Nicht invasive Vagus-Stimulation auch im klinischen Alltag wirksam und sicher

2019 ◽  
Vol 35 (1) ◽  
pp. 14-14
Author(s):  
Barbara Kreutzkamp
Keyword(s):  
Vagus Stimulation

scholarly journals STUDIES WITH THE ELECTROCARDIOGRAPH ON THE ACTION OF THE VAGUS NERVE ON THE HUMAN HEART

1911 ◽  
Vol 14 (3) ◽  
pp. 217-234 ◽  
Author(s):  
G. Canby Robinson ◽  
George Draper
Keyword(s):  
Vagus Nerve ◽  
Mechanical Stimulation ◽  
Human Heart ◽  
Appreciable Effect ◽  
Vagus Stimulation ◽  
Ventricular Systole ◽  
Constant Change ◽  
The Right ◽  
Stimulation Of

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.

Effects of vagus nerve on heart rate and ventricular contractility in chicken

1989 ◽  
Vol 256 (5) ◽  
pp. H1295-H1302
Author(s):  
S. A. Lang ◽  
M. N. Levy
Keyword(s):  
Vagus Nerve ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Ventricular Contractility ◽  
Ventricular Contraction ◽  
Vagus Stimulation ◽  
Constant Frequency ◽  
The Right ◽  
Contraction And Relaxation ◽  
Left Vagus

We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.

Parasympathetic inhibition of sympathetic effects on sinus rate in anesthetized dogs

1996 ◽  
Vol 271 (1) ◽  
pp. H44-H50 ◽  
Author(s):  
Y. Furukawa ◽  
Y. Hoyano ◽  
S. Chiba
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Pulmonary Veins ◽  
Fatty Tissue ◽  
Sympathetic Stimulation ◽  
Vagus Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Chronotropic Response ◽  
Sinus Rate ◽  
Isoproterenol Infusion

The intracardiac parasympathetic neural elements that control sinus rate are found in the fatty tissue overlying the atrial junctions of the right pulmonary veins of mammalian hearts. We refer to these nerves as the sinus rate-related parasympathetic nerves (SRRPN). Thus, to elucidate the role of SRRPN, we studied the effects of cervical vagus stimulation on the positive chronotropic responses to cardiac sympathetic nerve stimulation and isoproterenol infusion before and after the SRRPN were removed in the open-chest anesthetized dog heart. Before SRRPN denervation, cervical vagus stimulation suppressed the sinus rate and the positive chronotropic response to sympathetic nerve stimulation or isoproterenol infusion. After SRRPN denervation, cervical vagus stimulation hardly decreased the sinus rate. On the other hand, even after SRRPN denervation, cervical vagus stimulation suppressed the rate increased by sympathetic stimulation. Cervical vagus stimulation also attenuated the sinus rate increased by isoproterenol. The inhibition by vagus stimulation of the chronotropic response to sympathetic stimulation was greater than that of the response to isoproterenol. The attenuation by cervical vagus stimulation was abolished by atropine. These results suggest that 1) a small number of vagus nerves to the sinoatrial nodal area different from the SRRPN decrease the sinus rate increased by adrenergic interventions and 2) the same activation that causes relatively small effects on sinus rate is capable of causing much larger changes in sinus rate during increased sympathetic tone or in the case of beta-adrenoceptor agonist treatment in the heart in situ.

EXCITABILITY OF THE TURTLE AURICLE DURING VAGUS STIMULATION

1931 ◽  
Vol 98 (1) ◽  
pp. 109-120 ◽  
Author(s):  
Richard Ashman ◽  
Walter E. Garrey
Keyword(s):  
Vagus Stimulation

319 In Contrast to Vagus Stimulation, Vagotomy Increases the Severity of Food Allergy

2013 ◽  
Vol 144 (5) ◽  
pp. S-67
Author(s):  
Annick de Vries ◽  
Ine Vanderleyden ◽  
Gianluca Matteoli ◽  
Pedro J. Gomez-Pinilla ◽  
Martina Di Giovangiulio ◽  
...  
Keyword(s):  
Food Allergy ◽  
Vagus Stimulation

scholarly journals Cardiac sympathetic dysfunction in the prehypertensive spontaneously hypertensive rat

2013 ◽  
Vol 305 (7) ◽  
pp. H980-H986 ◽  
Author(s):  
Julia Shanks ◽  
Sotiria Manou-Stathopoulou ◽  
Chieh-Ju Lu ◽  
Dan Li ◽  
David J. Paterson ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Calcium Transients ◽  
Vagus Stimulation ◽  
Spontaneously Hypertensive ◽  
Sympathetic Dysfunction ◽  
The Difference ◽  
Wistar Kyoto ◽  
The Right ◽  
Right Atria

Recent studies in prehypertensive spontaneously hypertensive rats (SHR) have shown larger calcium transients and reduced norepinephrine transporter (NET) activity in cultured stellate neurons compared with Wistar-Kyoto (WKY) controls, although the functional significance of these results is unknown. We hypothesized that peripheral sympathetic responsiveness in the SHR at 4 wk of age would be exaggerated compared with the WKY. In vivo arterial pressure (under 2% isoflurane) was similar in SHRs (88 ± 2/50 ± 3 mmHg, n = 18) compared with WKYs (88 ± 3/49 ± 4 mmHg, n = 20). However, a small but significant ( P < 0.05) tachycardia was observed in the young SHR despite the heart rate response to vagus stimulation (3 and 5 Hz) in vivo being similar (SHR: n = 12, WKY: n = 10). In isolated atrial preparations there was a significantly greater tachycardia during right stellate stimulation (5 and 7 Hz) in SHRs ( n = 19) compared with WKYs ( n = 16) but not in response to exogenous NE (0.025–5 μM, SHR: n = 10, WKY: n = 10). There was also a significantly greater release of [3H]NE to field stimulation (5 Hz) of atria in the SHR (SHR: n = 17, WKY: n = 16). Additionally, plasma levels of neuropeptide Y sampled from the right atria in vivo were also higher in the SHR (ELISA, n = 12 for both groups). The difference in [3H]NE release between SHR and WKY could be normalized by the NET inhibitor desipramine (1 μM, SHR: n = 10, WKY: n = 8) but not the α2-receptor antagonist yohimbine (1 μM, SHR: n = 7, WKY: n = 8). Increased cardiac sympathetic neurotransmission driven by larger neuronal calcium transients and reduced NE reuptake translates into enhanced cardiac sympathetic responsiveness at the end organ in prehypertensive SHRs.

PACAP-(1-38) as neurotransmitter in pig pancreas: receptor activation revealed by the antagonist PACAP-(6-38)

1997 ◽  
Vol 273 (2) ◽  
pp. G436-G446 ◽  
Author(s):  
K. Tornoe ◽  
J. Hannibal ◽  
J. Fahrenkrug ◽  
J. J. Holst
Keyword(s):  
Glucagon Secretion ◽  
Receptor Activation ◽  
Immunohistochemical Localization ◽  
Nerve Fibers ◽  
Relative Importance ◽  
Vagus Stimulation ◽  
Porcine Pancreas ◽  
Endocrine Secretion ◽  
Induced Flow

The pituitary adenylyl cyclase-activating polypeptide PACAP-(1-38) has potent pancreatic secretory effects. We studied its immunohistochemical localization, release, and contribution to secretion induced by electrical vagus stimulation using isolated perfused porcine pancreas and the PACAP receptor antagonist PACAP-(6-38) (10(-7) M). PACAP was found in nerve fibers throughout the pancreas but, in particular, encircling ganglionic vasoactive intestinal polypeptide (VIP)-positive nerve cell bodies and, mostly, colocalized with VIP. Vagus stimulation caused its release. PACAP-(1-38)(4 x 10(-9) M) stimulated exocrine and endocrine secretion and released VIP. PACAP-(6-38) decreased PACAP-induced flow of juice to 59 +/- 7.8% and insulin secretion and VIP release to 12 +/- 6.8 and 57 +/- 13%, respectively. Glucagon secretion was unaffected. PACAP-(6-38) reduced vagus-stimulated flow rate to 63 +/- 7.6%, insulin and glucagon responses to 31.8 +/- 13 and 6 +/- 4%, respectively, and VIP release to 23 +/- 8.4% and reduced VIP-induced (2 x 10(-9) M) juice and insulin (but not glucagon) outputs to 8.3 +/- 4.2 and 67 +/- 14%, respectively. In conclusion, 1) pancreatic PACAP fibers seem to activate intrapancreatic VIPergic neurons, 2) PACAP-(6-38) antagonism documents the role of VIP/PACAP for neural regulation but cannot distinguish their relative importance, and 3) a PACAP receptor with low affinity for PACAP-(6-38), associated with glucagon cells, may exist.

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