1
40
3
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/0196-9781(90)90016-x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/0196-9781(90)90016-x</a>
Pages
955–961
Issue
5
Volume
11
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Influence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbits.
Publisher
An entity responsible for making the resource available
Peptides
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1990-10
Subject
The topic of the resource
Female; Male; Animals; Rabbits; Myocardial Contraction/drug effects; Hemodynamics/drug effects; Blood Pressure/*drug effects; Carotid Sinus/*innervation; Chemoreceptor Cells/*drug effects; Hindlimb/blood supply; Phrenic Nerve/drug effects; Pressoreceptors/*drug effects; Substance P/*pharmacology
Creator
An entity primarily responsible for making the resource
Qu L; Stuesse S L
Description
An account of the resource
Substance P (SP) is abundant in the carotid sinus nerve (CSN) and has been implicated in baro- and chemoreceptor reflexes. We examined the effect of SP on blood pressure, heart rate, phrenic nerve activity, hindlimb perfusion pressure, and cardiac contractile strength in urethane-anesthetized rabbits with bilaterally cut cervical sympathetic, vagus, and aortic depressor nerves. Retrograde simultaneous injection of SP (0.5-2.7 micrograms/kg in 0.2-0.3 ml saline) into both carotid sinus areas via the internal carotid arteries decreased blood pressure (by 56%), heart rate (by 13%), cardiac contractility (by 25%) and phrenic nerve activity (by 77%). The effect on hindlimb perfusion pressure was variable. There was both a reflex effect and direct hindlimb vasodilation. In another group of rabbits, the carotid sinus areas were vascularly isolated and perfused with SP (0.19 micrograms/min dissolved in Locke's solution) or Locke's solution alone for 5 min. While carotid sinus perfusion pressure was maintained in the range of 80-120 mmHg, mean arterial blood pressure, heart rate, and unit activity from the CSN were recorded. SP increased the activity of 11 of 18 baroreceptor fibers and inhibited all of 20 chemoreceptor fibers. SP decreased mean arterial blood pressure and heart rate, but the changes were less than those obtained with injection of SP into nonisolated carotid sinus arteries because systemic effects of SP, which in some cases counteracted the reflex effects, were eliminated.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0196-9781(90)90016-x" target="_blank" rel="noreferrer noopener">10.1016/0196-9781(90)90016-x</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1990
Animals
Blood Pressure/*drug effects
Carotid Sinus/*innervation
Chemoreceptor Cells/*drug effects
Female
Hemodynamics/drug effects
Hindlimb/blood supply
Male
Myocardial Contraction/drug effects
Peptides
Phrenic Nerve/drug effects
Pressoreceptors/*drug effects
Qu L
Rabbits
Stuesse S L
Substance P/*pharmacology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3181/00379727-193-43030" target="_blank" rel="noreferrer noopener">http://doi.org/10.3181/00379727-193-43030</a>
Pages
225–231
Issue
3
Volume
193
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Excessive sympathetic nervous system activity decreases myocardial contractility.
Publisher
An entity responsible for making the resource available
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1990-03
Subject
The topic of the resource
Female; Male; Animals; Rabbits; Epinephrine/blood; Norepinephrine/blood; Cisterna Magna; Hemodynamics/drug effects; Sympathetic Nervous System/drug effects/*physiology; Citrates/administration & dosage/pharmacology; Citric Acid; Extravascular Lung Water/drug effects; Heart Ventricles/drug effects/ultrastructure; Myocardial Contraction/*physiology; Ventricular Function; Veratrine/administration & dosage/pharmacology
Creator
An entity primarily responsible for making the resource
Pilati C F; Clark R S; Gilloteaux J; Bosso F J; Holcomb P; Maron M B
Description
An account of the resource
The objective of this study was to determine whether myocardial contractility is depressed by intense activation of the sympathetic nervous system. A massive sympathetic discharge was produced by injecting veratrine or sodium citrate into the cisterna magna of anesthetized rabbits (n = 10). Two and one-half hr later, the hearts were isolated and their left ventricular (LV) performance evaluated and compared with the LV performance of hearts isolated from control animals (n = 10). LV performance was evaluated from steady-state peak isovolumic systolic and end-diastolic pressures that were generated at various end-diastolic volumes (LV function curves). The relationship between peak LV systolic pressure (or the average peak developed LV wall stress) and LV end-diastolic volume was rotated downward (P less than 0.01) in the hearts removed from rabbits treated with veratrine or citrate. The LV end-diastolic pressure or LV end-diastolic wall stress of these hearts was not different from control at any end-diastolic volume. The diminished ability of the experimental hearts to develop systolic pressure or wall stress suggests that intense sympathetic activation depressed contractility. Severely damaged myofibers, located largely in the subendocardium, were found in these hearts. Furthermore, the depressed contractility was not related to pulmonary edema since only 2 of 10 rabbits developed edema.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3181/00379727-193-43030" target="_blank" rel="noreferrer noopener">10.3181/00379727-193-43030</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1990
Animals
Bosso F J
Cisterna Magna
Citrates/administration & dosage/pharmacology
Citric Acid
Clark R S
Epinephrine/blood
Extravascular Lung Water/drug effects
Female
Gilloteaux J
Heart Ventricles/drug effects/ultrastructure
Hemodynamics/drug effects
Holcomb P
Male
Maron M B
Myocardial Contraction/*physiology
Norepinephrine/blood
Pilati C F
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
Rabbits
Sympathetic Nervous System/drug effects/*physiology
Ventricular Function
Veratrine/administration & dosage/pharmacology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/jappl.1995.78.5.1642" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jappl.1995.78.5.1642</a>
Pages
1642–1650
Issue
5
Volume
78
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation.
Publisher
An entity responsible for making the resource available
Journal of applied physiology (Bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
1995
1995-05
Subject
The topic of the resource
Animals; Arginine/analogs & derivatives/pharmacology; Epinephrine/blood; Extravascular Lung Water/drug effects/metabolism; Hemodynamics/drug effects; In Vitro Techniques; Left/*physiopathology; Nitric Oxide/antagonists & inhibitors/biosynthesis/*physiology; Nitroarginine; Norepinephrine/blood; Pulmonary Circulation/drug effects; Pulmonary Edema/*physiopathology; Rabbits; Right/drug effects/physiology; Sympathetic Nervous System/drug effects/*physiology; Ventricular Dysfunction; Ventricular Function; Veratrine/pharmacology
Creator
An entity primarily responsible for making the resource
Pilati C F; Maron M B; Bosso F J
Description
An account of the resource
This study was undertaken to determine whether endothelium-derived relaxing factor (EDRF) modulates the pulmonary and systemic hemodynamic responses to massive sympathetic nervous system (SNS) activation and, in so doing, also modulates the degree of SNS-induced left ventricular (LV) dysfunction and the likelihood for pulmonary edema formation. The SNS of 13 anesthetized untreated rabbits and 14 anesthetized rabbits pretreated with the EDRF inhibitor, N omega-nitro-L-arginine (L-NNA, 20 mg/kg), was massively activated with an intracisternal injection of veratrine. Pulmonary and systemic arterial pressures increased to the same extent in both groups, but LV end-diastolic pressure was significantly lower in untreated rabbits. During this time, cardiac output decreased by 37% in L-NNA pretreated rabbits compared with 8% in untreated animals. Peak systemic and pulmonary vascular resistances increased significantly in L-NNA rabbits, whereas only systemic vascular resistance increased significantly in untreated rabbits. However, this increase in systemic vascular resistance was threefold less than that observed for L-NNA-treated animals. Although the degree of LV dysfunction was greater in the L-NNA rabbits, pulmonary edema developed less frequently in this group. We suggest that when EDRF release is inhibited during massive SNS activity, pulmonary vascular resistance increases markedly, which causes the right ventricle to fail. We further suggest that the reduced right ventricular output maintains pulmonary microvascular pressure below levels required for edema development.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.1995.78.5.1642" target="_blank" rel="noreferrer noopener">10.1152/jappl.1995.78.5.1642</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1995
Animals
Arginine/analogs & derivatives/pharmacology
Bosso F J
Epinephrine/blood
Extravascular Lung Water/drug effects/metabolism
Hemodynamics/drug effects
In Vitro Techniques
Journal of applied physiology (Bethesda, Md. : 1985)
Left/*physiopathology
Maron M B
Nitric Oxide/antagonists & inhibitors/biosynthesis/*physiology
Nitroarginine
Norepinephrine/blood
Pilati C F
Pulmonary Circulation/drug effects
Pulmonary Edema/*physiopathology
Rabbits
Right/drug effects/physiology
Sympathetic Nervous System/drug effects/*physiology
Ventricular Dysfunction
Ventricular Function
Veratrine/pharmacology