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Inflammation-induced vasoconstrictor hyporeactivity is caused by oxidative stress
Johannes Pleiner1, Friedrich Mittermayer, Georg Schaller
1Department of Clinical Pharmacology, University of Vienna, Vienna, Austria.
Journal of the American College of Cardiology
|November 11, 2003
Summary
Oxidative stress contributes to vascular dysfunction during inflammation. Vitamin C administration corrected impaired vasoconstrictor responses, suggesting it as a potential therapeutic target for inflammation-induced vascular issues.
Area of Science:
- Cardiovascular Physiology
- Inflammation and Immunology
- Oxidative Stress Research
Background:
- Acute inflammation is characterized by reduced responsiveness to vasoconstrictors.
- Oxidative stress is a significant factor in inflammation and may underlie this impaired vascular response.
- Antioxidant interventions may potentially reverse inflammation-induced vascular dysfunction.
Purpose of the Study:
- To investigate the role of oxidative stress in inflammation-induced vascular dysfunction.
- To determine if antioxidant therapy can ameliorate impaired vascular responses during endotoxemia.
Main Methods:
- Healthy volunteers underwent randomized, double-blind, cross-over studies.
- Systemic inflammation was induced using low-dose Escherichia coli endotoxin (lipopolysaccharide [LPS]).
- Forearm blood flow (FBF) responses to vasoconstrictors (norepinephrine, angiotensin II, vasopressin) were measured before and after LPS, with or without vitamin C co-administration.
Main Results:
- LPS administration induced vasodilation, increased white blood cell count, fever, and decreased plasma vitamin C levels.
- Lipopolysaccharide significantly reduced FBF responses to norepinephrine (59%), angiotensin II (25%), and vasopressin (51%).
- Intra-arterial vitamin C completely restored vascular responsiveness to norepinephrine and angiotensin II.
Conclusions:
- Endotoxemia caused by E. coli reduces forearm blood flow responsiveness to vasoconstrictors.
- High-dose vitamin C effectively corrected this hyporeactivity, indicating its potential therapeutic value.
- These findings suggest that targeting oxidative stress is a promising strategy for managing inflammation-induced vascular dysfunction.