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:
| 1979-81 | Postdoctoral Fellow | Cardiovascular Physiology | | 1979 | Ph.D. | Biology/Physiology, Kent State University | | 1969 | B.S. | Zoology, Kent State University |
Professional Experience:
| 1991 - present | Associate Professor of Physiology and Pharmacology | Northeastern Ohio Universities College of Medicine | | 1986 - 1991 | Assistant Professor of Physiology | Northeastern Ohio Universities College of Medicine | | 1981 - 1986 | Instructor in Physiology | Northeastern 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.
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