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Department of Cell Biology and Physiology, and Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
Studies of
the effect of nitric oxide (NO) synthesis inhibition were performed in
the isometrically contracting blood-perfused canine
gastrocnemius-plantaris muscle group. Muscle blood flow (
) was controlled with a pump during continuous NO
blockade produced with either 1 mM
L-argininosuccinic acid
(L-ArgSA) or NG-nitro-L-arginine methyl ester
(L-NAME) during repetitive
tetanic contractions (50-Hz trains, 200-ms duration, 1/s). Pump
was set to match maximal spontaneous
(1.3-1.4
ml · min
1 · g
1)
measured in prior, brief (3-5 min) control contraction trials in
each muscle. Active tension and oxygen uptake were 500-600 g/g and
200-230
µl · min
1 · g
1,
respectively, under these conditions. Within 3 min of
L-ArgSA infusion, vascular
resistance across the muscle
(Rv) increased significantly
(from ~100 to 300 peripheral resistance units;
P < 0.05), whereas
Rv increased to a lesser extent
with L-NAME (from ~100 to 175 peripheral resistance units; P < 0.05). The increase in Rv with
L-ArgSA was unchanged by
simultaneous infusion of 0.5-10 mM
L-arginine but was reduced with
1-3 µg/ml sodium nitroprusside (41-54%). The increase in
Rv with
L-NAME was reversed with 1 mM of
L-arginine. Increased fatigue
occurred with infusion of
L-ArgSA; active tension and
intramuscular pressure decreased by 62 and 66%, whereas passive
tension and baseline intramuscular pressure increased by 80 and 30%,
respectively. These data indicate a possible role for NO in the control
of Rv and contractility within the canine gastrocnemius-plantaris muscle during repetitive tetanic contractions.
canine; endothelium-derived relaxation factor; fatigue; gastrocnemius muscle; hyperemia; intramuscular pressure; passive tension
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