Circulatory effects of interruption and stimulation of cardiac vagal afferents.
TL;DR: The influence of the rhythmic activity in cardiac vagal afferents on the circulation was analyzed in chloralose-anesthetized cats by observing the cardiovascular responses to sudden interruption of this activity and to afferent stimulation of the cardiac nerves.
Abstract: The influence of the rhythmic activity in cardiac vagal afferents on the circulation was analyzed in chloralose-anesthetized cats by observing the cardiovascular responses to sudden interruption of this activity and to afferent stimulation of the cardiac nerves. The evoked responses were compared with those produced by “unloading” and stimulation of arterial baroreceptors. — Elimination of the impulse traffic in vagal afferents produced a blood pressure rise, a tachycardia and vasoconstrictions in skeletal muscle, intestine and kidney, indicating a tonic restraint of these afferents on the medullary vasomotor centre. The responses were generally moderate in the presence of normally functioning arterial baroreceptors but were pronounced after elimination of “buffering” influences from these receptors. — Comparisons of the inhibitory influences from vagal cardiac afferents and baroreceptor afferents, respectively, on the vasomotor centre indicated that the former were preferentially directed to neurons controlling the efferent discharge to the heart and the renal vessels. There was no evidence for a particularly strong engagement of the capacitance vessels in reflex patterns mediated through cardiac afferents. — Low frequency afferent stimulation of the cardiac nerves generally induced a profound brady-cardia, which was probably due to stimulation of fibres not normally tonically active.
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TL;DR: Environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias.
Abstract: Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.
288 citations
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TL;DR: The sections in this article are: Carotid Sinus Massage, Arterial Baroreceptor Control of Heart Rate, and Modification of Arteria Baroreflexes by Drugs.
Abstract: The sections in this article are:
1
Techniques
1.1
Carotid Sinus Massage
1.2
Electrical Stimulation of Carotid Sinus Nerves
1.3
Section or Anesthesia of Carotid Sinus Nerves and Vagi
1.4
Occlusion of Common Carotid Arteries
1.5
Neck Chamber
1.6
Vasoactive Drugs
1.7
Nonselective Techniques
2
Arterial Baroreceptor Control of Heart Rate
2.1
Autonomic Mediation
2.2
Other Properties
2.3
Relationship to Base-Line R-R Interval
2.4
Relationship to Respiratory Cycle
3
Arterial Baroreceptor Control of Atrioventricular Conduction and Ventricles
4
Carotid Baroreceptor Control of Blood Pressure
5
Carotid Baroreceptor Influence on Cardiac Output and Total Peripheral Resistance
6
Arterial Baroreceptor Control of Regional Circulations
7
Arterial Baroreceptor Control of Veins
8
Set Point of Carotid Baroreflex
9
Aortic Baroreflexes
10
Factors That Modify Arterial Baroreceptor Control of Circulation
10.1
Age
10.2
Exercise
10.3
Mental Stress
10.4
Sleep
10.5
Anesthesia
10.6
Central Blood Volume and Posture
11
Pathological States
11.1
Hypertension
11.2
Heart Disease
11.3
Carotid Sinus Syndrome
11.4
Other Pathological Conditions
12
Modification of Arterial Baroreflexes by Drugs
12.1
β-Adrenergic Antagonists
12.2
Cardiac Glycosides
12.3
Antihypertensive Drugs
283 citations
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TL;DR: The physiology of the Bezold–Jarisch reflex and its possible physiologic role in a number of clinical situations are focused on and discussion of the limited relevance of this reflex in regional anesthesia is provided.
Abstract: THE idea that reflexes originating in the heart can play a role in normal physiology dates to the 1860s. Until the 1950s, these reflexes, and the Bezold–Jarisch reflex (BJR) in particular, were regarded largely as pharmacological curiosities with the only practical application of the study of the BJR being the clinical use of a veratrum alkaloid as an antihypertensive agent. Since the 1860s, it had been known that injection of minute amounts (0.005 mg) of veratrine or its pure alkaloid components (veratrum) initiates a reflex which causes a rapid fall in blood pressure and heart rate in association with apnea. This “Von Bezold reflex” was classically defined in association with arrest of breathing, but more recently, it has been called the BJR and includes the triad of bradycardia, hypotension, and peripheral vasodilation. It is now understood that certain inhibitory reflexes, which have origin with cardiac sensory receptors, play a role in cardiovascular homeostasis. Activation of a subset of these receptors by diverse stimuli increases parasympathetic nervous system activity, inhibits sympathetic activity and is responsible for eliciting the BJR. Some anesthesiologists have suggested that the BJR may explain cardiovascular collapse reported during regional anesthesia techniques. This review focuses on the physiology of the BJR and its possible physiologic role in a number of clinical situations. It also provides discussion of the limited relevance of this reflex in regional anesthesia. The topic of clinical management will not be addressed given the paucity of data on this matter, but suggestions for future experimental direction are offered.
278 citations
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TL;DR: The sections in this article are: Intrinsic Properties of the Cardiovascular System: How They Permit the Rise in Cardiac Output, and Control of the Circulation During Exercise and Heat Stress: Competing Reflexes.
Abstract: The sections in this article are:
1
I. Intrinsic Properties of the Cardiovascular System: How They Permit the Rise in Cardiac Output
2
The Heart
2.1
Intrinsic Properties of the Heart
2.2
Pericardial Constraints
3
The Vascular System
3.1
Distribution of Resistance, Conductance, and Compliance
3.2
Dependency of CVP on Cardiac Output
3.3
Mechanical Effects on the Circulation—Auxiliary Pumps
3.4
Does Exercise Reduce Systemic Vascular Compliance?
3.5
Neural Control of the Vascular System during Exercise: How Important?
3.6
Balance between Mechanical and Neural Effects on Blood Flow and Blood Volume Distribution
4
II. Reflex Control of the Cardiovascular System During Dynamic Exercise: What Variables are Sensed and then Regulated by the Autonomic Nervous System During Dynamic Exercise?
4.1
Central Command
4.2
Reflexes from Active Muscles
5
Isometric Contractions: Testing Hypotheses
5.1
Isometric Contractions vs. Dynamic Exercise
5.2
Open-Loop vs. Closed-Loop Conditions
5.3
Does the Pressor Response to Voluntary Isometric Contraction have Chemoreflex or Mechanoreflex Origin?
6
Functional Importance of Muscle Chemoreflexes During Dynamic Exercise
6.1
Basic Concepts and Theory
6.2
Changes in MSNA as Evidence for Chemoreflex Activity in Dynamic Exercise
6.3
Does the Muscle Chemoreflex Initiate Increased SNA during Dynamic Exercise with Unimpaired Flow?
6.4
Does Activation of the Muscle Chemoreflex Correct Blood Flow Errors, and if so, How?
7
Baroreflex Regulation of Arterial Pressure (SAP) and Vascular Conductance in Dynamic Exercise
7.1
Does the Arterial Baroreflex Control SAP During Exercise?
7.2
Characterization and Analysis of Arterial Baroreflex Function
7.3
Baroreflex Sensitivity in Dynamic Exercise
7.4
Importance of Arterial Baroreflexes at the Onset of Exercise
7.5
Evidence Indicating “Resetting” of the Arterial Baroreflex
7.6
Central Command and Resetting of the Arterial Baroreflex—An Hypothesis
8
Role of Cardiopulmonary Baroreceptors in Dynamic Exercise
8.1
The Cardiopulmonary, or Low-Pressure, Baroreflex
8.2
Interaction between the Cardiopulmonary and Arterial Baroreflexes at Rest
8.3
Role of Cardiopulmonary Baroreflex during Dynamic Exercise
8.4
Interaction between Cardiopulmonary Baroreflex and Muscle Chemoreflex
8.5
Interaction between Cardiopulmonary and Arterial Baroreflexes in Exercise
8.6
Importance of Cardiopulmonary Baroreflexes during Dynamic Exercise
9
Control of the Circulation During Exercise and Heat Stress: Competing Reflexes
9.1
Cardiovascular Demands of Heat Stress
9.2
Overall Neural Control of the Cutaneous Circulation
9.3
Reflex Control of the Cutaneous Circulation during Exercise
9.4
Baroreflex v. Thermoregulatory Reflex Control of the Cutaneous Circulation during Exercise
10
How Does Physical Conditioning Alter Cardiovascular Function?
10.1
Range of Adjustment in Overall Cardiovascular Function
10.2
What Cardiovascular Adjustments Explain the Rise in ?
10.3
How does Maximal SV Increase with Physical Conditioning?
10.4
Does Physical Conditioning Change Autonomic Control of the Circulation?
11
Synthesis
11.1
What is the Autonomic Nervous System Controlling during Exercise?
11.2
What Errors Are Sensed and then Corrected by the Autonomic Nervous System during Exercise?
236 citations
References
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01 Dec 1962TL;DR: The cervical vagus consists of about 30 thousand fibres of which about 24 000 are sensory in function and about 3 thousand are myelinated and have been the centre of attraction in electrophysiological studies chiefly owing to the relative ease with which impulses can be recorded in them.
Abstract: The cervical vagus consists of about 30 thousand fibres of which about 24 000 are sensory in function (Agostoni, Chinnock, Daly and Murray 1957). Of the latter about 3 thousand are myelinated and have been the centre of attraction in electrophysiological studies chiefly owing to the relative ease with which impulses can be recorded in them. In the 19th International Physiological Congress, Whitteridge reviewed briefly all that was known about these myelinated afferent fibres which arose from endings of various kinds in the heart and lungs (Whitteridge 1953) and although more detailed information about certain myelinated sensory endings has been gained since that time, the main advance has been in the direction of recording impulse in non-medullated fibres from endings in the gastro-intestinal tract [Paintal 1953 (d), 4954 (a), (b); Iggo 1955, 1957 (b)]. Till Iggo’s clear demonstration (Iggo 1958) that the fibres concerned are mostly non-medullated, it was generally imagined that unitary discharges in non-medullated fibres could be recorded only with great difficulty owing to their small size. It was felt that if recording impulses in single fibres of small myelinated fibres presented certain difficulties, it would be still more difficult to record impulses in nonmedullated fibres. However, as pointed out by Iggo (1958), the situation is probably not comparable because non-medullated fibres occur in small bundles which can probably be dissected as such. Since there are many more non-medullated afferent fibres (21 000) than medullated ones (3 000) (Fig. 1), this therefore opens up a practically unexplored field for future work.
225 citations
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TL;DR: It will be shown that all such receptors encountered so far arose in the right and left atria of the heart; these will be referred to as type B atrial receptors.
Abstract: The satisfactory recording of impulses in afferent fibres from receptors in the great veins and atria has been accomplished by a number of investigators (Amann & Schaifer, 1943; Walsh, 1947; Whitteridge, 1948; Jarisch & Zotterman, 1948; Dickinson, 1950; Neil & Zotterman, 1950), and it has been shown that their frequency of discharge is related to the pressure in the great veins and atria (Whitteridge, 1948; Dickinson, 1950). The receptors so far described are known to arise from the atria and are characterized by the presence of an a volley of impulses in time with the a wave of the venous pressure curve. Hereafter these will be referred to as type A atrial receptors. The existence of another kind of cardiovascular fibre in the vagus was reported by Walsh & Whitteridge (1944) and confirmed by Whitteridge (1948). It was shown that this fibre differed in many ways from venous and depressor fibres and, for several reasons, it was believed that it arose from receptors in the small vessels of the lung. Later, Pearce & Whitteridge (1951) showed that a linear relationship existed between the activity of these 'pulmonary vascular' fibres and the pulmonary arterial pressure. The blocking temperature of these fibres was shown to be about 8 to 40 C (Torrance & Whitteridge, 1948) which corresponded well with their conduction velocity (Paintal, 1952). However, no experiments with the view to locating these pulmonary vascular receptors had been undertaken with the open chest so far. This was recently achieved, and in this paper the results of these experiments will be described. It will be shown that all such receptors encountered so far arose in the right and left atria of the heart; these will be referred to as type B atrial receptors. METHODS
200 citations