Day 2 :
Dalhousie University, Canada
Keynote: ATP Metabolism in the Red Blood Cells as Potential Biomarker for Post Exercise Hypotension and Cardiovascular Protection
Time : 10:15-10:55
Pollen Yeung completed his Ph.D at the age of 30 years from University of Saskatchewan (Saskatoon, SK, Canada) and is currently Professor of Pharmacy and Medicine at Dalhousie University in Halifax, NS, Canada. He has published more than 90 peer reviewed articles in reputed journals and is currently serving as an editorial board member for Recent Review of Clinical Trials, Drug Metabolism Open Journal, Medical Sciences Monitor, Metabolites, Cardiovascular Pharmacology Open Access, and Natural Products Chemistry and Research Open Access.
The importance of adenosine and ATP in regulating many biological functions has long been recognized, especially for their effects on the cardiovascular homeostasis which may be used for management of hypertension and cardiovascular diseases. In response to ischemia, ATP is broken down to release adenosine. The activity of adenosine is very short lived because it is rapidly taken up by myocardial and endothelial cells, erythrocytes (RBC), and also rapidly metabolized to oxypurine metabolites and other adenine nucleotides. Extracellular and intracellular ATP is broken down rapidly to ADP and AMP and finally to adenosine by 5’-nucleotidase. These metabolic events are known to occur in the myocardium as well as in RBC. We investigate in this study the feasibility of exploiting ATP metabolism in the RBC as systemic biomarker for post exercise hypotension and cardiovascular protection. An experimental exercise rat model was used to probe the relationship between post exercise hypotension and ATP metabolism in the RBC. The cardiovascular protective effect of exercise preconditioning was further investigated in an acute myocardial infarction model using mortality and ATP metabolism in the RBC as endpoints. We have shown post-exercise hypotension correlated significantly with RBC concentrations of ATP, and that exercise pre-conditioning reduced cardiovascular mortality and breakdown of ATP in the RBC. The post exercise effect was greater in hypertensive than in normotensive rats. The presentation will also discuss the opportunities, challenges and obstacles of exploiting ATP metabolism as targets for drug development and personalized medicine. Suppored in part by CIHR, NSHRF and DPEF.
The Johns Hopkins University, USA
Time : 11:10-11:40
Robert S. Fitzgerald received his PhD from The University of Chicago. He did post-doctoral training at UCSF/CVRI in San Francisco and in France at Universite de Nancy and Universite de Paris. Returning to his faculty position at The Johns Hopkins Medical Institutions, he eventually became Associate Chair, then Acting Chair of the Dept. of Environmental Health Sciences in the Bloomberg School of Public Health with Joint Appts. in the Depts. of Physiology and of Medicine in the School of Medicine. His CV includes over 200 contributions to peer-reviewed publications.
Chronic Heart Failure (CHF) is among the several cardiopulmonary disorders that are responsible for 74.5% of deaths world wide according to the report from WHO in 2013. The malfunctioning carotid body (CB) is responsible for increasing output from the sympathetic nervous system (SNS). This increase affects breathing patterns, cardiac performance, kidney function. Experiments in animal models have uncovered ways in which the CB can return to normal. It is perhaps an opportune time to understand this interoreceptor, arguably the most important in the organism. Located bilaterally at the junction of the carotid arteries bifurcation into external and internal branches, this structure in humans is tiny…weighing 18 mg. Yet measured blood flow through the feline version exceeds 2 L/min/100gm tissue. CBs are the sole detector of decreases in PaO2; it also is stimulated by increases in PaCO2 and H+, and glucopenia. Stimulation produces reflex responses in the cardiopulmonary, endocrine, and renal systems. CHF reduces the production of nitric oxide (NO) in the CBs, allowing for a greater release of ACh and ATP which stimulates the increase in SNS output. Efforts to reduce CB output in both humans and animal models have uncovered three techniques which show promise. Reduction in CB neural output is the key factor to restore normal cardiac function and reduce hypertension.