| Michael F. Callahan, Ph.D.
Assistant Professor
Department of Orthopaedic Surgery
Wake Forest University Health Sciences |
Address: | Department of Orthopaedic Surgery
Wake Forest University Health Sciences
Medical Center Boulevard
Winston-Salem, North Carolina 27157-1070 | |
Research Office: (336) 716-8901
Facsimile: (336) 716-7310
E-Mail:callahan@wfubmc.edu
Undergraduate School:
University of Southern Mississippi (B.A. Psychology), Hattiesburg, Mississippi
University of Alabama (Master’s Psychology), Birmingham, Alabama
Doctoral School:
University of Health Sciences, The Chicago Medical School (Ph.D. Pharmacology), North Chicago, Illinois
Professional Interests:
My primary research focus employs a multidisciplinary approach to neuroendocrine and metabolic control of cardiovascular and fluid/electrolyte homeostasis during conditions of hyper‑ and hypo-osmotic and hemorrhagic challenges. This research primarily focuses on the role of vasopressin and oxytocin peptidergic systems in four directions which impact on the control of arterial blood pressure: sympathetic nervous system activation, salt intake, stress responsiveness, and body fluid balance.
Work in collaboration with Dr. Thomas Smith, Department of Orthopedic Surgery, is progressing in the development of chronic hemodynamic (arterial pressure, cardiac output, and renal blood flow) measurements in unanesthetized mice. Our work in the area of chronic arterial pressure regulation centers on the angiotensin AT1a knockout mouse. In conjunction with Transonic Systems Inc., we have developed the ability to perform long term hemodynamic monitoring (direct cardiac output via ascending aorta flowmetry, renal and femoral blood flow) in mice. We have recently demonstrated the ability to determine cardiac output via small bolus saline ultrasound dilution of blood flowing through an arteriovenous shunt, i.e. Ultrasound dilution. We are beginning testing to determine whether this technique can be used on flow signals derived from peripheral organs (i.e. renal or femoral blood flow) in mice. I have recently organized surgical training workshops to train investigators how to implant blood flow and telemetry physiological devices in rats and mice. This workshop also included sessions of ventricular pressure volume relationships in anesthetized mice.
We are also exploring the hemodynamic microvascular effects of a new class of antidiabetic compounds, i.e. insulin sensitizing compounds which activate the peroxisome proliferator activator receptor-g (PPAR-g agonists). These compounds not only lower insulin levels in typeII diabetics but lower plasma lipids and arterial pressure. Our work has demonstrated that these agents decrease systematic vascular resistance in part by a vasodilation of skeletal muscle beds. Current studies are directed toward examining the macro- and microvascular actions of these agents and PPAR-α agonists in mice that are lacking the receptors in selected tissues. We are performing long term continuous monitoring of cardiac output, renal blood flow and arterial pressure in these mice.
Publications:
For a listing of recent publications, refer to PubMed, a service provided by the National Library of Medicine