Dr Richard Rainbow BSc PhD

Our research interests in the cardiovascular system extend from mechanistic investigations of ion channel modulation right up to modulation of whole tissue function. We use electrophysiological, imaging, myography and other phenotypic modelling to investigate protective or toxic alterations in cardiovascular tissue function. With our collaborators in Liverpool and in the Liverpool region through the LCCS and CDSS we are working in a number of exciting areas including exercise physiology, remote ischaemic conditioning, cardiotoxicity of chemotherapeutics and the effects of gender & sex hormones on cardiovascular function.

Cardioprotection is a broad term that can be applied to any stimuli that protects the heart from the damage caused by ischaemia, or that protects from arrhythmias. Despite nearly 40 years of research into cardioprotection, and despite the clear protective effects seen in cellular and preclinical animal models, to date, no successful cardioprotective intervention has made it into routine clinical practice. The mechanisms underlying cardioprotection are complex and involve modulation of intracellular signalling, however the phenotypic outcome in cardiac cells is always similar; a reduced accumulation of calcium during ischaemia, prolonged production of ATP by the mitochondria and a slight shortening of the action potential duration at the cellular level. We have demonstrated that artificially shortening the action potential by direct channel modulation can impart protection to the cell, causing reduced calcium loading and reduced ATP consumption. Our work in this area has focused on controlling intracellular calcium loading by manipulating channel activity using pharmacological modulators.

At the time of a heart attack, the amount of glucose in the blood is fundamentally important. If your blood glucose is too high then the damage to your heart can be more severe. Despite this appearing to be linked to diabetes, it has been shown that this can happen to anyone irrespective of a prior diagnosis of diabetes. Our data suggest that glucose plays a role in modulating contraction, intracellular Calcium signalling and ion channel function in the heart and blood vessels. In short, the blood vessels contract more strongly, so increasing blood pressure or making the tissue more prone to ischaemia, and the cardiac cells can develop potentially lethal arrhythmias. My group is working to try and understand the mechanisms underlying this “poisonous” effect of high glucose and what could be done to attenuate the glucose-induced damage.