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

gfr2f@virginia.edu

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.

Recent Publications

de Klaver MJ, Weingart GS, Obrig TG, Rich GF
Local anesthetic-induced protection against lipopolysaccharide-induced injury in endothelial cells: the role of mitochondrial adenosine triphosphate-sensitive potassium channels.

Plachinta RV, de Klaver MJ, Hayes JK, Rich GF
The protective effect of protein kinase C and adenosine triphosphate-sensitive potassium channel agonists against inflammation in rat endothelium and vascular smooth muscle in vitro and in vivo.

Hayes JK, Havaleshko DM, Plachinta RV, Rich GF
Isoflurane pretreatment supports hemodynamics and leukocyte rolling velocities in rat mesentery during lipopolysaccharide-induced inflammation.

de Klaver MJ, Buckingham MG, Rich GF
Isoflurane pretreatment has immediate and delayed protective effects against cytokine-induced injury in endothelial and vascular smooth muscle cells.

de Klaver MJ, Buckingham MG, Rich GF
Lidocaine attenuates cytokine-induced cell injury in endothelial and vascular smooth muscle cells.

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