Clinical implications of turbulence in the cardiovascular system: Its relation to cardiac murmurs, arterial bruits, and some characteristics of arterial pressure

2016 ◽  
Vol 1 (2) ◽  
pp. 197-213
Author(s):  
Paul D. Stein
Keyword(s):  
Arterial Pressure ◽  
Cardiovascular System ◽  
Clinical Implications

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Influence of central nervous system on arterial pressure during endotoxin shock

1983 ◽  
Vol 244 (2) ◽  
pp. H178-H185
Author(s):  
H. F. Janssen ◽  
L. O. Lutherer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Endotoxin Shock ◽  
Shock State ◽  
Induced Hypotension ◽  
Ventriculocisternal Perfusion

Some investigators have suggested that the hypotensive effects of endotoxin are exerted at the level of central nervous system (CNS). Others feel the effects are exerted peripherally and that the CNS is involved in the regulation of the cardiovascular system during the shock state. Still other data suggest that endotoxin shock is entirely a peripheral phenomenon. The present study used ventriculocisternal perfusion of endotoxin, a pretrigeminal brainstem transection, two midcollicular decerebrate preparations, and Cushing's reflex to investigate the involvement of the CNS during endotoxin shock. The results suggest the following: 1) endotoxin perfused centrally at a concentration equivalent to the maximum obtainable after peripheral injection will not alter mean arterial pressure (MAP); 2) either the forebrain is not involved in the MAP response or the remaining regions can compensate for its absence; and 3) Cushing's reflex will block the initial endotoxin-induced hypotension.

Vasodepressor responses elicited by diencephalic stimulation in dogs

1964 ◽  
Vol 207 (4) ◽  
pp. 915-920 ◽  
Author(s):  
Ralph J. Gorten ◽  
Orville A. Smith ◽  
Robert F. Rushmer
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
System Control ◽  
Experimental Conditions ◽  
Nervous Control ◽  
Anesthetized Dogs ◽  
Systemic Arteries ◽  
Central Nervous System Control

Tachycardia and peripheral vasoconstriction are the usual means by which the cardiovascular system, under nervous control, attempts to compensate for a lowering of pressure in the systemic arteries. When such compensatory efforts are absent during sudden, unexpected periods of hypotension, an alteration in central nervous system control should be suspected. The possibility of producing such alterations in the control of the circulation under experimental conditions was studied in five anesthetized dogs. Diencephalic areas were found in which electrical stimulation evoked a lowering of arterial pressure in the absence of tachycardia. Electrodes were chronically implanted in these areas so that stimulation could be performed in the unanesthetized state. The observed effects on the cardiovascular system were not always the same as those induced while the animals were anesthetized. The decrease in arterial pressure was usually less in extent. Occasionally an actual rise in pressure occurred, followed after the period of stimulation by a decrease in arterial pressure and heart rate.

scholarly journals SARS-CoV-2 receptor ACE2-dependent implications on the cardiovascular system: From basic science to clinical implications

2020 ◽  
Vol 144 ◽  
pp. 47-53 ◽  
Author(s):  
Sonja Groß ◽  
Christopher Jahn ◽  
Sarah Cushman ◽  
Christian Bär ◽  
Thomas Thum
Keyword(s):  
Cardiovascular System ◽  
Basic Science ◽  
Clinical Implications

What Goes Around Comes Around—Venous Return

2011 ◽  
pp. 48-54
Author(s):  
James R. Munis
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Venous Return ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Interconnected System ◽  
The Mean

By its nature, circulatory physiology is also susceptible to circular reasoning because every part of an interconnected system is affected by, and affects, every other part. If we're not careful, we end up saying things like ‘venous return equals cardiac output’ when, in the steady state, that is true by definition and nothing new is gained. If we grant that right atrial pressure (PRA) is the ‘downstream’ pressure for venous return, then it follows that PRA should be inversely related to venous return (and therefore, to cardiac output). If we simply apply Ohm's law to the cardiovascular system, we forget that the mean arterial pressure not only contributes to venous return but also is sustained by venous return. If venous return fails for any other reason (unrelated to arterial pressure), so too will mean arterial pressure eventually fail.

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