Über das angebliche Vorkommen von Accelerausfasern im Halsvagus der Säugetiere

Hering, H. E.

doi:10.1007/bf01722424

Cited by 9 publications

(6 citation statements)

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“…were placed distally on the cervical vagal nerve trunk after decentralization to eliminate afferent nerve activation. Cervical vagal nerve stimulation in the cat, as opposed to other species, produces a pure parasympathetic response because there are no sympathetic fibers coursing with the feline vagal nerve trunk (21). Parameters of stimulation wvere: 2-ins impulse duration, 5 V, and variable frequency ranging from 10 to 25 Hz adjusted to produce complete atrioventricular dissociation with a constant ventricular escape rate.…”

Section: Methodsmentioning

confidence: 99%

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Sheridan¹,

Penkoske²,

Sobel³

et al. 1980

J. Clin. Invest.

373

106

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A B S T R A C T Alpha compared to beta adrenergic contributions to dysrhythmias induced by left anterior descending coronary occlusion and by reperfusion were assessed in chloralose-anesthetized cats (n = 96). Alpha receptor blockade with either phentolamine or prazosin significantly reduced the number of premature ventricular complexes during coronary reperfusion (321±62-14±10 premature ventricular complexes, P <0.001), abolished early ventricular fibrillation (from 25% in controls to 0%), and prevented the increase in idioventricular rate seen with coronary reperfusion. However, ,8-receptor blockade was without effect. Ventricular dysrhythmias induced by coronary occlusion alone (without reperfusion) were attenuated markedly by a-receptor blockade under conditions in which perfusion (measured with radiolabeled microspheres) within ischemic zones was not affected. Alternative sympatholytic interventions including pretreatment with 6-hydroxydopamine to deplete myocardial norepinephrine from 8.8±+1.4 to 0.83+0.2 ng/mg protein and render the heart unresponsive to tyramine (120 gg/kg) attenuated dysrhythmias induced by both coronary occlusion and reperfusion in a fashion identical to that seen with a-receptor blockade. Although efferent sympathetic activation induced by left stellate nerve stimulation increased idioventricular rate from 66+6 to 144±7 beats/min (P < 0.01) before coronary occlusion, this response was blocked by propranolol but not by phentolamine. In contrast, during reperfusion the increase in idioventricular rate induced by left stellate nerve stimulation (to 203±14) was not inhibited by propranolol but was abolished by phentolamine (79 ± 10). Intracoronary methoxamine (0.1 uM) in animals depleted of myocardial catecholamines by 6-hydroxy-

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Section: Methodsmentioning

confidence: 99%

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Sheridan¹,

Penkoske²,

Sobel³

et al. 1980

J. Clin. Invest.

373

106

View full text Add to dashboard Cite

show abstract

“…Cervical vagal nerve stimulation in the cat, as opposed to other species, produces a pure parasympathetic response, since there are no sympathetic fibers coursing with the feline vagal trunk. 36 Parameters of stimulation were: 2 msec impulse duration, 5 V and variable frequency ranging between 10-25 Hz adjusted to produce complete atrioventricular dissociation with a constant ventricular escape rate.…”

Section: Methodsmentioning

confidence: 99%

Disparate electrophysiological alterations accompanying dysrhythmia due to coronary occlusion and reperfusion in the cat.

Penkoske¹,

Sobel²,

Corr³

1978

Circulation

133

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The electrophysiologic changes associated with dysrhythmias induced by coronary occlusion and by subsequent reperfusion were characterized with six complimentary approaches in chloralose-anesthetized cats (n = 57) with proximal occlusion of the left anterior descending (LAD) coronary artery. Occlusion led to reproducible ventricular dysrhythmia which abated in 35 minutes. The electrophysiologic effects of reperfusion initiated at this time could be studied. Simultaneous bipolar electrograms (epi-, myo- and endocardial) from ischemic and normal zones were analyzed by computer. Before the onset of the dysrhythmia induced by occlusion, conduction was markedly slowed, with dV/dt decreasing to 34% +/- 6% of control and conduction time (endo- to epicardial activation) prolonged to 328 +/- 77% of control. However, these values returned toward normal with reperfusion, even though it also consistently induced dysrhythmia. The idioventricular escape rate (determined by intense vagal stimulation) was 62 +/- 6 beats/min during the dysrhythmia induced by occlusion (equal to control), but increased during the reperfusion dysrhythmia to 188 +/- 12 beats/min. The occlusion dysrhythmia was exacerbated, but the reperfusion dysrhythmia was suppressed by rapid atrial pacing. The refractory period progressively shortened after occlusion and remained decreased during early reperfusion. Thus, increased conduction time through myocardial and epicardial regions, asynchronous depolarization and shortening of the refractory period accompanied dysrhythmia induced by occlusion. In contrast, the dysrhythmia induced by reperfusion was characterized by normal conduction time, through myocardial regions with continued significant epicardial delay, overdrive suppression, synchronous depolarization and a high idioventricular rate.

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“…Dale and his co-workers incline to the former more direct explanation, but as Hering [1924] points out their evidence is strongly in favour of the latter explanation. Thus the acceleration was usually absent or at most very slight until a marked and prolonged cardiac slowing developed after each tetanic stimulation, and acceleration during the stimulation usually just sufficed to restore the rhythm to the rate obtaining before the appearance of this slowing.…”

Section: Single Vagal Volley On Heartmentioning

confidence: 94%

“…Anatomically there is no evidence that sympathetic fibres to the heart arise from the superior cervical ganglion [Perman, 1924], and physiological evidence is also against the existence of such fibres [Dale, Laidlaw and Symons, 1910;Hering, 1924]. Recently Morgan and Goland [1932] have found that cardiac acceleration is sometimes produced by prolonged tetanic stimulation of the vago-sympathetic trunk of the dog after the vagus has been cut proximal to the nodose ganglion and allowed to degenerate.…”

Section: Single Vagal Volley On Heartmentioning

confidence: 99%

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The action of a single vagal volley on the rhythm of the heart beat

Brown¹,

Eccles²

1934

The Journal of Physiology

182

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IT may now be taken as established that the vagus exerts its inhibitory action on the heart by liberating a substance which biological tests have been unable to distinguish from acetylcholine and which in this paper will be called A.C. substance (see Feldberg and Krayer [1933] for a recent survey of the evidence). Three problems arise out of this first important step towards a solution of the vagal action on the heart:(1) How do impulses in the postganglionic nerve fibres of the vagus liberate A.c. substance? (2) What factors govern the transport of A.c. substance from the region of its liberation to the site of its action? (3) How does A.c. substance exert its inhibitory effect on the heart, e.g. how does it act on the rhythmic mechanism of the pacemaker? This paper and the next are for the most part concerned with the third problem, but some of the evidence also bears on the first and second problems. In the present paper a detailed study has been made of the effect on heart rate produced by a single volley of impulses down either the right or left vagus of the cat. A preliminary account of some of this work has already been published [Brown, Eccles and Hoff, 1932].The inhibitory effect of single stimuli applied to the vagus was first described by Donders [1868], who found that the slowing of the heart rhythm persisted for several beats. Niiel [1874] stated that a single stimulus to the frog's vagus had no effect on the heart, but Heidenhain [1882] found that a very definite slowing was produced. Gaskell [1883] observed that a single shock applied to the vagus produced a prolonged diminution in the contraction of the tortoise heart, and recently Gilson 14-2

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Über das angebliche Vorkommen von Accelerausfasern im Halsvagus der Säugetiere

Cited by 9 publications

References 0 publications

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Disparate electrophysiological alterations accompanying dysrhythmia due to coronary occlusion and reperfusion in the cat.

The action of a single vagal volley on the rhythm of the heart beat

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