Electrophysiological effects of ouabain in 6-hydroxydopamine pretreated dogs

1983 ◽  
Vol 61 (3) ◽  
pp. 229-236 ◽  
Author(s):  
Diane Godin ◽  
Claude Guimond ◽  
Réginald Nadeau
Keyword(s):  
Heart Rate ◽  
Sinus Bradycardia ◽  
Cardiac Pacing ◽  
Refractory Periods ◽  
Ventricular Extrasystoles ◽  
Additional Group ◽  
Sinus Cycle Length ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Therapeutic Doses

Chemical sympathectomy and bilateral vagotomy were used to evaluate the contribution of each division of the autonomic nervous system in the electrophysiological actions of ouabain. Intact and chemically sympathectomized dogs were given successive and cumulative doses of ouabain until toxicity became manifest (ventricular extrasystoles and (or) ventricular tachycardia). An additional group of normal and sympathectomized animals was also submitted to bilateral vagotomy in the presence of a therapeutic dose of ouabain. Sinus cycle length, AH interval of the His bundle electrogram, atrioventricular junctional effective and functional refractory periods were increased by ouabain at therapeutic doses. These effects were no different in sympathectomized dogs than in intact dogs, indicating the absence of any significant contribution of efferent sympathetic neural activity. However, our results suggested that vagal enhancement was the main mechanism whereby ouabain produced sinus bradycardia and depression of atrioventricular conduction. Sympathectomy with 6-OHDA did not modify nor abolish ouabain toxicity. However, toxic doses were significantly higher in sympathectomized animals than in normal animals. Considering that increasing heart rate by cardiac pacing or vagotomy significantly lowered toxic doses of ouabain in both intact and sympathectomized dogs, it is possible that sympathectomy could influence ouabain toxicity by altering heart rate alone.

Abstract 17124: Severe Bradycardia in Critically Ill Patients With COVID-19

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Julie Larue ◽  
Patrick De Jode ◽  
Jean-François Timsit ◽  
Guillaume Franchineau ◽  
Fabrice Extramiana ◽  
...  
Keyword(s):  
Heart Rate ◽  
Beta Blockers ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Cardiac Pacing ◽  
Multiple Organ ◽  
Physical Stimulation ◽  
Node Disease ◽  
Cardiac Manifestations ◽  
Mean Heart Rate

Cardiac manifestations of severe Covid19 infection are still poorly understood. From January to May 2020, 113 consecutive patients were admitted in intensive care units for severe Covid19 and 10 out of them presented an episode of bradycardia. Patients had a median age of 63 years, 6/10 were men, 7/10 were under mechanical ventilation for severe acute respiratory distress syndrome and 4/10 received a veno-venous extracorporeal membrane oxygenation. All bradycardias were due to sinus node bradycardia with a median heart rate of 36 bpm (range 10 - 45 bpm). For 6 patients, bradycardia was persistent and 3 required continuous isoprenaline infusion (Figure, patient A). Bradycardia was sudden for 4 patients and required brief resuscitation maneuvers for one (Figure, patient B) . Patients had normal baseline ECG and echocardiography, except for two patients who were under beta-blockers. For those two patients beta blockers were interrupted several days before bradycardia. A comprehensive review of patient’s files ruled out bradycardia due to drug-drug interactions, myocarditis, hyperkalemia, hypoxia or vagal physical stimulation. Holter ECG was performed for 7 patients: 3 recordings evoked vagal hyperactivity (low mean heart rate and elevated pNN50 / RMSSD, Figure Patient A), 3 others cardiac dysautonomia (SDNN<100ms, Figure Patient B). Amongst these 10 patients, 5 were discharged from ICU among which 2 returned home and five died from covid-19 associated multiple-organ failure. None of them required temporary or permanent cardiac pacing. To conclude, sinus bradycardia occurred commonly in severe Covid19 infection. This highlights the need to monitor cardiac rhythm. Even if the pathophysiology remains unclear, cardiac dysautonomia and vagal hyperactivity could be hypothesized rather than an intrinsic sinus node disease.

scholarly journals Amiodarone-Induced Hypothyroidism

2019 ◽  
Vol 26 (6) ◽  
pp. 127-134
Author(s):  
Svetlana A. Chepurnenko ◽  
Galina V. Shavkuta ◽  
Alina D. Nasytko
Keyword(s):  
Heart Rate ◽  
Antiarrhythmic Drugs ◽  
Sinus Bradycardia ◽  
Thyroid Stimulating Hormone ◽  
Amiodarone Therapy ◽  
Thyroid Gland Function ◽  
Ventricular Extrasystoles ◽  
St Segment ◽  
Gland Function ◽  
Electrocardiogram Ecg

Aim: to present a clinical case of amiodarone-induced hypothyroidism in a patient with paroxysmal atrial fi brillation.Results. Before taking amiodarone, the patient suffered from subclinical hypothyroidism. The level of thyroid stimulating hormone (TSH) was 6.2 mIU/L, thyroxine (T4) — 9.2 pmol/L. Against the background of taking amiodarone in a maintenance dose of 200 mg per day 5 days a week with a break of 2 days, clinically severe hypothyroidism developed with a TSH level of more than 16 mIU/L. An electrocardiogram (ECG) recorded sinus bradycardia with a heart rate (HR) of 37 beats per minute. Paroxysms of atrial fi brillation have stopped. According to the daily ECG monitoring recorded throughout the sinus rhythm with maximum heart rate of 92 beats/min., minimum of 35 beats/min. The circadian rhythm profi le was correct. No pauses were detected for more than two seconds. Transient atrioventricular block was of 1 degree (during sleep). Ectopic activity was represented by supraventricular extrasystoles 112 per day: 107 single, 1 pair, 1 group. Ventricular extrasystoles: 55 per day: polymorphic, solitary. No diagnostically signifi cant elevation or depression of the ST segment was detected. After the abolition of amiodarone, thyroid function was recovered. Levothyroxine was not prescribed. However, paroxysms of atrial fi brillation began to occur again. For the prevention of paroxysms, sotalol 160 mg per day was prescribed.Conclusion. Thus, the development of clinically pronounced amiodarone-induced hypothyroidism has contributed to the existing thyroid dysfunction in the patient. The assessment of the thyroid gland function and its further monitoring in the process of taking the drug is prescribed. Amiodarone therapy is performed in case of ineffectiveness of other antiarrhythmic drugs and, as a rule, is not used for primary prescription.

scholarly journals Rate Control in Atrial Fibrillation by Cooling: Effect of Temperature on Dromotropy in Perfused Rabbit Hearts

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Karl Mischke ◽  
Markus Zarse ◽  
Christian Knackstedt ◽  
Patrick Schauerte
Keyword(s):  
Atrial Fibrillation ◽  
Heart Rate ◽  
Rate Control ◽  
Therapeutic Option ◽  
Effect Of Temperature ◽  
Significant Drop ◽  
Refractory Periods ◽  
Sinus Cycle Length ◽  
The Mean ◽  
The Impact

Background. Cooling has emerged as a therapeutic option in critically ill patients (especially after cardiac resuscitation) and might also have a negative dromotropic effect in atrial fibrillation. We sought to determine the impact of cooling on electrophysiologic properties of Langendorff-perfused rabbit hearts.Methods and Results. In 20 isolated Langendorff-perfused rabbit hearts, the temperature of the tissue bath was changed between 17 and 42°C. With decreasing temperature, significant increases of the spontaneous sinus cycle length, decreases of the mean ventricular heart rate during atrial fibrillation, and relevant increases of atrial and ventricular refractory periods were observed (ANOVAP<.01).Conclusions. Cardiac hypothermia leads to a significant drop of mean ventricular heart rate during atrial fibrillation. Negative chronotropy and dromotropy induced by moderate cardiac hypothermia might be a feasible therapeutic approach in patients with hemodynamically relevant tachyarrhythmias in a CCU/ICU setting.

Vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol

1992 ◽  
Vol 70 (6) ◽  
pp. 872-881 ◽  
Author(s):  
Menashe B. Waxman ◽  
John A. Asta ◽  
Douglas A. Cameron ◽  
Laszlo Endrenyi
Keyword(s):  
Heart Rate ◽  
Present Experiment ◽  
Inferior Vena ◽  
Venous Return ◽  
Adrenergic Stimulation ◽  
Cardiac Volume ◽  
Inferior Vena Caval ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Heart Rate Slowing

Testing for the susceptibility for vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. To explore the basis of the vasodepressor test in humans, the present experiment examined whether a reduced cardiac volume coupled with adrenergic stimulation causes a vasodepressor reaction in rats. Vasodepressor reaction was defined as paradoxical heart rate slowing in conjunction with hypotension during inferior vena caval occlusion. Inferior vena caval occlusion was performed for 60 s and the maximum changes in R-R were measured during seven states as follows. (A) Under control conditions inferior vena caval occlusion alone accelerated the rate in 32 of 32 rats (ΔR-R, −13.9 ± 1.7 ms, p < 0.001). (B) When inferior vena caval occlusion was performed during an infusion of isoproterenol (0.5–1.0 μg∙min−1), a vasodepressor reaction was observed in all rats as the heart rate slowed (ΔR-R, +138.1 ± 14.8 ms, p < 0.001). The vasodepressor reaction was further examined during isoproterenol and inferior vena caval occlusion under five additional states. (C) After atropine the vasodepressor reaction was unchanged (ΔR-R, +132.7 ± 24.8 ms, p < 0.001). (D) After bilateral vagotomy the paradoxical slowing was eliminated. (E) After intrapericardial lidocaine the paradoxic slowing was eliminated. (F) After bilateral stellectomy nonsignificant slowing was still present, but this was markedly reduced when compared with B (p < 0.001). (G) Following chronic chemical sympathetic denervation with 6-hydroxydopamine the paradoxic bradycardia was eliminated. Conclusions: (1) Reduced cardiac volume combined with adrenergic stimulation can stimulate a vasodepressor reaction; (2) the vasodepressor reaction requires signalling by the afferent but not efferent vagal fibers; (3) the bradycardia is mainly due to withdrawal of sympathetic efferent tone.Key words: vasodepressor reaction, venous return, isoproterenol.

Symptomatic Bradycardia Caused by Mianserin at Therapeutic Doses

1991 ◽  
Vol 10 (5) ◽  
pp. 383-384 ◽  
Author(s):  
Bernard Carcone ◽  
Thierry Vial ◽  
Nicolas Chaillet ◽  
Jacques Descotes
Keyword(s):  
Heart Rate ◽  
Female Patient ◽  
Therapeutic Dose ◽  
Sinus Bradycardia ◽  
Acute Episode ◽  
First Report ◽  
Cardiac Abnormalities ◽  
Conduction Defect ◽  
Symptomatic Bradycardia ◽  
Therapeutic Doses

An acute episode of symptomatic sinus bradycardia, occurred in a 50-year-old female patient after she had been given a single therapeutic dose of mianserin. Heart rate was corrected by atropine injection. Re-administration of mianserin resulted in the recurrence of bradycardia. Further examination showed no cardiac abnormalities. This case is the first report of conduction defect in a patient given therapeutic doses of mianserin.

scholarly journals Computational Analysis of Coronary Blood Flow: The Role of Asynchronous Pacing and Arrhythmias

Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Long Qt Syndrome ◽  
Premature Ventricular Contraction ◽  
Cardiac Pacing ◽  
Long Qt ◽  
Computational Evaluation ◽  
Qt Syndrome

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.

Stimulation of the nigrostriatal dopamine system produces hypertension and tachycardia in rats

1994 ◽  
Vol 266 (6) ◽  
pp. H2489-H2496 ◽  
Author(s):  
M. T. Lin ◽  
J. J. Yang
Keyword(s):  
Corpus Striatum ◽  
Substantia Nigra Pars Compacta ◽  
Dopamine System ◽  
Arterial Blood ◽  
Nigrostriatal Dopamine ◽  
Induced Hypertension ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Da Release ◽  
Stimulation Of

To test for the ability of the nigrostriatal dopamine (DA) system to influence cardiovascular function, experiments were carried out to assess the effects of electrical or chemical stimulation of the nigrostriatal DA system on arterial blood pressure, heart rate, and striatal DA release in anesthetized rats. Electrical stimulation of the substantia nigra pars compacta (SNC), in addition to enhancing the DA release in the corpus striatum (CS), elicited proportional hypertension and tachycardia. This could be mimicked by microinjection of two excitatory amino acids, kainic acid and glutamate, into the SNC area of rat brain. The SNC stimulation-induced hypertension, tachycardia, and increased striatal DA release were attenuated by prior destruction of the nigrostriatal DA system produced by intramedial forebrain bundle injection of 6-hydroxydopamine and by prior blockade of postsynaptic DA receptors produced by intra-CS injection of DA receptor antagonists, haloperidol or pimozide. The SNC stimulation-induced hypertension was attenuated by spinal transection, whereas the SNC stimulation-induced tachycardia was attenuated by bilateral vagotomy. The data suggest that stimulation of the nigrostriatal DA system produces both hypertension and tachycardia in rats.

scholarly journals Possibilities of cardioselective beta - blocker bisoprolol therapy in patients having coronary artery disease and bronchial asthma

2019 ◽  
Vol 91 (9) ◽  
pp. 26-31
Author(s):  
N Y Grigorieva ◽  
T P Ilyushina ◽  
E M Yashina
Keyword(s):  
Coronary Artery Disease ◽  
Heart Rate ◽  
Coronary Artery ◽  
Calcium Antagonist ◽  
Beta Blocker ◽  
Ventricular Extrasystoles ◽  
Group 3 ◽  
Group 2 ◽  
Artery Disease ◽  
Group 1

Aim: to compare the antianginal and pulse slowing effects, the impact on the ectopic myocardial activity as well as the safety of the treatment with beta - adrenoblocker bisoprolol, calcium antagonist verapamil and the combination of bisoprolol with amlodipine in patients with stable angina (SA) and bronchial asthma (BA). Materials and methods. The study included 90 patients with SA II-III functional class (FC) having concomitant persistent asthma of moderate severity, controlled, without exacerbation. The patients were divided into three groups with 30 individuals in each one depending on the main antianginal drug prescribed. Group 1 patients received a cardio - selective beta - adrenergic blocker bisoprolol (Concor) at the dose of 5 mg/day, patients of group 2 were treated by a calcium antagonist verapamil at the dose of 240 mg/day, patients of group 3 received combined therapy with bisoprolol at the dose of 5 mg/day and amlodipine at the dose of 5 mg/day given as a fixed combination (Concor AM 5/5). All the patients were investigated by the methods of daily ECG monitoring and respiratory function study (RFS) in addition to physical examination at baseline and after 4 weeks of treatment. Results. After 4 weeks of treatment, patients of group 1 and group 3 did not complain of angina attacks and did not use nitroglycerin unlike patients of group 2. The achieved heart rate (HR) in group 1 patients was 68.6±8.5 beats/min, in group 2 - 74.3±5.6 beats/min, in group 3 - 67.3±4.8 beats/min. A significant decrease in the number of supraventricular and ventricular extrasystoles occurred in patients of group 1 and group 3 only. Thus, the pulse slowing, antianginal, antiischemic and antiarrhythmic effect of the calcium antagonist verapamil, even at the dose of 240 mg/day, is not always sufficient for the patients with SA II-III FC and concomitant BA, unlike therapy with the inclusion of beta - blocker bisoprolol. During the study there was no registered deterioration in the indices of bronchial patency according to the RFS data in the patients of all three groups. Conclusion. In patients with coronary artery disease and concomitant asthma, all three types of pulse slowing therapy do not have any negative effects on bronchial patency. Therapy with the inclusion of beta - blockers (bisoprolol or its combination with amlodipine), in contrast to verapamil, reliably reduces heart rate and the number of supraventricular and ventricular extrasystoles in addition to a good antianginal effect.

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