Proceedings of The Physiological Society

University of Cambridge (2004) J Physiol 555P, PC15


The role of prostaglandins (PGs) in the vasodilatation that follows isometric contraction in human subjects

Thet Su Win and Janice M. Marshall

Department of Physiology, The Medical School, Birmingham B15 2TT, UK

The issue of whether or not PGs contribute to the vasodilatation associated with muscle contraction is controversial (see Kilbom & Wennmalm, 1976; Shoemaker et al. 1996). In the present, double-blind cross-over study with approval of the University Ethics Review Committee, we tested the role of PGs in the dilatation that follows isometric contraction of the forearm.

In 11 healthy volunteers aged 21.5±0.8 years (mean ± S.E.M.), forearm blood flow (FBF) was measured by venous occlusion plethysmography and forearm cutaneous red cell flux (cRCF) by means of a laser Doppler probe. Measurement of arterial blood pressure (ABP) with a semiautomatic sphygmomanometer allowed calculation of forearm and cutaneous vascular conductance (FVC, CVC: FBF or cRCF divided by ABP).

In Protocol 1, measurements were made before and at 0, 0.5, 1, 2 and 3 min after a 2 min period of isometric contraction of the forearm at 60 % maximum voluntary contraction. This was performed after placebo or after aspirin (600 mg, a dose that blocks cyclooxygenase, Heavey et al, 1985). Following the contraction there was an increase in FVC (post-contraction dilatation), but no change in CVC, indicating the vasodilatation occurred predominantly in forearm muscle. Aspirin substantially reduced the post-contraction increase in FVC: from a baseline of 0.09±0.01 conductance units (CU), the peak FVC at 0 min was reduced from 0.24±0.03 to 0.14±0.01* CU (*:P < 0.05, placebo vs. aspirin, ANOVA and Bonferroni/Dunn post hoc test.

In Protocol 2, which was comparable to Protocol 1 except subjects breathed 40 % O2 throughout, after placebo, the post contraction increase in FVC was smaller than during air breathing: the peak FVC at 0 min was 0.15±0.02* CU. Further, when breathing 40 % O2, aspirin had no further effect on the post-contraction increase in FVC: the peak FVC at 0 min after aspirin and with 40 % O2 was 0.16±0.02 CU.

These results indicate that PGs make a substantial contribution to the vasodilatation that follows isometric contraction of the forearm. Given aspirin and breathing 40 % O2 had similar effects on the post-contraction dilatation, we propose the stimulus for PG synthesis is hypoxia of the vascular endothelium in forearm muscle that arises during the period of contraction.

Where applicable, experiments conform with Society ethical requirements