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Vol. 83, Issue 6, 1933-1940, December 1997
Division of Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6300; and Clinical Research Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Received 20 March 1997; accepted in final form 4 August 1997.
Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor,
and John R. Wilson. Prostaglandin production contributes to
exercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933-1940, 1997.
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 F1
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
F1
(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.
congestive heart failure; indomethacin; regional blood flow
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