Regulation of blood flow by aspirin following muscle ischemia

S. J. Cameron, Styliani Goulopoulou, B. R. Weil, J. A. Kanaley

Research output: Contribution to journalReview article

Abstract

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 arachidonic acid-derived mediators such as the prostaglandins.

Original languageEnglish
Pages (from-to)143-150
Number of pages8
JournalEuropean Review for Medical and Pharmacological Sciences
Volume16
Issue number2
StatePublished - 1 Feb 2012

Fingerprint

Hyperemia
Aspirin
Ischemia
Muscles
Placebos
Forearm
Area Under Curve
Blood Vessels
Placebo Effect
Vascular Endothelium
Arachidonic Acid
Prostaglandins
Healthy Volunteers
Eating
Lipids

Keywords

  • Aspirin
  • Forearm blood flow (FBF)
  • High density lipoprotein (HDL)
  • Prostaglandins
  • Reactive hyperemia (RH)

Cite this

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title = "Regulation of blood flow by aspirin following muscle ischemia",
abstract = "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 arachidonic acid-derived mediators such as the prostaglandins.",
keywords = "Aspirin, Forearm blood flow (FBF), High density lipoprotein (HDL), Prostaglandins, Reactive hyperemia (RH)",
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Regulation of blood flow by aspirin following muscle ischemia. / Cameron, S. J.; Goulopoulou, Styliani; Weil, B. R.; Kanaley, J. A.

In: European Review for Medical and Pharmacological Sciences, Vol. 16, No. 2, 01.02.2012, p. 143-150.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Regulation of blood flow by aspirin following muscle ischemia

AU - Cameron, S. J.

AU - Goulopoulou, Styliani

AU - Weil, B. R.

AU - Kanaley, J. A.

PY - 2012/2/1

Y1 - 2012/2/1

N2 - 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 arachidonic acid-derived mediators such as the prostaglandins.

AB - 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 arachidonic acid-derived mediators such as the prostaglandins.

KW - Aspirin

KW - Forearm blood flow (FBF)

KW - High density lipoprotein (HDL)

KW - Prostaglandins

KW - Reactive hyperemia (RH)

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M3 - Review article

C2 - 22428464

AN - SCOPUS:84859515943

VL - 16

SP - 143

EP - 150

JO - European Review for Medical and Pharmacological Sciences

JF - European Review for Medical and Pharmacological Sciences

SN - 1128-3602

IS - 2

ER -