George F. Rich George F. Rich

Professor and Chair of Anesthesiology
Professor of Biomedical Engineering

B.S., Mechanical Engineering, University of Utah, 1979
Ph.D., Bioengineering, University of Utah, 1985
M.D., University of Utah, 1985


Research Interests

Our research involves the role of endogenous nitric oxide/guanylate cyclase and other endothelial pathways in the control of vascular resistance. We are also interested in the effect of inhaled nitric oxide on pulmonary vascular resistance and its use in the treatment of pulmonary hypertension. Experiments are designed to model human diseases and to be clinically relevant. We perform acute and longterm experiments of induced pulmonary hypertension, utilizing a chronic hypoxia rat model. Other experiments include evaluation of inflammatory responses and the effects of inhibiting inducible endothelial enzymes, which may be partially responsible for sepsis-induced hypotension. Isolated lung and kidney models are used to study functional changes in vascular tone, associated with alterations of various endogenous endothelial pathways. We also evaluate protein and enzyme levels using western blots, light microscopy, and radioimmunoassays.

Selected Publications

D. U. Frank, S. M. Lowson, C. M. Roos, and G. F. Rich. Endotoxin alters hypoxic pulmonary vasoconstriction in isolated rat lungs. Journal of Applied Physiology, 81:1316-1322, 1996.

D. U. Frank, D. J. Horstman, G. N. Morris, R. A. Johns, and G. F. Rich. Regulation of the endogenous NO pathway by prolonged inhaled NO in rats. Journal of Applied Physiology, 85:1070-1078, 1998.

L. G. Fischer, D. J. Horstman, K. Hahnenkamp, N. E. Kechner, and G. F. Rich. Selective iNOS inhibition attenuates acetylcholine- and bradykinin-induced vasoconstriction in lipopolysaccharide-exposed rat lungs. Anesthesiology, 91:724-732, 1999.

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