Andreas Deussen

Coronary flow and metabolism

Previous and current research

The coronary vessels provide supply of oxygen, nutrients and circulating humoral factors to the myocardium. A failure of coronary vessel function is without any doubt killer number 1 in the industrial nations. Impairment of coronary vessel function is largely aggravated in association with common diseases, e.g. diabetes, obesitas and high blood pressure. Under such circumstances an unspecific inflammatory response of the coronary vessel wall is observed.

Focus of our research is the comprehensive understanding of coronary vessel function under physiological and pathophysiological conditions.

To maintain a continuous blood flow (cardiac output) to the various organs of the body cardiac muscle depends on continuous aerobic energy generation. If coronary blood flow is interrupted, this is followed by myocardial failure (pump failure) within seconds. Thus, coronary flow regulation must always keep pace with the rise of myocardial oxygen demand, as it may occur under conditions of physical exercise. A specific feature of heart muscle is that heart muscle contraction generates the force for its own blood perfusion. This contraction counteracts myocardial perfusion.

In addition to a dense adrenergic innervation and the presence of a well developed autoregulation metabolic and endothelial factors play an important role for the adjustment of coronary blood flow.

 
    Fig. Isolated perfused mouse heart

Future prospects and goals

We are specifically interested in the functional role and metabolism of adenosine, a degradation product of the adenine nucleotides, and of nitrogen monoxide (NO) and oxygen radicals (O2-, OH.).

As experimental models we use isolated perfused organs (heart, vessels) and isolated cells (endothelial cells, smooth muscle cells, cardiomyocytes). In addition to classical pharmacological blocking experiments we employ knock out and overexpression models of mice. For analytical purposes we make use of highly sensitive analytical techniques.

A detailed analysis of metabolic processes in tissues is compromised by the complex arrangement of the various cellular and subcellular steps involved. In addition, coronary flow provides substrate and product supply and washout. The evaluation of experimental data by intuition only has therefore led to erroneous conclusions. Therefore, we add mass balanced mathematical model analysis to the planning and evaluation of experimental studies.

About

1982-1990: Research Assistant and Research Associate at the Department of Physiology, University of Duesseldorf 1991-1992: Visiting Assistant Professor at the Center for Bioengineering, University of Washington, Seattle, USA  1992-1996: Heisenberg-Fellow and guest scientist at the Department of Physiology, University of Duesseldorf and the Center for Bioengineering, University of Washington, Seattle, USA since 1996: Full Professor and chairman of the Department for Physiology of the Medical Faculty Carl Gustav Carus, TU Dresden since 2005: present Dean of Research

Selected publications   

B.M. Lewis, A. Pexa, K. Francis, V. Verma, A.M. McNicol, M. Scanlon, A. Deussen, W.H. Evans, D.A. Rees, J. Ham (2006): Adenosine stimulates connexin 43 expression and gap junctional communication in pituitary folliculostellate cells. FASEB J, published online

O. Frobert, G. Haink, U. Simonsen, C.H. Gravholt, M. Levin, A. Deussen (2006): Adenosine concentration in the coronary artery wall and A2A-receptor involvement in hypoxia-induced vasodilation. J Physiol.; 570: 375-384.

A. Pexa, A. Deussen (2005): Modulation of ecto-5´-nucleotidase by phospholipids in human umbilical vein endothelial cells (HUVEC). Naunyn-Schmiedeberg´s Arch. Pharmacol. 372: 131-138

A. Heintz, Th. Koch, A. Deussen (2005): Intact nitric oxide production is obligatory for the sustained flow response during hypercapnic acidosis in guinea pig heart. Cardiovasc. Res. 66: 55-63

T. Lauer, M. Preik, T. Rassaf, B.E. Strauer, A. Deussen, M. Feelisch, M. Kelm (2001): Plasma nitrite rather than nitrate reflects regional endothelial nitric oxide synthase activity but lacks intrinsic vasodilator activity. Proc. Natl. Acad. Sci. 98: 12814-12819

Home page