SYMPATHETIC NERVOUS SYSTEM-INDUCED CARDIAC DYSFUNCTION

 

Charles F. Pilati, Ph.D.

 

Associate Professor Emeritus
Department of Physiology and Pharmacology

 

Northeastern Ohio Universities
College of Medicine
4209 St. Rt. 44, P.O. Box 95
Rootstown, Ohio 44272-0095
Phone: (330) 325-6423
Fax: (330) 325-5912
E-mail: pc@neoucom.edu
Community of Science Expertise


 

Education:

1979-81Postdoctoral FellowCardiovascular Physiology
1979Ph.D.Biology/Physiology, Kent State University
1969B.S.Zoology, Kent State University

 

Professional Experience:

1991 - presentAssociate Professor of Physiology and Pharmacology Northeastern Ohio Universities College of Medicine
1986 - 1991Assistant Professor of PhysiologyNortheastern Ohio Universities College of Medicine
1981 - 1986Instructor in PhysiologyNortheastern Ohio Universities College of Medicine

Research Interests:

The sympathetic nervous system (SNS) plays a major role in maintaining cardiovascular homeostasis at rest as well as during physical activity. Although normal levels of SNS activity are essential, massive activation of the SNS can be detrimental to the heart. Seizures and various injuries to the brain are typical events that cause massive SNS activation. Under these conditions, large concentrations of sympathetic neurochemicals are released which can damage the heart and impair its pumping ability. In my laboratory, we are trying to find out why excessive concentrations of these neurochemicals cause cardiac depression and whether there are ways to protect the heart. This research is important because poor cardiac function would affect the outcome of patients with a variety of brain injuries that massively activate the SNS. Furthermore, this type of cardiac dysfunction has important implications regarding the success of transplanted hearts because these hearts are obtained from brain-dead donors, and massive SNS activation frequently occurs at the onset of brain death.

 


 

Selected Publications:

  • Pilati, C.F., R.S. Clark, F.J. Bosso, P. Holcomb, and M.B. Maron. Excessive sympathetic nervous system activity decreases myocardial contractility. Proc. Soc. Exp. Biol. Med. 193: 225-231, 1990.
  • Pilati, C.F., F.J. Bosso, and MB Maron. Factors involved in LV dysfunction after massive sympathetic activation. Amer. J. Physiol. 263 (Heart Circ. Physiol.): H784-H791, 1992.
  • Bosso, F.J., F.D. Allman, and C.F. Pilati. Myocardial workload is a major determinant of norepinephrine-induced LV dysfunction. Amer. J. Physiol. 266 (Heart Circ. Physiol.): H531-H539, 1994.
  • Lang, S.A., MB Maron, F.J. Bosso, and C.F. Pilati. Temporal changes in LV function after massive SNS activation. Can. J. Physiol. Pharmacol. 72: 693-700, 1994.
  • Pilati, C.F., MB Maron, and F.J. Bosso. Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation. J. Appl. Physiol. 78: 1642-1650, 1995.
  • Allman, FD, W. Herold, F. Bosso, and C.F. Pilati. Norepinephrine cardiomyopathy: time-dependent changes in left ventricular function and histopathology. Journal of Heart and Lung Transplantation 17: 991-997, 1998.
  • Bosso, F.J., Jarjoura, D.G., and C.F. Pilati. Role of angiotensin II in sympathetic nervous system induced left ventricular dysfunction. Can. J. Physiol. Pharmacol. 77: 806-812, 1999.
  • Smith, J.M. and C.F. Pilati. Effect of massive SNS activation on coronary vascular hemodynamics and myocardial energy pools. Exp. Biol. Med. 227:125-132, 2002.