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Departments of Anesthesiology and of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905
Received 9 November 1995; accepted in final form 13 May 1996.
Engelke, Keith A., John R. Halliwill, David N. Proctor, Niki
M. Dietz, and Michael J. Joyner. Contribution of nitric oxide and
prostaglandins to reactive hyperemia in the human forearm. J. Appl. Physiol. 81(4):
1807-1814, 1996.
We investigated the separate and combined
contributions of nitric oxide (NO) and vasodilating prostaglandins as
mediators of reactive hyperemia in the human forearm. Forearm blood
flow (FBF) was measured with venous occlusion plethysmography after 5 min of ischemia. In one protocol (n = 12), measurements were made before and after intra-arterial
administration of the NO synthase inhibitor
NG-monomethyl-L-arginine
(L-NMMA) to one forearm. In a
separate protocol (n = 7),
measurements were made before and after systemic administration of the
cyclooxygenase inhibitor ibuprofen and again after
L-NMMA.
L-NMMA reduced baseline FBF at
rest (2.7 ± 0.4 to 1.6 ± 0.2 ml · 100 ml
1 · min1;
P < 0.05) and had a modest
effect on peak forearm vascular conductance and flow (forearm vascular
conductance = 31.1 ± 3.1 vs. 25.7 ± 2.5 ml · min1 · 100 ml
forearm1 · 100 mmHg of perfusion
pressure1 · min1,
P < 0.05; FBF = 26.6 ± 2.9 vs.
22.8 ± 2.6 ml · 100 ml1 · min1,
P = 0.055). Total excess
flow above baseline during reactive hyperemia was unaffected by
L-NMMA (14.3 ± 3.0 vs. 13.1 ± 2.3 ml/100 ml; P < 0.05).
Ibuprofen did not change FBF at rest, reduced peak FBF from 27.6 ± 1.9 to 20.3 ± 2.7 ml · 100 ml1 · min1
(P < 0.05), but had no effect on
total excess flow above baseline. Infusion of
L-NMMA after ibuprofen reduced
FBF at rest by 40%, had no effect on peak flow, but reduced total
excess flow above baseline from 12.0 ± 2.5 to 7.6 ± 1.3 ml/100
ml (P < 0.05). These data
demonstrate that NO synthase inhibition has a modest effect on peak
vasodilation during reactive hyperemia but plays a minimal role later.
Prostaglandins appear to be important determinants of peak flow. The
effects of NO synthase inhibition during reactive hyperemia may also be
potentiated by concurrent cyclooxygenase inhibition.
blood flow; prostaglandins; endothelium; vasodilation
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