Integration of afferent information on ganglion nodosum neurons

Mikhailova, S. D.; Bebyakova, N. A.; Semushkina, T. M.

doi:10.1007/bf00841222

Cited by 3 publications

(6 citation statements)

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“…1). Moreover, shifts in the hemodynamic parameters in these animals were less pronounced than in the control (occlusion without BE injection), in whom arterial pressure dropped as follows: systolic and diastolic arterial pressures by 24% and 27%, respectively, mean diastolic pressure by 24% and pulse pressure by 17%, and heart rate decreased by 21% [8]. The latter agrees with the relationship between the arterial pressure reduction during the early stages of myocardial ischemia and the occurrence of VF [3].…”

Section: Resultsmentioning

confidence: 75%

“…Arrhythmias were recorded during a 15-min occlusion and subsequent 15-min reperfusion periods. We showed Russian State Medical University, Moscow that under these conditions idioventricular arrhythmia developes in 72% of cases, ventricular tachycardia (VT) in 28% of cases, and ventricular fibrillation (VF) in 55% of cases [8].13-Endorphin, a nonselective agonist of opiate receptors (Laboratory of Peptide Synthesis, Cardiology Research Center, Russian Academy of Medical Sciences) was injected intravenously (50 gg/kg, bolus) 5 min before occlusion of the coronary artery [6,13]. In some experiments, vagus nerves were cut on the neck, or the lower cardiac nerve and caudal loop were cut near the stellate ganglion.…”

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confidence: 99%

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The role of heart vegetative nerves in antiarrhythmic effect of β-endorphin in experimental myocardial ischemia

et al. 1997

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Acute experiments on narcotized cats showed that premedication with 13-endorphin promotes the development of ventricular tachycardia and decreases the occurrence of ventricular fibrillation caused by myocardial ischemia. The antifibrillatory effect of 13-endorphin is related to central nervous structures regulating the function of the cardiovascular system and is mediated through the vagus nerves. Key Words: ~-endorphin; myocardial ischemia; cardiac arrhythmias; vagus nerves; stellate gangliaClinical studies revealed that reduced blood concentration of [3-endorphin (BE) in patients with myocardial infarction is characteristic of grave disorders accompanied by marked circulatory insufficiency and cardiac arrhythmias [1]. Moreover, experiments on animals showed that BE injected prior to infarction considerably restricts necrotic zone, preserves myocardial contractility in zones with normal circulation, and reduces mortality [6]. Taking into consideration these data and the important role of changed activity of the bulbar cardiovascular center and sympathetic influences in the development of ischemic cardiac arrhythmias, we decided to estimate the interrelationship between the protective effect of BE and functioning of different cardiac nerves. MATERIALS AND METHODSExperiments were carried out on 39 cats of both sexes weighing 2-4 kg narcotized with Nembutal (40 mg/kg, intraperitoneally). Myocardial ischemia was modeled by occluding the circumflex branch of the left coronary artery near the main vessel. Arrhythmias were recorded during a 15-min occlusion and subsequent 15-min reperfusion periods. We showed Russian State Medical University, Moscow that under these conditions idioventricular arrhythmia developes in 72% of cases, ventricular tachycardia (VT) in 28% of cases, and ventricular fibrillation (VF) in 55% of cases [8].13-Endorphin, a nonselective agonist of opiate receptors (Laboratory of Peptide Synthesis, Cardiology Research Center, Russian Academy of Medical Sciences) was injected intravenously (50 gg/kg, bolus) 5 min before occlusion of the coronary artery [6,13]. In some experiments, vagus nerves were cut on the neck, or the lower cardiac nerve and caudal loop were cut near the stellate ganglion. ECG and blood pressure in the femoral artery were recorded with a Biokomb-8 polyphysiograph (Orion/EMG). Statistical significance of differences was evaluated using the Student's t and )~2 tests. RESULTSIn 10 experiments, the effects of preliminary BE injection on the development of arrhythmias induced by occlusion of coronary artery were studied. Neither BE, nor subsequent occlusion of the coronary artery (during a 30-sec period) produced considerable shifts of hemodynamic parameters. Myocardial ischemia in these animals was accompanied by cardiac rhythm disturbances (Fig. 1). The occurrence of VT was

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Section: Resultsmentioning

confidence: 75%

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confidence: 99%

The role of heart vegetative nerves in antiarrhythmic effect of β-endorphin in experimental myocardial ischemia

et al. 1997

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“…This indicates that antiarrhythmic effects of BE are determined by afferent impulses conducted into the central nervous system along myelinated VN fibers. The information which is conducted to the bulbar cardiovascular center from cardiovascular and integrative neurons of the nodose ganglion plays an important role in the genesis of ischemic arrhythmia [3,6,8]. Therefore, in the third series of experiments we studied the influence of BE on the impulse activity of neurons belonging to these groups.…”

Section: Resultsmentioning

confidence: 99%

“…The development of arrhythmia was observed during 15-min arterial occlusion and 15-min Russian State Medical University, Moscow reperfusion. Under these conditions idioventricular rhythm, ventricular tachycardia, and ventricular fibrillation were observed in 72%, 28%, and 55% of animals, respectively [7]. Electrocardiogram and blood pressure in the femoral artery were recorded with a BIOKOMB-8 polyphysiograph (ORLON/ EMG).…”

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Effects of β-endorphin on cardiac afferent systems

et al. 1998

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Studies performed on cats have shown that the antifibdUatory effect of 13-endorphin under acute myocardial ischemia is mediated by afferent pathways of the vagus nerves and sympathetic components of arrhythmogenesis. This effect is associated with the ability of 13-endorphin to change the impulse activity of cardiovascular and integrative neurons of the nodose ganglion. Key Words: ~-endorphin, vagus nerves, nodose ganglion, myocardial ischemia, cardiac adrenergic reactivityClinical and experimental data point to a relationship between the severity of ischemic heart disease and the decrease in the plasma level of 13-endorphin (BE). A moderate increase in the BE content is generally associated with good prognosis in patients with myocardial ischemia [1,2,5]. Our previous studies revealed a protective effect of BE in respect of the development of isehemic ventricular fibrillation. Bilateral vagotomy abolished this effect [9]. Vagotomy interrupts the conduction of impulses over afferent and efferent pathways of the vagus nerves CON). Therefore, it is unclear what a pathway mediates the antifibrillatory effects of BE. Cardiac afferent systems play an important role in the pathogenesis of ischemic ventricular fibrillation. This work was designed to determine the role of vagal afferents in the antiarrhythmic effect of BE. MATERIALS AND METHODSExperiments (n=82) were performed on male and female eats weighing 2-4 kg narcotized with Nembutal (40 mg/kg intraperitoneally). Myocardial ischemia was induced by ligation of the left circumflex coronary artery at the site of its origin from the main branch. The development of arrhythmia was observed during 15-min arterial occlusion and 15-min Russian State Medical University, Moscow reperfusion. Under these conditions idioventricular rhythm, ventricular tachycardia, and ventricular fibrillation were observed in 72%, 28%, and 55% of animals, respectively [7]. Electrocardiogram and blood pressure in the femoral artery were recorded with a BIOKOMB-8 polyphysiograph (ORLON/ EMG). Single and multiple extrasystoles, ventricular taehyeardia, and ventricular fibrillation were considered in the analysis of arrhythmia.In the lust series of experiments, 8 cats were subjected to coronary artery occlusion accompanied by the injection of BE under differentiated blockade of the impulse conduction along myelinated VN fibers induced by cooling VN to 6"C [11]. Cervical VNs were separated from the sympathetic nerves and placed on a special nerve-cooling device equipped with a thermistor registering the nerve temperature. These nerves were thoroughly isolated from surrounding tissues. The nerve temperature was lowered using a cooling liquid which was pumped with a vacuum device 5 min before coronary artery occlusion and during ischemia and 15-min reperfusion. In the second series of experiment, 10 cats were subjected to similar procedures without administering BE. In the third series of experiments (24 animals), the pulse activity of the nodose ganglion neurons was extracellularly registered with a ...

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“…During myocardial ischemia aggravated by ventricular fibrillation local changes in the myocardium are accompanied by important disintegration of neural activity in the bulbar cardiovascular center [1,2,5,6]. The important role in this rearrangement of the activity of bulbar cardiovascular neurons (CVN) is played by changes in impulse activity of nodose ganglion neurons [4]. In light of this, our aim was to study impulse activity of nodose ganglion neurons of various types during intraatrial injection of dalargin.…”

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confidence: 99%