resistance in ischemic heart muscle within hours.
    • This phenomenon suggests alterations in vascular smooth muscle tone within the affected area.

    Purpose of the Study:

    • To investigate the mechanisms behind the progressive increase in vascular resistance in ischemic myocardium.
    • To differentiate between vasoconstrictor release and reduced vasodilator release as causes of increased vascular tone.

    Main Methods:

    • Pharmacological studies on ischemic canine hearts to test vasoconstrictor hypotheses.
    • Measurement of adenosine release from isolated guinea pig hearts to assess vasodilator release.

    Main Results:

    • Pharmacological interventions ruled out norepinephrine, PGF2 alpha, thromboxane A2, and high K+ as primary causes of vasoconstriction.
    • Reduced release of metabolic vasodilators, such as adenosine, was supported as a key factor.
    • Myocardial function and blood flow remained significantly impaired throughout the ischemic period.

    Conclusions:

    • The increased vascular resistance in ischemic myocardium is primarily linked to a decrease in metabolic vasodilator release.
    • A positive feedback cycle exists where reduced myocardial function and coronary blood flow exacerbate each other during moderate ischemia.

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