Effect of Tea on Endothelial Function and Ischaemia-reperfusion Injury
Tea consumption may impact upon the decrease in endothelial function after IR-injury. However, no previous study directly examined the potential of tea to impact upon the change in endothelial function after IR-injury.
The investigators hypothesize that tea consumption counteracts endothelial damage in response to ischaemia reperfusion injury in healthy humans.
Ischaemia Reperfusion Injury
|Study Design:||Observational Model: Case-Crossover
Time Perspective: Cross-Sectional
|Official Title:||Effect of Black Tea Consumption on Endothelial Function and Ischaemia-reperfusion Injury in Humans|
- Change in Endothelial Function after ischaemia reperfusion injury [ Time Frame: three weeks ]Change in endothelial function (measured with flow mediated dilation) after ischaemia reperfusion injury (induced by 20 minutes ischemia and 20 min reperfusion) with and without precedence of tea consumption
- Change in baseline flow mediated dilation after water/tea consumption [ Time Frame: three weeks ]Change in baseline flow mediated dilation after water/tea consumption
|Study Start Date:||August 2011|
|Study Completion Date:||February 2012|
|Primary Completion Date:||February 2012 (Final data collection date for primary outcome measure)|
Black tea ingestion
Rationale: Occlusion of an artery (causing ischemia) is a frequently reported condition, e.g. myocardial infarction, cerebral infarction or during organ transplantations. The period of ischemia will be followed by reperfusion (possibly after an operation). The ischaemic period as well as the reperfusion are both associated with damage to the tissue, including the endothelium. It is hypothesised that production of oxidative stress and reduced NO bioactivity (through increased reactive oxygen production) during ischaemia and reperfusion is involved in the development of tissue damage to the endothelium. Interventions that can prevent or attenuate endothelial dysfunction in response to ischemia-reperfusion (IR)-injury have a potential clinical relevance to prevent (complications of) cardiovascular disease.
Several studies have examined the effect of tea consumption on the endothelial function. These studies demonstrated a dose-dependent improvement of tea to improve endothelial function in healthy and diseased humans, possibly through the vasoactive effects of flavonoids, which may involve increased nitric oxide bioactivity and inhibition of NADPH oxidase. Based on the ability of flavonoids to decrease (the impact of) oxidative stress, tea consumption may also impact upon the decrease in endothelial function after IR-injury. However, no previous study directly examined the potential of tea to impact upon the change in endothelial function after IR-injury.
Objective: To examine whether tea consumption counteracts endothelial damage in response to ischaemia reperfusion injury in healthy humans.
Main study parameters: Change in endothelial function (measured with flow mediated dilation) after ischaemia reperfusion injury (induced by 20 minutes ischemia and 20 min reperfusion) with and without precedence of tea consumption.
Nature and extent of the burden and risks associated with participation, benefit and group relatedness: Non-invasive cuff occlusion is used to examine endothelial function (5-minute ischaemia) and produce the stimulus that induces ischaemia-reperfusion injury (20-minute ischaemia). This repeated cuff inflation is non-invasive and not associated with a health risk for the subject. Tea consumption is safe and, most likely, daily routine for most participants. The only difference is that this study will monitor and instruct participants regarding their tea consumption in the week preceding the tests. The volunteers will not benefit directly from participating in this study.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01660516
|Radboud University Nijmegen Medical Centre|
|Nijmegen, Gelderland, Netherlands, 6525 EX|
|Principal Investigator:||Dick Thijssen, Dr.||Radboud University Medical Centre Nijmegen|
|Principal Investigator:||Maria Hopman, Prof. Dr.||Radboud University|