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Editorial
For over a century, the prevailing view has been that the smooth
muscle wall of large conduit arteries does not undergo rhythmic
contractile activity in synchrony with the cardiac cycle. This
behavior was described by Otto Frank and denoted the Windkessel
Hypothesis [1]. Considering the wide acceptance of the Windkessel
Hypothesis, potential targets for new therapeutic agents have not
considered rhythmic activation during the cardiac cycle.
In contrast to the Windkessel Hypothesis, evidence has
accumulated that the smooth muscle wall of large arteries
undergoesrhythmicactivationinsynchronywiththeheartbeat.This
rhythmic contractile activity has been denoted pulse synchronized
contractions (PSCs) [2-6]. PSCs have been demonstrated in dogs,
cats, rats, and, notably, humans [2-13]. Specifically, activity has been
seen in aorta, carotid, femoral, pulmonary, and brachial arteries [2-
13]. Much attention has been paid to confirming that PSCs are not
due to a movement artifact secondary to the pulse wave or cardiac
contractions [2,13]. PSCs are not abolished in bled animals, in
which there is no pulse wave, and when animals have a dissociation
between ventricular contractile activity and right atrial activity,
PSCs are coupled to atrial not ventricular rate [2].
The pacemaker for PSCs resides in the right atrium [2,13],
allowing speculation that this may allow coordination between
cardiac and vascular contractile activity. Generation of PSCs is
through a neurogenic not myogenic mechanism [2,12,13], although
the specific neural pathway has not been elucidated.
AlthoughdataincontradistinctiontotheWindkesselHypothesis
have been published for over 50 years [2-13] and these findings
have been demonstrated in several independent laboratories, PSCs
have not been accepted, and, therefore, a potential therapeutic site
for the treatment of certain cardiovascular diseases has not been
explored. PSCs may potentially serve a protective function limiting
vessel distension with the pulse wave as the upstroke of the PSC
appears to slightly precede the upstroke of the pulse wave. This
specific timing of the pulse wave and PSC may serve to limit vessel
distension, reducing the Laplacian forces acting on the vessel wall.
References
1.	 Frank O (1899) Die Grundform des Arteriellen Pulses. Zeitschrift fur
Biologie 37: 483-526.
2.	 Mangel A, Fahim M, Van Breemen (1982) Control of vascular contractility
by the cardiac pacemaker. Science 215(4540): 1627-1629.
3.	 Mangel AW (2014) Does the aortic smooth muscle wall undergo
rhythmic contractions during the cardiac cycle. Experimental & Clinical
Cardiology 20(11): 6844-6851.
4.	 Mangel AW (2017) A changing paradigm for understanding the behavior
of the cardiovascular system. J Clin Exp Cardiol 8: 496.
5.	 Mangel A, Lothman K (2017) Emergence of a new paradigm in
understanding the cardiovascular system: pulse synchronized
contractions. Cardiovasc Pharmacol Open access 6(5): 220.
6.	 Marion SB, Mangel AW (2014) From depolarization-dependent
contractions in gastrointestinal smooth muscle to aortic pulse
synchronized contractions. Clin Exp Gastroenterol 7: 61-66.
7.	 Ravi K, Fahim M (1987) Rhythmic contractile activity of the pulmonary
artery studied in vivo in cats. J Auton Nerv Syst 18(1): 33-37.
8.	 Heyman F (1955) Movements of the arterial wall connected with
auricular systole seen in cases of atrioventricular heart block. Acta Med
Scand 152(2): 91-96.
9.	 Heyman F (1957) Comparison of intra-arterially and extra-arterially
recorded pulse waves in man and dog. Acta Medica Scandinavica 157(6):
503-510.
10.	Heyman F (1959) Extra- and intra-arterial records of pulse waves and
locally introduced pressure waves. Acta Medica Scandinavica 163(6):
473-475.
11.	Heyman F (1961) Pulse synchronous movements of the arterial wall
peripheral to an obstruction in the circulation of the arm. Acta Medica
Scand 169: 87-93.
12.	Heyman F, Stenberg K (1962) The effect of stellate ganglion block on the
relationship between extra- and intra-arterially recorded brachial pulse
waves in man. Acta Medica Scandinavica 171(1): 9-11.
13.	Sahibzada N, Mangel AW, Tatge JE, Dretchen KL, Franz MR, et al. (2015)
Rhythmic aortic contractions induced by electrical stimulation in vivo in
the rat. PLoS One 10(7): e0130255.
Allen W Mangel*and Kate Lothman
RTI Health Solutions, Research Triangle Park, USA
*Corresponding author: Allen Mangel, RTI Health Solutions, PO Box 12194, Research Triangle Park, NC 27514, USA, Tel: 919-485-5668; Fax: 919-541-
1275; Email:
Submission: January 17, 2018; Published: January 29, 2018
Pulse Synchronized Contractions (PSCs):
A Call to Action!
Editorial Open J Cardiol Heart Dis
Copyright © All rights are reserved by Allen Mangel. 1(2). OJCHD.000508. 2018.
CRIMSONpublishers
http://www.crimsonpublishers.com
Keywords: Cardiovascular; Windkessel; PSCs
Volume 1 - Issue - 2
ISSN 2578-0204

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Pulse Synchronized Contractions (PSCs): A Call to Action!_Crimson Publishers

  • 1. 1/1 Editorial For over a century, the prevailing view has been that the smooth muscle wall of large conduit arteries does not undergo rhythmic contractile activity in synchrony with the cardiac cycle. This behavior was described by Otto Frank and denoted the Windkessel Hypothesis [1]. Considering the wide acceptance of the Windkessel Hypothesis, potential targets for new therapeutic agents have not considered rhythmic activation during the cardiac cycle. In contrast to the Windkessel Hypothesis, evidence has accumulated that the smooth muscle wall of large arteries undergoesrhythmicactivationinsynchronywiththeheartbeat.This rhythmic contractile activity has been denoted pulse synchronized contractions (PSCs) [2-6]. PSCs have been demonstrated in dogs, cats, rats, and, notably, humans [2-13]. Specifically, activity has been seen in aorta, carotid, femoral, pulmonary, and brachial arteries [2- 13]. Much attention has been paid to confirming that PSCs are not due to a movement artifact secondary to the pulse wave or cardiac contractions [2,13]. PSCs are not abolished in bled animals, in which there is no pulse wave, and when animals have a dissociation between ventricular contractile activity and right atrial activity, PSCs are coupled to atrial not ventricular rate [2]. The pacemaker for PSCs resides in the right atrium [2,13], allowing speculation that this may allow coordination between cardiac and vascular contractile activity. Generation of PSCs is through a neurogenic not myogenic mechanism [2,12,13], although the specific neural pathway has not been elucidated. AlthoughdataincontradistinctiontotheWindkesselHypothesis have been published for over 50 years [2-13] and these findings have been demonstrated in several independent laboratories, PSCs have not been accepted, and, therefore, a potential therapeutic site for the treatment of certain cardiovascular diseases has not been explored. PSCs may potentially serve a protective function limiting vessel distension with the pulse wave as the upstroke of the PSC appears to slightly precede the upstroke of the pulse wave. This specific timing of the pulse wave and PSC may serve to limit vessel distension, reducing the Laplacian forces acting on the vessel wall. References 1. Frank O (1899) Die Grundform des Arteriellen Pulses. Zeitschrift fur Biologie 37: 483-526. 2. Mangel A, Fahim M, Van Breemen (1982) Control of vascular contractility by the cardiac pacemaker. Science 215(4540): 1627-1629. 3. Mangel AW (2014) Does the aortic smooth muscle wall undergo rhythmic contractions during the cardiac cycle. Experimental & Clinical Cardiology 20(11): 6844-6851. 4. Mangel AW (2017) A changing paradigm for understanding the behavior of the cardiovascular system. J Clin Exp Cardiol 8: 496. 5. Mangel A, Lothman K (2017) Emergence of a new paradigm in understanding the cardiovascular system: pulse synchronized contractions. Cardiovasc Pharmacol Open access 6(5): 220. 6. Marion SB, Mangel AW (2014) From depolarization-dependent contractions in gastrointestinal smooth muscle to aortic pulse synchronized contractions. Clin Exp Gastroenterol 7: 61-66. 7. Ravi K, Fahim M (1987) Rhythmic contractile activity of the pulmonary artery studied in vivo in cats. J Auton Nerv Syst 18(1): 33-37. 8. Heyman F (1955) Movements of the arterial wall connected with auricular systole seen in cases of atrioventricular heart block. Acta Med Scand 152(2): 91-96. 9. Heyman F (1957) Comparison of intra-arterially and extra-arterially recorded pulse waves in man and dog. Acta Medica Scandinavica 157(6): 503-510. 10. Heyman F (1959) Extra- and intra-arterial records of pulse waves and locally introduced pressure waves. Acta Medica Scandinavica 163(6): 473-475. 11. Heyman F (1961) Pulse synchronous movements of the arterial wall peripheral to an obstruction in the circulation of the arm. Acta Medica Scand 169: 87-93. 12. Heyman F, Stenberg K (1962) The effect of stellate ganglion block on the relationship between extra- and intra-arterially recorded brachial pulse waves in man. Acta Medica Scandinavica 171(1): 9-11. 13. Sahibzada N, Mangel AW, Tatge JE, Dretchen KL, Franz MR, et al. (2015) Rhythmic aortic contractions induced by electrical stimulation in vivo in the rat. PLoS One 10(7): e0130255. Allen W Mangel*and Kate Lothman RTI Health Solutions, Research Triangle Park, USA *Corresponding author: Allen Mangel, RTI Health Solutions, PO Box 12194, Research Triangle Park, NC 27514, USA, Tel: 919-485-5668; Fax: 919-541- 1275; Email: Submission: January 17, 2018; Published: January 29, 2018 Pulse Synchronized Contractions (PSCs): A Call to Action! Editorial Open J Cardiol Heart Dis Copyright © All rights are reserved by Allen Mangel. 1(2). OJCHD.000508. 2018. CRIMSONpublishers http://www.crimsonpublishers.com Keywords: Cardiovascular; Windkessel; PSCs Volume 1 - Issue - 2 ISSN 2578-0204