Richard E. Klabunde, Ph.D.

Associate Professor
Ph.D., University of Arizona
Cardiovascular Physiology

Office: 304 Irvine Hall
Phone: 740-593-9468
Fax: 740-593-2778
Email: klabunde@ohio.edu

Other URLs:

Richard Klabunde's Homepage


Research Summary:

     The long-term goal of my research is to determine the mechanisms causing cardiovascular dysfunction in septic shock so that new therapeutic approaches for treatment can be developed. Bacterial infections can cause a systemic inflammatory response that depresses cardiac function and systemic vascular tone, leading to hypotension, organ failure, and death. Septic shock is the leading cause of death in hospital intensive care units. Presently, I am determining the role of platelet activating factor, nitric oxide and reactive oxygen species in microvascular dysfunction (arteriolar function and microvascular permeability) and cardiac depression during septic shock. Microcirculatory studies use the hamster cheek pouch microcirculation and intravital video microscopy coupled with digital image analysis. Cardiac studies utilize the isolated, Langendorff-perfused rat heart preparation that enables detailed assessment of ventricular and coronary function in vitro.

     Another area of recent research focus has been on the role of reactive oxygen species in vascular dysfunction associated with acute hyperglycemia. These studies are utilizing both microcirculatory preparations and the isolated, perfused rat heart model.

Selected References:

  • Klabunde, RE and DE Anderson. Role of nitric oxide and reactive oxygen species in PAF-induced microvascular leakage. FASEB J 15:A47, 2001.

  • Klabunde, RE and DE Anderson. Obligatory role of nitric oxide in PAF-induced leakage in the hamster cheek pouch microcirculation. Eur J Pharmacol 404:387-394, 2000.

  • McHugh, NA, A Solowiej, RE Klabunde and GF Merrill. Acute coronary vascular and myocardial perfusion effects of conjugated equine estrogen in the anesthetized dog. Basic Res Cardiol 93:470-476, 1998.

  • Klabunde, RE and LJ Mulligan. The ferret as a model for myocardial infarct size reduction by a selectin inhibitor. Lab Animal Sci 48:529-532, 1998

  • Klabunde, RE, J Tse and HR Weiss. Guanylyl cyclase inhibition reduces contractility and decreases cGMP and cAMP in isolated rat hearts. Cardiovasc Res 37:676-683, 1998.

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