Regulation of blood flow by aspirin following muscle ischemia

S.J. Cameron 1,3, S. Goulopoulou 2, B.R. Weil 2, J.A. Kanaley 1,2

1 Department of Medicine, SUNY Upstate Medical University, Syracuse, (USA)
2 Department of Exercise Science, Syracuse University, Syracuse, NY, (USA)
3 Present address: Department of Medicine, Weill Medical College of Cornell University, Department of Medicine, New York, NY, (USA)

---

• Pharmacology

Background: The vascular endothelium secretes a balance of dilator and constrictor substances which regulate vascular tone. During ischemic stress, this balance changes. After a short period of ischemia, a protective mechanism known as reactive hyperemia (RH) contributes to a post-ischemic increase in blood flow. The agents regulating this phenomenon remain controversial.

Aim: The purpose of this study was to examine whether aspirin regulates vascular endothelial function following ischemia. Methods: Sixteen healthy volunteers presented for two visits, each serving as their own control, and randomized to receive 500 mg aspirin or placebo. Forearm blood flow (FBF) was measured at baseline and during reactive hyperemia (RH) which was induced by five minutes of arterial occlusion. Blood samples were analyzed for vWF and lipids. Results: After ischemia, RH was attenuated when subjects were pre-medicated with 500 mg aspirin compared to placebo: AUC[aspirin]=1450 ± 201 mL/100 mL tissue/min vs. AUC[placebo]= 2207 ± 294 mL/100 mL tissue/min; (p < 0.05). Separation of the subjects with high HDL or low HDL levels resulted in a similar peak FBF response with placebo, but in the high-HDL group only, aspirin ingestion attenuated peak FBF after ischemia compared to the placebo condition (22.6 ± 1.7 mL/100 mL tissue/min vs. 33.5 ± 3.2 mL/100 mL tissue/min, respectively) (p < 0.05).

Conclusions: Aspirin partially regulates the RH response following ischemia compared to placebo, and this effect appears to be more profound when adjusting for plasma HDL concentration in healthy individuals. This suggests that the post-ischemic RH response may be partially mediated by arachadonic acid-derived mediators such as the prostaglandins.

Corresponding Author: Jill A. Kanaley, Ph.D.; e-mail: kanaleyj@missouri.edu

Free PDF Download