Amadou K.S. Camara, PhD
Associate Professor of Anesthesiology
Medical College of Wisconsin
8701 Watertown Plank Road
Milwaukee, WI 53226-0509
Dr. Camara received his PhD in Cardiovascular Physiology from the Medical College of Wisconsin in 1995. His dissertation work was to elucidate the role of the central renin-angiotensin system in the regulation of arterial pressure and the modulating effects of chronic dietary salt intake on the etiology of renal neurogenic hypertension. After receiving his PhD, Dr. Camara joined the laboratory of Dr. Zeljko Bosnjak in the Department of Anesthesiology as a postdoctoral fellow. Under the auspices of Drs. Bosnjak and Wai-Meng Kwok, Dr. Camara studied cardiac electrophysiology; specifically how volatile anesthetics modulate isolated cardiac myocyte L- and T- type calcium channel currents and the potential implications of these findings in understanding anesthetic protection against ischemia and reperfusion injury. In 1999, Dr. Camara, now a department faculty member, joined Dr. David F Stowe’s research team to study the role of mitochondria in ischemia and reperfusion and cardiac preservation in the isolated Langendorff heart.
Mitochondria are increasingly recognized as the lynch pin in the determination of cell survival and death. Mitochondrial dysfunction has been implicated in the etiology of ischemic heart disease. Understanding the role of mitochondria in ischemia and reperfusion injury and in organ preservation for transplant has gained enormous attention lately, with huge clinical implications.
Dr. Camara’s recent research interests focus on the role of mitochondria (respiration, inner membrane potential, redox potential, reactive oxygen species) in cardiac preservation during hypothermic and normothermic ischemia and reperfusion in isolated cardiac cells (myocytes and endothelial cells) and isolated guinea pig hearts. One aspect of this research is the demonstration that hypothermic preservation also leads to deleterious production of reactive oxygen and nitrogen species (ROS and RNS) that could lead to the compromise of organ storage and reduce their clinical utility. Understanding the source and mechanism of ROS/RNS generation could lead to the development of a more effective preservation solution for organ storage. Other research interests include regulation of mitochondrial ion flux (hydrogen, potassium and calcium fluxes), mitochondrial pH, membrane potential and mitochondrial ROS, and the effects of derangement in these processes in the potential sequelae of activation of cellular injury.
To contact Dr. Camara, please call 414-955-5624 or e-mail email@example.com.