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Pretreatment with intravenous ascorbic acid preserves endothelial function during acute hyperglycaemia (R1)
Brian A Mullan1, Ciaran N Ennis, Howard J P Fee
1Department of Anaesthesia and Intensive Care Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK. brian@mullan99.fsnet.co.uk
Clinical and Experimental Pharmacology & Physiology
|April 28, 2005
Summary
Intravenous ascorbic acid (vitamin C) prevents endothelial dysfunction caused by acute hyperglycemia. This finding suggests vitamin C may be a potential therapy for conditions involving high blood sugar.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Nutritional Science
Background:
- Acute hyperglycemia can impair endothelial function, affecting blood vessel dilation.
- Intra-arterial ascorbic acid has previously shown potential to improve vasodilation during hyperglycemia.
- The efficacy of intravenous ascorbic acid in preventing systemic endothelial dysfunction during hyperglycemia requires investigation.
Purpose of the Study:
- To investigate the effect of intravenous ascorbic acid on endothelial function during acute systemic hyperglycemia in healthy humans.
- To determine if ascorbic acid pretreatment can prevent hyperglycemia-induced endothelial dysfunction.
- To assess the relationship between plasma ascorbate levels and endothelial function index (EFI) during hyperglycemia.
Main Methods:
- A randomized, double-blind, placebo-controlled, cross-over study involving nine healthy male volunteers.
- Endothelial function assessed via forearm blood flow responses to endothelium-dependent and independent vasodilators, calculating the endothelial function index (EFI).
- Measurements taken at baseline and after a 2-hour systemic hyperglycemic clamp (14 mmol/L), with subjects receiving either placebo or 2g intravenous ascorbic acid prior to the clamp.
Main Results:
- Systemic hyperglycemia significantly reduced the EFI in the placebo group (1.08 to 0.74, P < 0.001).
- Ascorbic acid pretreatment prevented the decline in EFI during hyperglycemia (1.11 to 1.12, P = 0.938), a significant difference compared to placebo (P < 0.001).
- Decreased plasma ascorbate levels during hyperglycemia correlated directly with reduced EFI (r = 0.798, P < 0.001).
Conclusions:
- Intravenous ascorbic acid effectively prevents endothelial dysfunction induced by acute systemic hyperglycemia.
- Ascorbic acid demonstrates potential therapeutic value in clinical scenarios complicated by acute hyperglycemia.
- Maintaining adequate ascorbate levels may be crucial for preserving endothelial function during hyperglycemic states.