Our laboratory is interested in studying the basic cellular electrophysiologic mechanisms which determine cardiac excitation, conduction and refractoriness with a view to understanding the causes of cardiac arrhythmias and developing modalities to control them. Our experiments utilize in vitro animal models to study the mechanisms of cardiac arrhythmias. We derive information about the underlying membrane electrophysiologic characteristics which contribute to the abnormal conduction and automaticity at the basis of arrhythmias. Much of our past work has focused on a canine model of "healed" myocardial infarction which has proven to be a useful analog of the human condition. Our current investigations involve studying how antiarrhythmic agents cause arrhythmias (proarrhythmia). In this regard we are focusing on an animal model of drug induced long Q-T syndrome. We are also studying ways of salvaging ischemic myocardium at risk for infarction. Our goal is to generate new information which may be useful in designing new therapeutic modalities.
Key Words:
Cardiac Arrhythmias
Myocardial Ischemia
Myocardial Infarction
Myocardial preconditioning
Joseph F. Spear, Subbuswamy K. Prabu, Domenico Galati, Haider Raza Hindupur K. Anandatheerthavarada, and Narayan G. Avadhani Beta-1 adrenoreceptor activation contributes to ischemia/reperfusion damage as well as plays a role in ischemic preconditioning Am J Physiol, Heart and Circ Physiol 292: H2459-H2466, 2007.Ji-Kang Fang, Subbuswamy K. Prabu, Haider Raza, Naresh B Sepuri, Hindupur K. Anandatheerthavarada, Domonico Galati, Joseph Spear, and Narayan G. Avadhani Site specific phosphorylation of cytochrome c oxidase subunits I, IVi1 and Vb in rabbit hearts subjected to ischemia/reperfusion FEBS 581: 1302-1310, 2007.Subbuswamy K. Prabu, Hindupur K. Anandatheerthavarada, Haider Raza, Satish Srinivasan, Joseph F. Spear, and Narayan G. Avadhani Protein kinase A-mediated phosphorylation modulates cytochrome c oxidase function and augments hypoxia and myocardial ischemia-related injury J. Biol. Chem., 281: 2061–2070, 2006.Spear JF and Moore EN Preconditioning attenuates the shortening of recovery during coronary occlusion in isolated rabbit hearts with d-sotalol induced long-QT intervals J. Cardiovasc. Pharmacol. 39: 761-776, 2002.Spear JF and Moore EN Effect of acute global low-flow ischemia on triggered arrhythmias in d-sotalol induced long-QT intervals in perfused rabbit hearts J. Cardiovasc. Pharmacol. 37: 196-208, 2001.Spear JF and Moore EN Gender and seasonal related differences in myocardial recovery and susceptibility to sotalol induced arrhythmias in isolated rabbit hearts. J. Cardiovasc. Electrophys. 11: 880-887, 2000.
B.S. (Biology) Loyola College, Baltimore, 1965Ph.D. (Physiology) University of Pennsylvania, 1969
University of Pennsylvania
Department of Medicine
School of Medicine (1970 to 1971)
Pennsylvania Heart Association, Research Fellowship
University of Pennsylvania
Department of Medicine
School of Medicine (1971 to 1972)
U.S.P.H.S. Post Doctoral Traineeship in Cardiovascular Physiology