scholarly journals Age-related changes in cardiac electrophysiology and calcium handling in response to sympathetic nerve stimulation

2018 ◽  
Vol 596 (17) ◽  
pp. 3977-3991 ◽  
Author(s):  
Samantha D. Francis Stuart ◽  
Lianguo Wang ◽  
William R. Woodard ◽  
G. Andre Ng ◽  
Beth A. Habecker ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Cardiac Electrophysiology ◽  
Calcium Handling ◽  
Sympathetic Nerve Stimulation ◽  
Age Related ◽  
Age Related Changes

Elevated sympathetic response of epicardium proximal to healed myocardial infarction

1983 ◽  
Vol 245 (4) ◽  
pp. H646-H652 ◽  
Author(s):  
M. S. Gaide ◽  
R. J. Myerburg ◽  
P. L. Kozlovskis ◽  
A. L. Bassett
Keyword(s):  
Myocardial Infarction ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Cardiac Electrophysiology ◽  
Coronary Artery Ligation ◽  
Sympathetic Nerve Stimulation ◽  
Artery Ligation ◽  
Refractory Periods ◽  
Marked Disparity ◽  
Normal Area

Sympathetic nerve interaction with cardiac electrophysiology was evaluated in healed myocardial infarction by monitoring the effects of sympathetic nerve stimulation on local epicardial refractoriness in cats. Single-stage distal coronary artery ligation was used to induce myocardial infarction. Regions overlying and surrounding infarcts 3 mo after healing and comparable regions in sham-operated and normal unoperated hearts were studied. Local ventricular muscle refractory periods were measured by the extrastimulus technique from 1) the epicardium overlying the infarct, 2) the area bordering the infarct, and 3) a normal area proximal to the infarct on the anterior free wall of the left ventricle. Bilateral stimulation of the ansa subclavia induced significant and disparate refractory period shortening (P less than or equal to 0.01) in hearts with healed myocardial infarction. Shortening was greatest in the normal area [-26 +/- 8 (+/-SD) ms], less in the border area (-15 +/- 6), and least in the infarct area (-7 +/- 2). In contrast, refractory periods measured in noninfarcted hearts shortened significantly (P less than or equal to 0.01) but uniformly and to a lesser extent during sympathetic stimulation. We conclude 1) the effects of sympathetic nerve stimulation are more pronounced in the areas proximal to healed infarction than in similar areas of noninfarcted hearts and 2) a marked disparity in sympathetic responsiveness occurs in hearts with healed myocardial infarction.

Interactive Effects of Verapamil and Sympathetic Nerve Stimulation on the Sinus and AV Nodes in the Canine Hearts.

1992 ◽  
Vol 33 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Katsusuke YANO ◽  
Masanobu HIRATA ◽  
Takao MITSUOKA ◽  
Yoriaki MATSUMOTO ◽  
Tetsuya HIRATA ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Interactive Effects ◽  
Sympathetic Nerve Stimulation

scholarly journals Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Srinivas Tapa ◽  
Lianguo Wang ◽  
Samantha D. Francis Stuart ◽  
Zhen Wang ◽  
Yanyan Jiang ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Cardiac Electrophysiology ◽  
Neural Control ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Post Surgery ◽  
Dopamine Beta Hydroxylase ◽  
Perfused Hearts ◽  
Insight Into

Abstract Myocardial infarction (MI) can result in sympathetic nerve loss in the infarct region. However, the contribution of hypo-innervation to electrophysiological remodeling, independent from MI-induced ischemia and fibrosis, has not been comprehensively investigated. We present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing a targeted-toxin (dopamine beta-hydroxylase antibody conjugated to saporin, DBH-Sap), and measure resulting electrophysiological and Ca2+ handling dynamics. Five days post-surgery, sympathetic nerve density was reduced in the anterior left ventricular epicardium of DBH-Sap hearts compared to control. In Langendorff-perfused hearts, there were no differences in mean action potential duration (APD80) between groups; however, isoproterenol (ISO) significantly shortened APD80 in DBH-Sap but not control hearts, resulting in a significant increase in APD80 dispersion in the DBH-Sap group. ISO also produced spontaneous diastolic Ca2+ elevation in DBH-Sap but not control hearts. In innervated hearts, sympathetic nerve stimulation (SNS) increased heart rate to a lesser degree in DBH-Sap hearts compared to control. Additionally, SNS produced APD80 prolongation in the apex of control but not DBH-Sap hearts. These results suggest that hypo-innervated hearts have regional super-sensitivity to circulating adrenergic stimulation (ISO), while having blunted responses to SNS, providing important insight into the mechanisms of arrhythmogenesis following sympathetic nerve loss.

What do antagonists tell us about α-adrenoceptors?

1985 ◽  
Vol 68 (s10) ◽  
pp. 15s-19s ◽  
Author(s):  
G. M. Drew
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Isolated Heart ◽  
Coupling Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Stimulus Response ◽  
Adrenoceptor Agonist ◽  
Tissue Responses ◽  
Cat Spleen ◽  
Relative Potencies

The early proposals that pre- and post-junctional α-adrenoceptors might be different stemmed largely from two separate observations. Firstly, the orders of potency of a series of agonists at inhibiting the response to sympathetic nerve stimulation and in increasing inotropic activity in the rabbit isolated heart were different [1, 2]. Secondly, phenoxybenzamine was more potent in inhibiting vasoconstrictor responses to sympathetic nerve stimulation than in increasing transmitter overflow from the cat spleen [3]. These experiments illustrate the most fundamental, pharmacological ways of distinguishing between receptors: namely, by comparing the relative potencies of agonists and/or antagonists in producing, or preventing, pharmacological effects. There are, however, difficulties in using agonists to classify receptors because their ability to generate a response depends not only upon their intrinsic properties of affinity for, and efficacy at, the receptors but also upon the capacity of the tissue to translate the stimulus into a response. Thus agonists with a relatively low intrinsic efficacy may produce a small response, or no response at all, in a tissue in which the efficiency of the stimulus-response coupling mechanism is low. The importance of this phenomenon in influencing tissue responses to agonists with low efficacy has been demonstrated for the α-adrenoceptor agonist prenalterol [4] and for the α-adrenoceptor agonist oxymetazoline [5].

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