Influence of Pentobarbital and Chloralose Anesthesia on Quinidine-Induced Effects on Atrial Refractoriness and Heart Rate in the Dog

Boucher, Michel; Dubray, Claude; Li, J. H.; Paire, M; Duchêne-Marullaz, P

doi:10.1097/00005344-199102000-00004

Cited by 16 publications

(4 citation statements)

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“…In dogs, pentobarbital increases the fibrinogen receptor antagonist L‐734,217 plasma concentrations by ∼2‐fold immediately after bolus infusion compared with awake dogs, whereas isoflurane increases verapamil plasma levels ∼3‐fold after a 10 minutes infusion period compared with awake animals . Although not all drugs display increased plasma concentrations upon anesthesia, the absence of anesthesia in our investigation may cause the lower PA‐6 plasma levels observed here compared with the previous experimental study . Furthermore, we observed high variability of PA‐6 plasma levels in contrast to the previous study.…”

Section: Discussioncontrasting

confidence: 85%

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Szatmári

Yuan

Herwijnen

et al. 2018

Veterinary Internal Medicne

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BackgroundThe inward rectifier inhibitor pentamidine analogue 6 (PA‐6) is effective in cardioversion of goats with persistent rapid pacing induced atrial fibrillation (AF) and is not proarrhythmic in dogs with experimental chronic 3rd‐degree AV block. Efficacy and safety in the clinical setting are unknown.HypothesisThat PA‐6 would be effective in converting AF to sinus rhythm (SR) in dogs with naturally occurring AF, without the presence of overt adverse effects.AnimalsTen client‐owned large and giant breed dogs.MethodsAnimals with persistent or permanent AF were recruited for our prospective study. PA‐6 was administered IV as a bolus of 2.5 mg/kg 10 min−1 followed by a maintenance infusion of 0.04 mg/kg min−1 for a maximum of 50 minutes in conscious dogs. Standard 6 lead limb ECG was recorded during the infusion. Visible and audible signs of adverse effects were scored during the entire procedure.ResultsPA‐6 did not induce changes in QRS duration (54.7 ± 4.6 versus 56.7 ± 6.1 ms, P = .42), QTc interval (241.1 ± 19.5 versus 258.7 ± 19.8 ms, P = .061) or RR interval (363.4 ± 84.6 versus 440.8 ± 96.3 ms, P = .072) at the end of the bolus. No cardioversion to SR was observed in any dog. Three dogs displayed no adverse effects. Five dogs had premature ventricular depolarizations during PA‐6 infusion on the ECG. Respiratory distress with laryngeal stridor, subtle muscle twitching, and mild generalized muscular weakness were noncardiac adverse effects observed in 5 dogs. Adverse effects resolved spontaneously.Conclusions and Clinical importanceChronic naturally occurring AF in large and giant breed dogs could not be cardioverted to SR by PA‐6.

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Section: Discussioncontrasting

confidence: 85%

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Szatmári

Yuan

Herwijnen

et al. 2018

Veterinary Internal Medicne

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“…This could suggest that blocking Na v 1.8 could avoid functional substrate forming in PV myocardium, probably as a result of inhibiting GP function and atrial electrical remodeling. Although we could not deny the fact that sodium pentobarbital has been reported vagolytic and may increase the ERP value when applying, the effect of A‐803467 on ERP in the present study is still established, since both groups were treated equally with the anesthetic to eliminate bias between groups, and the minimum dosage was used to reduce the possibility of unnecessary influence, as in our previously published studies …”

Section: Discussionmentioning

confidence: 76%

Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

Chen

Shu

et al. 2016

JAHA

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BackgroundGanglionated plexus have been developed as additional ablation targets to improve the outcome of atrial fibrillation (AF) besides pulmonary vein isolation. Recent studies implicated an intimate relationship between neuronal sodium channel Nav1.8 (encoded by SCN10A) and AF. The underlying mechanism between Nav1.8 and AF remains unclear. This study aimed to determine the role of Nav1.8 in cardiac electrophysiology in an acute AF model and explore possible therapeutic targets.Methods and ResultsImmunohistochemical study was used on canine cardiac ganglionated plexus. Both Nav1.5 and Nav1.8 were expressed in ganglionated plexus with canonical neuronal markers. Sixteen canines were randomly administered either saline or the Nav1.8 blocker A‐803467. Electrophysiological study was compared between the 2 groups before and after 6‐hour rapid atrial pacing. Compared with the control group, administration of A‐803467 decreased the incidence of AF (87.5% versus 25.0%, P<0.05), shortened AF duration, and prolonged AF cycle length. A‐803467 also significantly suppressed the decrease in the effective refractory period and the increase in effective refractory period dispersion and cumulative window of vulnerability caused by rapid atrial pacing in all recording sites. Patch clamp study was performed under 100 nmol/L A‐803467 in TSA201 cells cotransfected with SCN10A‐WT,SCN5A‐WT, and SCN3B‐WT. IN a,P was reduced by 45.34% at −35 mV, and IN a,L by 68.57% at −20 mV. Evident fast inactivation, slow recovery, and use‐dependent block were also discovered after applying the drug.ConclusionsOur study demonstrates that Nav1.8 could exert its effect on electrophysiological characteristics through cardiac ganglionated plexus. It indicates that Nav1.8 is a novel target in understanding cardiac electrophysiology and SCN10A‐related arrhythmias.

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“…In addition, the use of anesthetics could alter cardiac function. For instance, pentobarbital reduce the chronotropic effects of atrial and ventricular function (2). Second, we obtained LA volume and strain profiles only from the apical four-chamber images.…”

Section: Study Limitationsmentioning

confidence: 99%

Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase

Inoue

Asanuma

Masuda

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Inoue K, Asanuma T, Masuda K, Sakurai D, Higaki J, Nakatani S. Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase. Am J Physiol Heart Circ Physiol 308: H904 -H912, 2015. First published January 30, 2015 doi:10.1152/ajpheart.00530.2014.-Afterload mismatch can cause acute decompensation leading to an occurrence of acute heart failure. We investigated how the left atrium (LA) and left ventricle (LV) react to acute increases in afterload using speckle tracking echocardiography (STE). LA strain and volume were obtained by STE in 10 dogs during banding of descending aorta (AoB). Simultaneously, LA pressure was measured by a micromanometer-tipped catheter. LA peak negative strain during LA contraction, strain change during LA relaxation (early reservoir strain), and that during LA dilatation (late reservoir strain) were obtained from LA longitudinal strain-volume curves. From pressure-strain curves, the areas of A-loop and V-loops were computed as the work during active contraction and relaxation (A-work) and that during passive filling and emptying (V-work). AoB increased LV systolic pressure (105 Ϯ 15 vs. 163 Ϯ 12 mmHg, P Ͻ 0.01) and mean LA pressure (3.8 Ϯ 1.2 vs. 7.1 Ϯ 2.0 mmHg, P Ͻ 0.01). LV global circumferential strain decreased (Ϫ18.8 Ϯ 3.5 vs. Ϫ13.2 Ϯ 3.5%, P Ͻ 0.01), but LV stroke volume was maintained (8.4 Ϯ 2.3 vs. 9.6 Ϯ 3.6 ml). LA peak negative strain (Ϫ2.9 Ϯ 2.3 vs. Ϫ9.8 Ϯ 4.0%, P Ͻ 0.01) and early reservoir strain (4.5 Ϯ 2.1 vs. 7.7 Ϯ 2.4%, P Ͻ 0.05) increased by AoB, but late reservoir strain did not change (8.9 Ϯ 3.4 vs. 6.1 Ϯ 3.4%). A-work significantly increased (3.2 Ϯ 2.0 vs. 19.2 Ϯ 15.1 mmHg %, P Ͻ 0.01), whereas V-work did not change (13.3 Ϯ 7.1 vs. 13.1 Ϯ 7.7 mmHg %). In conclusion, LA external work during active contraction and relaxation increased as compensation for LV dysfunction during aortic banding. Atrial dysfunction may lead failure of this mechanism and hemodynamic decompensation. atrial function; speckle tracking echocardiography; external work ACUTE HEART FAILURE IS A MAJOR cause of hospitalizations and is associated with significant mortality (8, 9). The process of transition from asymptomatic to overt heart failure is complex and incompletely understood. Increased afterload is one of the key triggers for the sudden onset of life-threatening pulmonary edema. An acute increase of blood pressure results in a preload recruitment to maintain left ventricular (LV) stroke volume according to the Frank-Starling mechanism (21), and the left atrium (LA) immediately reacts to the hemodynamic overload by enhancing LA contraction and relaxation. Accordingly, the failure of LA adaptation leads to a decompensated state of heart failure (15).Echocardiography plays an important role in the assessment of LA structure and function. In an experimental study, Barbier et al.(1) measured LA reservoir function by calculating the expansion rate of the LA area with automated border detection echocardiography. That study identified the determinant...

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Influence of Pentobarbital and Chloralose Anesthesia on Quinidine-Induced Effects on Atrial Refractoriness and Heart Rate in the Dog

Cited by 16 publications

References 0 publications

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase

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Influence of Pentobarbital and Chloralose Anesthesia on Quinidine-Induced Effects on Atrial Refractoriness and Heart Rate in the Dog

Cited by 16 publications

References 0 publications

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Efficacy of pentamidine analogue 6 in dogs with chronic atrial fibrillation

Neuronal Na v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase

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Product

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Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention