Thursday 26 November 2026 1:00pm to 2:00pm
Heart and Lung Research Institute Cambridge Biomedical Campus, CB2 0BB
About
Beating Human Coronary Microvascular Dysfunction
The control of blood flow to the working heart is intricately controlled. The role of catecholamines in changing coronary microvascular diameter is poorly understood particularly in patients with microvascular dysfunction. In a healthy heart, the coronary resistance arteries develop myogenic, and the action of catecholamines in is to cause vasodilatation via β-adrenergic receptors. What is not known is whether this vasodilation also manifests as conducted vasodilation, which is addressed by the first aim of this study, including the underlying K+ channels responsible. The second aim was to establish how these responses are affected in patients with microvascular dysfunction. Patients without coronary artery disease undergoing elective valve surgery were consented and right atrial appendage biopsies taken. Resistance arteries (100-300 µm) were cannulated onto glass pipettes and pressurized to 80 mmHg. Confocal microscopy was used to record artery inner diameter and, for conduction experiments, a fluorescent dye mixed with each catecholamine was delivered from a micropipette positioned at the downstream end of each artery. Diameter was measured up to 1000 µm upstream from the site of direct agonist action. Vasodilatation to each catecholamine was sensitive to the β1-adrenergic antagonist atenolol; and responses to noradrenaline and adrenaline were augmented by the α1-adrenergic antagonist prazosin, in some cases from no vasodilation to full vasodilation. This profile was observed for both local and conducted vasodilation. The KATP channel blocker glibenclamide was effective in reducing conducted vasodilation. These data suggest that catecholamines not only cause vasodilation at the site of receptor activation but, due to opening K+ channels, can initiate conducted dilation that aides the drop in resistance to blood flow, aiding coronary blood flow. The extent of the α1-adrenergic constriction in resistance arteries would influence this coronary blood flow and proportionately contribute towards the ischaemia associated with microvascular dysfunction.
A light lunch will be provided from 12.30 pm
Please contact Anthony Davenport if you would like to arrange a meeting with the speaker
it would be great to see you in person, but if you need to attend attend remotely please contact Sarah Gibbings to receive a Teams link