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Am J Physiol Heart Circ Physiol (April 15, 2004). doi:10.1152/ajpheart.00153.2003
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Submitted on February 19, 2003
Accepted on April 12, 2004

The protective effects of ascorbic acid on arterial haemodynamics during acute hyperglycaemia

Brian A. Mullan1*, Ciaran N. Ennis2, Howard JP Fee3, Ian S. Young4, and David R. McCance2

1 Department of Anaesthesia & Intensive Care Medicine, Queen's University, Belfast, United Kingdom; Regional Centre for Endocrinology & Diabetes, The Royal Victoria Hospital, Belfast, United Kingdom
2 Regional Centre for Endocrinology & Diabetes, The Royal Victoria Hospital, Belfast, United Kingdom
3 Department of Anaesthesia & Intensive Care Medicine, Queen's University, Belfast, United Kingdom
4 Department of Medicine, Queen's University, Belfast, United Kingdom

* To whom correspondence should be addressed. E-mail: brian{at}mullan99.fsnet.co.uk.

Mortality increases when acute coronary syndromes are complicated by stressinduced hyperglycaemia. Early pulse wave reflection can augment central aortic systolic blood pressure and increase left ventricular strain. Altered pulse wave reflection may contribute to the increase in cardiac risk during acute hyperglycaemia. Chronic ascorbic acid (AA) supplementation has recently been shown to reduce pulse wave reflection in diabetes. We investigated the in vivo effects of acute hyperglycaemia, with and without AA pre-treatment, on pulse wave reflection and arterial haemodynamics. Healthy male volunteers were studied. Peripheral blood pressure (BP) was measured at the brachial artery and the SphygmoCorTM Pulse Wave Analysis System was used to derive central BP, the aortic augmentation index (AIx; measure of systemic arterial stiffness) and the time to pulse wave refection (Tr; measure of aortic distensibility), from non-invasively obtained radial artery pulse pressure waveforms. Haemodynamics were recorded at baseline and then every 30 minutes during a 120 minute systemic hyperglycaemic clamp (14mmol.l-1). The subjects, studied on two separate occasions, were randomised in a double-blind, crossover manner to placebo, or 2g intravenous AA, prior to the initiation of hyperglycaemia. During hyperglycaemia AIx increased and Tr decreased. Hyperglycaemia did not change peripheral pulse pressure (PP), but did magnify central aortic PP and diminished the normal physiological amplification of PP from the aorta to the periphery. Pulse wave reflection, as assessed from peripheral pulse wave analysis, is enhanced during acute hyperglycaemia. Pre-treatment with AA prevented the hyperglycaemia-induced haemodynamic changes. By protecting haemodynamics during acute hyperglycaemia, AA may have therapeutic use.




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