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Related Experiment Videos

Inflammation-induced endothelial dysfunction involves reduced nitric oxide bioavailability and increased oxidant

Brian R Clapp1, Aroon D Hingorani, Rajesh K Kharbanda

  • 1BHF Laboratories, Centre for Clinical Pharmacology, Department of Medicine, University College London, Rayne Institute, 5 University Street, London WC1E 6JJ, United Kingdom. b.clapp@ucl.ac.uk

Cardiovascular Research
|September 15, 2004
PubMed
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Inflammation causes endothelial dysfunction by reducing nitric oxide (NO) bioavailability and increasing oxidative stress. This dysfunction is partially reversible with antioxidants, suggesting a role for reactive oxygen species.

Area of Science:

  • Cardiovascular Research
  • Inflammation and Immunology
  • Endothelial Biology

Background:

  • Endothelial dysfunction is a key factor in cardiovascular disease.
  • Inflammation is known to impair endothelial function.
  • Mechanisms underlying inflammation-induced endothelial dysfunction require further investigation.

Purpose of the Study:

  • To investigate the mechanisms of inflammation-induced endothelial dysfunction in humans.
  • To assess the impact of a controlled inflammatory response on endothelial nitric oxide (NO) bioavailability.
  • To explore the potential of antioxidant and substrate supplementation in mitigating inflammation-induced endothelial dysfunction.

Main Methods:

  • Forearm venous plethysmography was used to measure endothelial function in healthy volunteers post-typhoid vaccination.

Related Experiment Videos

  • Endothelial NO bioavailability was assessed using N(G)-monomethyl-l-arginine (l-NMMA) and bradykinin.
  • Effects of l-arginine and ascorbic acid supplementation were evaluated.
  • Systemic inflammatory markers, anti-oxidant status, and urinary protein excretion were monitored.

    • Main Results:

    • Typhoid vaccination induced a systemic inflammatory response, decreased total anti-oxidant status, and increased urinary albumin excretion.
    • Endothelial function, assessed by responses to bradykinin and l-NMMA, was significantly reduced post-vaccination.
    • Ascorbic acid partially restored the blood flow response to bradykinin, while l-arginine had no significant effect.
    • Responses to glyceryl trinitrate and norepinephrine remained unaffected.

    Conclusions:

    • Acute inflammation leads to widespread endothelial dysfunction and reduced vascular nitric oxide (NO) bioavailability in humans.
    • Increased oxidative stress appears to play a significant role in inflammation-induced endothelial dysfunction.
    • Local antioxidant treatment offers partial reversal, highlighting the therapeutic potential of targeting reactive oxygen species.