Cardiac Sympathetics Research Articles

Participation of cardiac and peripheral sympathetics in carotid occlusion response

ARTICLESParticipation of cardiac and peripheral sympathetics in carotid occlusion responseHH Wang, CY Chai, JS Kuo, and SC WangHH Wang, CY Chai, JS Kuo, and SC WangPublished Online:01 Jun 1970https://doi.org/10.1152/ajplegacy.1970.218.6.1548MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPhysiological Sympathetic Activation Reduces Systemic Inflammation: Role of Baroreflex and Chemoreflex28 April 2021 | Frontiers in Immunology, Vol. 12Angiotensin-(1-7) improves cognitive function in rats with chronic cerebral hypoperfusionBrain Research, Vol. 1573A Population Model of Integrative Cardiovascular Physiology13 September 2013 | PLoS ONE, Vol. 8, No. 9Baroreceptor and chemoreceptor contributions to the hypertensive response to bilateral carotid occlusion in conscious miceR. M. Lataro, J. A. Castania, M. W. Chapleau, H. C. Salgado, and R. Fazan1 December 2010 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 299, No. 6Permanent, bilateral common carotid artery occlusion in the rat: A model for chronic cerebral hypoperfusion-related neurodegenerative diseasesBrain Research Reviews, Vol. 54, No. 1Pressure response to carotid occlusion in diabetic rats: effect of insulin therapyDiabetes Research and Clinical Practice, Vol. 68, No. 1Neurohumoral Mechanisms Involved in the Hypertensive Response Elicited by Bilateral Carotid Occlusion in Conscious Intact or Chronically Sympathectomized Rats13 October 2004 | Clinical and Experimental Hypertension, Vol. 26, No. 6Arterial Baroreceptors and Experimental Diabetes25 January 2006 | Annals of the New York Academy of Sciences, Vol. 940, No. 1Dynamic effects of carotid sinus baroreflex on ventriculoarterial coupling studied in anesthetized dogs.Circulation Research, Vol. 70, No. 5Neurohormonal control of gastrointestinal blood flow1 January 2011Pressure-flow relationships of the canine iliac periphery and systemic hemodynamics: Effects of sodiumnitroprusside and adenosinePfl�gers Archiv European Journal of Physiology, Vol. 407, No. 4Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Comparative effects of unilateral and bilateral carotid artery ligation in the spontaneously hypertensive rat.Stroke, Vol. 11, No. 1Carotid artery ligation-induced cerebral ischemia in old, male, Sprague-DawleyratsAGE, Vol. 2, No. 2Pharmacological effects of two new β-adrenoceptor blocking drugs: Kö 1366 and Kö 1313European Journal of Pharmacology, Vol. 17, No. 3 More from this issue > Volume 218Issue 6June 1970Pages 1548-1554 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.6.1548PubMed5446281History Published online 1 June 1970 Published in print 1 June 1970 Metrics

Reflex control of heart rate in the unanesthetized dog.

Reflex control of heart rate in the unanesthetized dog.

Participation of cardiac sympathetics in carotid occlusion pressor reflex.

Participation of cardiac sympathetics in carotid occlusion pressor reflex.

Vagal and sympathetic components of conditioned cardioacceleration in the pigeon

The present experiments were undertaken to assess the relative contributions of the vagi and cardiac sympathetics to conditioned heart rate changes in the pigeon. The cardiac response was established using a defensive conditioning paradigm in which light was paired with foot-shock. Birds with bilateral cervical vagotomy, beta-blockade (propranolol), or both were studied in this situation and their conditioning performances compared with those of control animals. Conditioned cardioacceleration in vagotomized birds was significantly below that of control animals, although substantial conditioning still occurred. However, following beta-blockade conditioned rate responses were markedly reduced, almost no conditioned cardioacceleration appearing until late in training. Bilateral vagotomy prolonged the latency of the response, while a short latency heart rate change could still occur following beta-blockade. Functional denervation with combined vagotomy and beta-blockade prevented the conditioned response completely. Successful differentiation performance was obtained in birds with either vagotomy or beta-blockade, but vagotomized animals required longer training to establish such differential responding. These results suggest the following conclusions: (a) Conditioned cardiocceleration is mediated entirely by the extrinsic cardiac nerves. (b) The principal contribution to the magnitude of the response is mediated by the cardiac sympathetic nerves. (c) The shortest latency component of the response in mediated by the vagi. (d) Either nerve supply is capable of mediating differentiation, but it is more difficult to establish with only excitatory innervation of the heart.

Propranolol in hypertension

Propranolol has been found to be an effective and potentially useful hypotensive drug, though, of course, only extensive and widespread clinical use can discover unexpected disadvantages. Its mode of action is different from potent drugs in common use. Its hypotensive action may arise from blockade of the cardiac sympathetics. The full hypotensive effect is not usually seen for several weeks after the commencement of propranolol therapy, and an explanation of this has been offered. Maximal therapeutic benefit is therefore frequently delayed.

Reflex control of the heart in complete A-V block: With special reference to the experimental creation of Adams-Stokes disease

The cardiac sympathetics and parasympathetics were directly and reflexly activated in dogs having complete heart block. Activation of the vagus produced a very slight decrease in ventricular rate and in blood pressure. The vagus had no direct effect upon the ventricles. It was concluded that vagal fibers may supply the bundle of His and its branches but not the ventricular muscle. Contrasted to the almost negligible effects of the vagus was the striking positive inotropic and chronotropic effects of stimulation of the cardiac sympathetics. Activation of the carotid sinus (carotid hypertension) reflexly induced a ventricular negative inotropic and chronotropic effect. This effect was mediated by reflex inhibition of the cardiac sympathetics, and the vagus played no role. It was concluded that the ventricle in complete A-V block is primarily under the control of the sympathetics. Ventricular asystole was produced in dogs with complete heart block by activation of the carotid sinus and by cessation of ventricular pacemaking. Similar mechanisms nay be active in the production of Adams-Stokes attacks in man.

Myocardial extraction and production of catechol amines.

Stimulation of the cardiac sympathetic efferent nerves is accompanied by a release of catechol amines in coronary blood. This release is a function of stimulation intensity and occurs even when stroke volume and coronary outflow are maintained constant. Comparison between the ethylenediamine and the trihydroxyindole methods for the analysis of plasma catechol amines shows both quantitative and qualitative differences, with only the results with the latter method showing a consistent relationship to the hemodynamic changes observed during cardiac sympathetic stimulation. The acutely synipatheetomized heart extracts catechol amines from coronary blood in the absence of nervous stimulation. The patterns of extraction observed indicate that the quantity of catechol amines in the myocardium can modify the extent of extraction in the unstimulated state as well as the extent of release during stimulation. Continued stimulation of the cardiac sympathetics is accompanied by at least a partial depletion of the myoeardial catechol amine stores. These stores appear to be repleted by circulating catechol amines, since the response to any given intensity of stimulation can be potentiated by a prior norepinephrine infusion. Dichloroisoproterenol prevents neither the myocardial extraction of catechol amines in the unstimulated state nor the release of catechol amines during sympathetic stimulation; it does lessen or abolish the cardiody-namic effects of sympathetic stimulation. Data are presented which indicate that a direct coronary vasoconstriction is one of the consequences of cardiac sympathetic nerve stimulation, the vasodilatation usually observed being due, at least in part, to overriding metabolic factors.

A cardiac sympathetic pathway not blocked by tetraethylammonium.

ArticleA CARDIAC SYMPATHETIC PATHWAY NOT BLOCKED BY TETRAETHYLAMMONIUMEfrain G. Pardo, Barbara R. Rennick, and Gordon K. MoeEfrain G. PardoFrom the Department of Pharmacology, University of Michigan, Barbara R. RennickFrom the Department of Pharmacology, University of Michigan, and Gordon K. MoeFrom the Department of Pharmacology, University of MichiganPublished Online:01 May 1950https://doi.org/10.1152/ajplegacy.1950.161.2.245MoreSectionsPDF (691 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 161Issue 2May 1950Pages 245-249 Copyright & PermissionsCopyright © 1950 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1950.161.2.245PubMed15425641History Received 19 September 1949 Published online 1 May 1950 Published in print 1 May 1950 Metrics

Enhancement of Epinephrine Induced Cardiac Arrhythmias by Tetraethylammonium Chloride (Etamon).

In the experiments to be reported herein tetraethylammonium chloride has been shown to intensify the cardiac arrhythmias occurring in dogs during cyclopropane anesthesia. Secondly, experiments on unanesthetized animals suggest that the choice of a pressor agent for use as an antidote after tetraethylammonium chloride may be critical. After tetraethylammonium injection epinephrine resulted in ventricular tachycardia whereas phenylephrine (Neo-Synephrine) caused no arrhythmias. Cardiac arrhythmias occurring during cyclopropane anesthesia have been demonstrated experimentally to depend upon reflex sensitization of the heart to epinephrine. Cyclopropane stimulates receptors located in the abdominal viscera, producing afferent impulses which pass to the cord by way of fibers travelling with the splanchnics. The reflex center is located in the brain, presumably in the hypothalamus. Efferent impulses pass to the heart by way of cardiac sympathetics. Since interruption of this pathway at any point has prevented the arrhythmias, the tetraethylammonium ion should theoretically block the reflex sensitization. This agent has been reported to interrupt sympathetic impulses by ganglionic blockade and consequently was expected to block the efferent impulses. When it was found that tetraethylammonium potentiated the cardiac effects of epinephrine under cyclopropane, the cardiac effects of the ion and epinephrine were also investigated in unanesthetized animals. Epinephrine has been recommended as an antidote for the profound hypotension which may follow the clinical administration of tetraethylammonium. Cyclopropane-epinephrine Ventricular tachycardia was produced in the dog by the method described by Meek et al. The only modification of this technic was reduction of the standard test dose of epinephrine in order to lower the mortality from ventricular fibrillation. After the control duration of ventricular tachycardia had been determined, tetraethylammonium chloride was administered intravenously over a period of 60 seconds in doses of 5 to 20 mg/kg.