WVU Home
Search:DepartmentHealth Sciences CenterWVU  Go
West Virginia University, Robert C. Byrd Health Sciences Center A-Z WVU Site Index Campus Map WVU Directory Contact Us WVU Home School of Medicine
Department of Physiology and Pharmacology
Center for Interdisciplinary Research in Cardiovascular Sciences

Jefferson C. Frisbee

Assistant Professor of Physiology and Pharmacology

Email: jfrisbee@hsc.wvu.edu


Research Interests

Our research program is targeted at understanding alterations to microvascular structure and function during the development of the metabolic syndrome. While individual projects examine alterations to microvascular reactivity to physiological and pharmacological stimuli, additional efforts are directed at understanding modifications to microvascular structure (at both the individual vessel and whole network levels of resolution) which develop with the metabolic syndrome.

Description of Research

A developing characteristic of the metabolic syndrome, defined as the combined presentation of obesity, insulin resistance/type II diabetes mellitus, dyslipidemia and hypertension, is a progressive inability to match blood flow to working tissues with metabolic demand arising from those tissues, such that an evolving ischemic condition develops. While this syndrome presently afflicts more than 47 million Americans (American Heart Association), defining specific causes underlying this perfusion/demand mismatch has been challenging, as previous studies in human subjects have determined that alterations to vascular reactivity, a progressive structural narrowing of individual vessels, and a developing reduction in the density of microvessels within skeletal muscle can all occur during the metabolic syndrome in afflicted individuals. Each of these conditions has the potential to elevate vascular resistance and compromise the ability of skeletal muscle to resist fatigue through impairments in the processes of mass transport and exchange.

Our research program is targeted at understanding alterations to microvascular structure and function during the development of the metabolic syndrome. While individual projects examine alterations to microvascular reactivity to physiological and pharmacological stimuli, additional efforts are directed at understanding modifications to microvascular structure (at both the individual vessel and whole network levels of resolution) which develop with the metabolic syndrome. However, the underlying purpose of these projects is the integrative understanding of how alterations to both structure and function of the microcirculation combine to impact perfusion to the individual organ or tissue in question in animals afflicted with the full metabolic syndrome or with individual components of it.

While the predominant research thrust of the laboratory employs the Zucker rat model of the metabolic syndrome (one brought on by hyperphagia), other avenues of investigation are employing models of the constituent elements of the metabolic syndrome (i.e., hypertension, insulin resistance, dyslipidemia). Further, while much of our previous investigation has focused on alterations to microvascular structure/function and perfusion within the skeletal muscle circulation, evolving projects focus on cerebrovascular behavior during the metabolic syndrome and on the regulation of pulmonary microvascular structure and function as well.

Seleted Publications

J.C. Frisbee, K.G. Maier, J.R. Falck, R.J. Roman and J.H. Lombard. Hypoxic dilation of skeletal muscle resistance arterioles: an integration of signaling mechanisms. Am. J. Physiol. Reg. Integ. Comp. Physiol. 283:R309-319, 2002.

J.C. Frisbee, K.G. Maier and D.W. Stepp. Elevated oxidant stress contributes to enhanced myogenic activation of skeletal muscle microvessels of obese Zucker rats Am. J. Physiol. Heart Circ. Physiol. 283:H2160-H2168, 2002

J.C. Frisbee. Remodeling of the skeletal muscle microcirculation increases resistance to perfusion in obese Zucker rats. Am. J. Physiol. Heart Circ. Physiol. 285:H104-H111, 2003

J.C. Frisbee. Impaired perfusion of skeletal muscle of obese Zucker rats. Am. J. Physiol. Reg. Integ. Comp. Physiol. 285:R1124-R1134, 2003.

J.C. Frisbee. Enhanced arteriolar a-adrenergic sensitivity impairs dilator responses and skeletal muscle perfusion in obese Zucker rats. J. Appl. Physiol. 97:764-772, 2004

S.A. Phillips, F.A. Sylvester and J.C. Frisbee. Oxidant stress and constrictor reactivity impair cerebral artery dilation in obese Zucker rats. Am. J. Physiol. Reg. Integ. Comp. Physiol. 288:R522-R530, 2005.