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  • 1
    Electronic Resource
    Electronic Resource
    Post-excitatory depression in thoracic sympathetic efferent neural traffic during a cardiogenic hypertensive chemoreflex (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 423-430 
    Details
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Serotonin bewirkt bei Injektion in den linken Vorhof von Hunden einen hypertensiven Chemoreflex. Um das Muster der nervalen Übermittlung zu klären, wurden bei 8 narkotisierten Hunden mit offenem Thorax Ableitungen von thorakalen sympathischen (efferenten) Nerven vorgenommen. Serotonin (200 μg) verursacht massive sympathische Entladungen während der Hypertension und Bradykardie, die für den Chemoreflex charakteristisch sind. Nach der initialen sympathischen Entladung kam es regelmäßig zu einer postexzitatorischen Depression auf ein Niveau, das eindeutig unter Kontrollbedingungen lag. Diese postexzitatorische Depression begann im Mittel 11 s nach der Serotoninjektion und durchschnittlich 6,6 s nach der neuralen Spitzenentladung. Sie dauerte im Mittel 140 s und erreichte initial maximale Werte mit allmählichem Rückgang. Komplette Blockierung der hypertensiven Reaktion durch kombinierte Verabreichung von Phentolamin. Propranolol und Nitroglycerin konnte die nervalen Vorgänge nicht beseitigen einschließlich der postexzitatorischen Depression (mit Ausnahme eines Hundes). Wir schließen daraus, daß die postexzitatorische Depression thorakaler sympathischer Efferenzen nicht ausschließlich durch die sekundäre Beteiligung eines Barorezeptormechanismus vermittelt werden kann. Sie gehört wahrscheinlich zum Wesen des kardiogenen hypertensiven Chemoreflexes.
    Notes: Summary Serotonin injected in the left atrium activates a cardiogenic hypertensive chemoreflex in dogs. To elucidate patterns of the neural traffic, records were obtained from thoracic sympathetic efferent nerves (either the anterior ansa of the left stellate ganglion or the T4 input to the left stellate) in 8 anesthetized dogs with chests open. Serotonin (200 μg, left atrium) caused a massive sympathetic discharge during the hypertension and bradycardia characteristic of the chemoreflex. Following the initial sympathetic discharge, there was a consistent post-excitatory depression of neural traffic, to a level significantly less than control discharge (two-tailed p≤.05). This post-excitatory depression began 11±5.4 (S.D.) seconds after injection of serotonin and 6.6±5.3 seconds after the peak neural discharge. It lasted 140±94 seconds, being maximal initially with gradual recovery. Complete block of the hypertension by the combined administration of phentolamine, propranolol, and nitroglycerin failed to abolish the efferent neural events, including postexcitatory depression, in all but one dog. We conclude that post-excitatory depression in thoracic sympathetic efferent neural traffic cannot be mediated exclusively through the secondary engagement of a baroreceptor mechanism and that it most likely is an integral part of the cardiogenic hypertensive chemoreflex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02005342
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  • 2
    Electronic Resource
    Electronic Resource
    Differential effects of sympathetic activity on AV junctional automaticity and AV conduction (1986)
    Springer
    Basic research in cardiology 81 (1986), S. 497-507 
    Details
    ISSN: 1435-1803
    Keywords: AV junctional automaticity ; retrograde VA conduction ; antegrade AV conduction ; sympathetic deficit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22±2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73±5 percent and retrograde VA conduction 56 ±13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 1∶1 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 1∶1 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907756
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The effects of negative chronotropic interventions on sinus node recovery time (1987)
    Springer
    Basic research in cardiology 82 (1987), S. 92-100 
    Details
    ISSN: 1435-1803
    Keywords: sinus node recovery time ; overdrive suppression ; sinus cycle length ; vagal stimulation ; verapamil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of multiple increases in sinus cycle length on sinus node recovery time (SNRT) were examined in 5 dogs. Pacing was performed from the left atrial appendage for 30 and 60 seconds using at least 4 different pacing cycle lengths selected between 230 and 620 msec. Each dog received propranolol (1 mg/kg, IV) prior to any measurements. The effects of increases in sinus cycle length on SNRT were first assessed during 2 levels (4 and 8 Hz) of continuous vagal stimulation. From a control cycle length of 439±28 msec (mean±SE), the vagal stimulations lengthened the sinus cycle lengths to 604±10 msec and 758±16 msec respectively. Sinus cycle length was then prolonged by combined muscarinic and beta-receptor blockade resulting in a sinus cycle length of 549±9 msec. Autonomic blockade plus verapamil (3–10 mg IV) resulted in sinus cycle lengths of 612±14 and 721±18 msec respectively, which were not significantly different from those obtained with vagal stimulation. Data relating SNRT to the sinus cycle length, pacing cycle length, duration of pacing and the negative chronotropic interventions used to achieve the changes in the sinus cycle length were analyzed via covariance analysis. The results demonstrate that the single most important determinant of SNRT is the sinus cycle length. Furthermore, equivalent increases in sinus cycle length whether obtained by vagal stimulation, autonomic blockade or intravenous verapamil results in SNRTs that are not significantly different. Therefore, in the sinus node, changes in the rate of pacemaker activity, regardless of how they are achieved, will largely determine the changes in SNRT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907057
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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