Key result
The bradykinin B2 receptor antagonist HOE-140 did not prevent the attenuation of vasodilatation by ischaemia-reperfusion injury (P=0.0002 with HOE-140 and P=0.04 with placebo).
Why the study?
Does intravenous HOE-140 (bradykinin B2 receptor antagonist) alter endothelium-dependent vasomotor dysfunction induced by ischaemia-reperfusion injury or the protection afforded by remote ischaemic preconditioning in healthy male volunteers?
Population
20 healthy male volunteers
Comparison
Intravenous infusion of the bradykinin B2… vs Saline placebo
Design
RCT, Randomised, double-blind
Authors
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B2 blockade confers no endothelial protection in IR injury; confirms bradykinin does not mediate this or RIPC effects in humans.
RCT (n=20)
Double-blind
cross-over
No
Does intravenous HOE-140 (bradykinin B2 receptor antagonist) alter endothelium-dependent vasomotor dysfunction induced by ischaemia-reperfusion injury or the protection afforded by remote ischaemic preconditioning in healthy male volunteers?
Endogenous bradykinin acting via the B2 receptor does not appear to mediate ischaemia-reperfusion injury or the protective effects of remote ischaemic preconditioning in humans.
Pedersen et al. (2011) conducted an RCT in Ischaemia-reperfusion injury (n=20). HOE-140 vs. saline placebo was evaluated on Bilateral forearm blood flow assessed using venous occlusion plethysmography during intra-arterial infusion of acetylcholine. The bradykinin B2 receptor antagonist HOE-140 did not prevent the attenuation of vasodilatation by ischaemia-reperfusion injury (P=0.0002 with HOE-140 and P=0.04 with placebo).
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