Neurocardiovascular Physiology Group
Our group aims to understand how the brain communicates with vital organs, like the heart and kidneys, during illness. By employing cutting-edge genetic engineering techniques, we explore ways to modify these interactions to improve patients’ outcomes. We focus on conditions such as heart failure, systemic infection, and inflammation.
About our research
- Autonomic neuroscience
- Cardiovascular disease
- Sepsis and inflammation
- Chronic sympathetic nerve activity recording
- Selective vagal nerve fibre stimulation
Current research projects include:
Selective vagal nerve stimulation using optogenetics
Vagal nerve stimulation (VNS) has enormous therapeutic potential as evidenced by ~200 current clinical trials assessing its therapeutic potential across multiple diseases (Clinicaltrials.gov). However, it is plagued by disabling side effects, such as cough and neck pain, and substantial variability in efficacy between subjects and within subjects over time. This is due to multiple factors, including that the: (i) vagus nerve is not homogeneous, containing both motor and sensory nerve axons, (ii) the anatomy of the vagus nerve is not consistent between people such that electrode placement affects which axons are stimulated and (iii) understanding of which axon groups need to be stimulated for effective therapy in different conditions remains poor. There is an urgent need for a greater understanding of the organisation of the components of the vagus nerve to increase efficacy. We are addressing these issues using cutting-edge optogenetic methods to specifically target efferent vagal fibres (the hardest fibre type to target electrically) in diseases, such as heart failure.
Neuroinflammation in cardiopulmonary bypass
Approximately 2 million cardiac surgical procedures requiring cardiopulmonary bypass (CPB) are performed annually worldwide1 and a major unresolved clinical complications arising from CPB is postoperative delirium.2, 3 It occurs in ~50% of patients and these patients have a >30% risk of developing long-term cognitive decline with dementia after 7.5 years.2 There is emerging evidence that one of the critical drivers of delirium after CPB is neuroinflammation.3 In close collaboration with the Translational Cardiovascular and Renal Research Group, we are determining how CPB drives neuroinflammation and investigating novel treatments targeting neuroinflammation.
1. Hu J et al. J Cardiothorac Vasc Anesth. 2016;30:82-9.
2. Greaves D et al. International journal of cardiology. 2019;289:43-49.
3. Jufar AH et al. Acta physiologica (Oxford, England). 2022;236:e13860.
Research and technical staff
- Baagavi Saseethran
- Sally Malone
- Anton Trask-Marino
- Rachel Peris
- Victoria Stock
- Booth, L.C., de Silva, R.A.U., Pontes, R.B., Yao, S.T., Hood, S.G., Lankadeva, Y.R., Kosaka, J., Eikelis, N., Lambert, G.W., Schlaich, M.P. and May, C.N. (2021). Renal, Cardiac, and Autonomic Effects of Catheter-Based Renal Denervation in Ovine Heart Failure. Hypertension, 78(3), pp.706–715. doi:https://doi.org/10.1161/hypertensionaha.120.16054.
- Booth, L.C., Yao, S., Korsak, A., Farmer, D.M., Hood, S.G., McCormick, D.J., Boesley, Q., Connelly, A., McDougall, S.J., Korim, W.S., Guild, S.-J., Mastitskaya, S., Le, P., Teschemacher, A.G., Sergey Kasparov, Ackland, G.L., Malpas, S.C., McAllen, R.M., Allen, A.E. and May, C.N. (2021). Selective optogenetic stimulation of efferent fibers in the vagus nerve of a large mammal. Brain Stimulation, 14(1), pp.88–96. doi:https://doi.org/10.1016/j.brs.2020.11.010.
- McArdle, Z., Pontes, R.B., Yao, S.T., Lankadeva, Y.R., Singh, R.R., Hood, S.G., Schlaich, M.P., May, C.N. and Booth, L.C. (2019). Blunted diuretic and natriuretic responses to acute sodium loading early after catheter-based renal denervation in normotensive sheep. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 317(2), pp.R319–R327. doi:https://doi.org/10.1152/ajpregu.00228.2018.