Prostaglandin production contributes to exercise-induced vasodilation in heart failure

Chim C. Lang, Don B. Chomsky, Javed Butler, Shiv Kapoor, John R. Wilson

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    23 Citations (Scopus)

    Abstract

    Endothelial release of prostaglandins may contribute to exercise-induced skeletal muscle arteriolar vasodilation in patients with heart failure. To test this hypothesis, we examined the effect of indomethacin on leg circulation and metabolism in eight chronic heart failure patients, aged 55 +/- 4 yr. Central hemodynamics and leg blood flow, determined by thermodilution, and leg metabolic parameters were measured during maximum treadmill exercise before and 2 h after oral administration of indomethacin (75 mg). Leg release of 6-ketoprostaglandin F1alpha was also measured. During control exercise, leg blood flow increased from 0.34 +/- 0.03 to 1. 99 +/- 0.19 l/min (P <0.001), leg O2 consumption from 13.6 +/- 1.8 to 164.5 +/- 16.2 ml/min (P <0.001), and leg prostanoid release from 54.1 +/- 8.5 to 267.4 +/- 35.8 pg/min (P <0.001). Indomethacin suppressed release of prostaglandin F1alpha (P <0.001) throughout exercise and decreased leg blood flow during exercise (P <0.05). This was associated with a corresponding decrease in leg O2 consumption (P <0.05) and a higher level of femoral venous lactate at peak exercise (P <0.01). These data suggest that release of vasodilatory prostaglandins contributes to skeletal muscle arteriolar vasodilation in patients with heart failure.
    Original languageEnglish
    Pages (from-to)1933-1940
    Number of pages8
    JournalJournal of Applied Physiology
    Volume83
    Issue number6
    Publication statusPublished - 1 Dec 1997

    Keywords

    • Congestive heart failure
    • Indomethacin
    • Regional blood flow

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    Lang, C. C., Chomsky, D. B., Butler, J., Kapoor, S., & Wilson, J. R. (1997). Prostaglandin production contributes to exercise-induced vasodilation in heart failure. Journal of Applied Physiology, 83(6), 1933-1940.