Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm

Keith A. Engelke, John R. Halliwill, David N. Proctor, Niki M. Dietz, Michael Joseph Joyner

Research output: Contribution to journalArticle

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Abstract

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 N(G)-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 · min-1; 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 · min-1 · 100 ml forearm-1 · 100 mmHg of perfusion pressure-1-min-1, P < 0.05; FBF = 26.6 ± 2.9 vs. 22.8 ± 2.6 ml · 100 ml-1 · min-1, 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 ml-1 · min-1 (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.

Original languageEnglish (US)
Pages (from-to)1807-1814
Number of pages8
JournalJournal of Applied Physiology
Volume81
Issue number4
StatePublished - Oct 1996

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Hyperemia
Forearm
Prostaglandins
Nitric Oxide
omega-N-Methylarginine
Ibuprofen
Nitric Oxide Synthase
Blood Vessels
Plethysmography
Cyclooxygenase Inhibitors
Prostaglandin-Endoperoxide Synthases
Vasodilation
Arginine
Ischemia
Perfusion
Pressure

Keywords

  • blood flow
  • endothelium
  • prostaglandins
  • vasodilation

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Engelke, K. A., Halliwill, J. R., Proctor, D. N., Dietz, N. M., & Joyner, M. J. (1996). Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm. Journal of Applied Physiology, 81(4), 1807-1814.

Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm. / Engelke, Keith A.; Halliwill, John R.; Proctor, David N.; Dietz, Niki M.; Joyner, Michael Joseph.

In: Journal of Applied Physiology, Vol. 81, No. 4, 10.1996, p. 1807-1814.

Research output: Contribution to journalArticle

Engelke, KA, Halliwill, JR, Proctor, DN, Dietz, NM & Joyner, MJ 1996, 'Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm', Journal of Applied Physiology, vol. 81, no. 4, pp. 1807-1814.
Engelke, Keith A. ; Halliwill, John R. ; Proctor, David N. ; Dietz, Niki M. ; Joyner, Michael Joseph. / Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm. In: Journal of Applied Physiology. 1996 ; Vol. 81, No. 4. pp. 1807-1814.
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