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PubMedDate not supplied

Preatrial activity recorded by intracavitary and transthoracic techniques.

Two methods to record preatrial activity, that is, sinus node potential are presented. One, during right atrial catheterization through an electrode catheter, and the other, using transthoracic recordings with a high amplification and derivation of the electric signals. The sinus node potential duration represents the sino-atrial conduction time (SACT), a useful parameter for the sinus node function evaluation.

Atrial Function↗
PubMed2006

Substrate mapping to detect abnormal atrial endocardium with slow conduction in patients with atypical right atrial flutter.

OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter. BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear. METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones. RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 +/- 0.3 cm and mean voltage at the isthmus was -0.91 +/- 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 +/- 0.18 m/s vs. 1.14 +/- 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%). CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.

Adult↗
PubMed1985

The conduction and cardiac sympathetic systems: metabolic aspects.

Compared with the myocardium, glycolytic enzymes are reduced by 50% and mitochondrial enzymes and space by 70% in the conduction system of the calf heart. In addition, on the basis of adenosine triphosphate activities energy demands are reduced by more than 50%; this is in parallel with the reduction in myofibrillar space. The increased tolerance of the conduction system against ischemia can be explained by a reduction of energy demands and a higher proportion of (anaerobic) glycolytic as opposed to aerobic mitochondrial energy production. Among the structures of the conduction system, the sinoatrial and atrioventricular nodes are markedly susceptible to hypoxia in contrast to atrial conduction and ventricular conduction by way of the His-Purkinje system. In the isolated perfused rat heart, an increased net release of noradrenaline during the first 10 minutes of ischemia is only noted after sympathetic stimulation. During this phase, catecholamine overflow is limited by the activity of the neuronal reuptake. At a later second phase, from 15 to 40 minutes after the onset of ischemia, the mechanism of noradrenaline net release is carrier-mediated efflux inhibited by neuronal uptake blocking agents. During the third phase of ischemia, after about 40 minutes, spontaneous noradrenaline release is greatly augmented, probably as a result of leakage caused by membrane damage.

Animals↗
PubMed1991

[Induction of ventricular tachycardia by esophageal stimulation. Apropos of 2 cases].

The utility of transesophageal atrial pacing in sustained left ventricular tachycardia is reported in two cases. A 46 year old man without any apparent cardiac disease presented with invalidating but undocumented palpitations. Transesophageal atrial pacing with isoproterenol infusion induced wide complex tachycardia with a right bundle branch block morphology and left axis deviation. Atrio-ventricular dissociation was observed and it was possible to reduce the ventricular complex width by rapid transesophageal atrial pacing: the tachycardia was terminated by an injection of verapamil. It was not possible to reinduce the tachycardia after treatment with atenolol 100 mg/day, introduced because of the catecholinergic nature of the arrhythmia. The patient is symptom free after 2 years of treatment with this drug. Regular wide complex tachycardia with right bundle branch block and left axis deviation without any detectable atrial activity was recorded in a 50 year old man without known cardiac disease. Transesophageal atrial pacing with isoproterenol infusion induced an identical tachycardia. The tachycardia started after a normally conducted atrial extrastimulus followed by ventriculo-atrial dissociation and it was possible to overdrive with atrial pacing. The tachycardia could not be reinduced after treatment with atenolol and the patient is asymptomatic 12 months later. These reports show that it is possible to study certain ventricular tachycardias by transesophageal atrial pacing. The efficacy of antiarrhythmic therapy can be controlled simply by this non-invasive technique.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

[Comparative study of endocavitary recording and the 24-hour electrocardiogram in the study of sinus function. Apropos of 174 cases].

We compared the results of electrophysiological investigations of sino-atrial node function in a series of 174 patients (including the sino-atrial conduction time (SACT) according to the method of Narula and Strauss, the corrected sino-atrial recovery time (CSART) and, in, 22 patients, the atropine test) with the results of 24 hour Holter monitoring. 73 patients presented a pathological Strauss curve, 47 had a prolonged SACT (Strauss' method) and 19 had a pathological CSART. Of the 22 bradycardic patients, the injection of atropine relieved the bradycardia in 45.5 per cent of cases. 19 patients showed signs of sino-atrial node dysfunction on the 24 hour Holter recording. Of the 35 patients with a surface electrocardiogram (ECG) suspicious of sino-atrial node dysfunction, 21 (60%) had a prolonged SACT and 13 (37.1%) had a pathological CSART: 15 of them (42.8%) showed major electrophysiological abnormalities and 19 (54.3%) had a positive Holter. In two-thirds of the cases of pure sino-atrial bradycardia, the results of electrophysiological and Holter investigations were normal; in 50 per cent of cases of sino-atrial block and/or pause on the surface ECG, major abnormalities were found on both electrophysiology and the Holter monitor. The SACT, estimated according to the method of Strauss, is discorsdant with the SACT estimated according to Narula's method in 46 p. cent of cases. It seems that Strauss' SACT was more sensitive in our study. In 102 cases (59.3%), the SACT and the CSART were concordant. In 10 cases, the SACT was normal while the CSART was pathological and in 42 cases, the SACT was pathological while the CSART was normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Electrophysiologic studies in atrial fibrillation. Slow conduction of premature impulses: a possible manifestation of the background for reentry.

Extrastimulus-induced intraatrial conduction delays were measured in 12 patients with documented episodes of atrial fibrillation (AF) by recording atrial electrograms at the high right atrium, His bundle region, and coronary sinus. Seventeen patients with and without heart disease, but without atrial arrhythmias served as the control group. During baseline-paced atrial rhythms, a conduction delay zone could be delineated, near the atrial effective refractory period, during which all extrastimuli produced conduction delays. When compared at the same paced cycle lengths (500 to 650 ms), the patients with AF had shorter atrial effective refractory periods (mean +/- standard deviation 206 +/- 24.1 versus 233 +/- 28.2 in control patients, p less than 0.02), wider conduction delay zones (79 +/- 21.7 ms versus 52 +/- 21 in control patients, p less than 0.01), and longer conduction delays both to the His bundle region (64 +/- 18.3 ms versus 35 +/- 21.7 in control patients, p less than 0.005) and the coronary sinus (76 +/- 18.9 ms versus 35 +/- 16.1 in control patients, p less than 0.001). Repetitive atrial responses were recorded in 6 patients with AF and in 9 control subjects. Sinus nodal function abnormalities were detected in 6 of the patients with fibrillation. Patients with AF had a higher tendency than control subjects to develop slow intraatrial conduction, as well as shorter effective refractory periods. Since both features would favor reentry, they may be the electrophysiologic manifestations of the abnormalities making these patients prone to atrial reentrant arrhythmias. Repetitive atrial responses were of no predictive value. Sinus nodal dysfunction was frequently found, but was not essential for the occurrence of AF.

Adult↗
PubMed1981

Mechanism of generation of body surface electrocardiographic P-waves in normal, middle, and lower sinus rhythms.

We used comprehensive electrophysiological/anatomical digital computer models of atrial excitation and the human torso to study the mechanisms of generation of body surface P-waves in normal sinus rhythm, and in middle and lower sinus rhythm. Simulated atrial surface isochrone maps for normal sinus rhythm support the validity of the atrial excitation model. The results suggest that the presence of specialized internodal tracts containing fast-conducting fibers is not essential to account for propagation of excitation in apparent preferential directions from the sinoatrial (SA) node to the atrioventricular node. However, in the absence of fast conducting fibers, a slowly conducting segment in the intercaval region is necessary to achieve proper excitation of the interatrial septum. P-wave notches occur in the absence of specialized fast conducting atrial tracts and anisotropies due to fiber orientation. These notches are due to the atrial geometry and the separate contributions of the right atrium, left atrium, and interatrial septum to the P-waves, and become more pronounced as the pacemaker site shifts downward in the SA node. Thus, slight changes in the origin of excitation, which result in subtle changes in the atrial excitation isochrones, produce significant and complex changes in the simulated body surface P-waves.

Adult↗
PubMed1997

Functional mechanisms underlying tachycardia-induced sustained atrial fibrillation in a chronic dog model.

BACKGROUND: Rapid atrial activation causes electrical remodeling that promotes atrial fibrillation (AF), but underlying mechanisms are incompletely understood. We applied epicardial mapping to evaluate atrial electrophysiology and AF duration in dogs subjected to rapid atrial pacing (400/min). METHODS AND RESULTS: Dogs paced for 1 (P1, n=7), 7 (P7, n=13), or 42 (P42, n=7) days were compared with sham dogs (P0, n=13). Atrial pacing progressively increased AF duration. Atrial effective refractory period (ERP) and ERP accommodation to rate were significantly decreased by pacing, with near-maximal changes within 7 days. Atrial conduction velocity decreased more slowly, with maximum changes at 42 days, contributing to increases in AF duration after ERP stabilized. Stepwise multilinear regression indicated that both wavelength (P=.02) and duration of pacing (P=.0001) were independent determinants of changes in AF duration. Mean atrial fibrillation cycle length (AFCL) at 112 recording sites decreased with increased duration of rapid pacing (P<.001), and the SD of AFCL increased progressively (P<.0001), together accounting for 72% of the variance in AF duration. Increases in AFCL variability were due to regionally determined differences in AFCL changes caused by rapid pacing. The number of zones of reactivation per cycle of AF increased as AF became more sustained, consistent with multiple-wavelet reentry. CONCLUSIONS: Rapid atrial activation causes time-dependent decreases in ERP, conduction velocity, and wavelength, which, along with increased regional heterogeneity, provide a substrate for AF. The conduction abnormalities and increased regional heterogeneity previously noted in patients with AF may be a consequence, as well as a cause, of the tachyarrhythmia.

Animals↗
PubMed2003

Feasibility of atrial sensing via a free-floating single-pass defibrillation lead for dual-chamber defibrillators.

BACKGROUND: Detection and misclassification of rapidly conducted atrial fibrillation (AF) and marked sinus tachycardia by implantable cardioverter defibrillators (ICD) can result in the delivery of inappropriate therapies. Continuous atrial sensing may improve the differentiation between supraventricular and ventricular tachycardia. The present approach is to implant a separate atrial pacing lead connected to a dual-chamber defibrillator. We hypothesized that a free-floating single-pass defibrillation lead reliably senses the atrial electrical activity. The aim of the study was to assess during implantation the efficacy of a custom-built free-floating single-pass defibrillation lead and to record sinus rhythm (SR), induced AF, and atrial flutter (Afl). METHODS: The free-floating single-pass defibrillation lead (Biotronik, Berlin, Germany) had an atrial bipole with 10 mm spacing and a distance between the atrial bipole and the electrode tip of 13.5, 15 or 17-cm. The lead was temporarily implanted in 15 patients during an ICD implantation. Fifteen seconds recordings were made during SR and after the induction of AF and Afl as well as during induced ventricular fibrillation. The amplitude and the time that the amplitude was less than 0.3 mV were assessed. RESULTS: The amplitude during SR (2.1 +/- 1.4 mV) was significantly higher compared with the amplitudes for Afl (1.3 +/- 0.5 mV; p < 0.02) and AF (0.7 +/- 0.5 mV; p < 0.001). Low amplitudes were not observed during SR and rarely during Afl (1.6 +/- 3.1%), but they were observed 19.9 +/- 15.9% of the time during AF (p < 0.05). The correlation coefficients between SR and AF amplitudes were r = 0.25, between SR and Afl amplitudes r = 0.31, and between AF and Afl amplitudes r = 0.41. During the ventricular fibrillation conversion test 9 patients were in continuous SR. The P-wave amplitude before the induction of ventricular fibrillation was 2.1 +/- 1.4 mV. The signal during ventricular fibrillation decreased to 1.1 +/- 0.7 mV and increased immediately after the termination of ventricular fibrillation to 1.6 +/- 0.8 mV. CONCLUSIONS: The recorded unfiltered signals indicate that SR as well as AF and Afl can immediately be detected after the implantation of the new free-floating single-pass defibrillation lead. High signal amplitude during SR did not predict high amplitude during AF or Afl. During induced ventricular fibrillation the P-wave amplitude decreased intermittently.

Aged↗
PubMedDate not supplied

[Ventricular response in atrial fibrillation : normal conduction, consequences of conduction disorders and preexcitation syndromes. Therapeutic implications].

Atrial fibrillation is the most common arrhythmia in man. It is characterized by: 1) a rapid and irregular atrial electrical activity, 2) an irregular ventricular response which follows complex laws in the absence of advanced disorder of atrio-ventricular conduction. The study of these laws of complex transformation which govern the ventricular response can be approached by histograms of the RR interval: the shortest interval between two QRS complexes corresponds approximately to the functional refractory period of the atrio-ventricular conduction pathways--the longest interval corresponds to the maximal intranodal hidden conduction in the central part of the node. Depending on the values obtained and the morphological type of the distribution, we can diagnose all degrees of atrio-ventricular conduction disorders. This has great practical significance in patients receiving or about to receive cardiotonics or antiarrhythmics. In the same way, in cases of pre-excitation syndrome, this method can be used to evaluate the refractory period of the accessory pathway and to guide treatment.

Atrial Fibrillation↗
PubMed1997

The relationship between the sinus node and the right atrial appendage.

BACKGROUND: The developmental anatomy of the right atrium, particularly the union between its sinus venarum (sinus) and atrial portions, has not been completely settled. Invagination of the embryonic sinus into the atrium brings about electrical and structural union between these primitive chambers but results in the formation of the terminal crest, a seemingly bulky and intrusive band of muscle separating sinus from atrium. However, it is unlikely that a structure that can be found in all mammalian species is merely a functionless remnant. Structural differences between the smooth sinus and the deeply trabeculated right atrial appendage emphasize the two-part shape of the right atrium, but it is hypothesized that the sinus and atrium form a single, well-knit chamber shaped for the supply of nutrient blood to atrial conducting tissues rather than for downstream bloodflow. METHODS AND RESULTS: The morphology of the right atrium was studied grossly and microscopically in 54 adult hearts. The distribution of Thebesian sinusoids arising from the right atrial appendage was identified by ink perfusion and clearing of several additional adult and fetal hearts. The sinus node was found to be precisely co-extensive with the undercut portion of the terminal crest and with pectinate muscles lining the pyramidal portion of the right atrial appendage. Sinusoids and interpectinate spaces related to the undercut portion of the terminal crest are limited to the area of the sinus node. CONCLUSION: These findings support the hypothesis that the right atrial appendage, pectinate muscles and terminal crest evolved to supply nutrient blood to conducting myocardium of the sinus portion of the right atrium, and that this chamber, like the right ventricle, is structured as a single and completely finished unit. Interpectinate spaces and Thebesian sinusoids offer clues to the location of conducting pathways, including the sinus node.

Adolescent↗
PubMed2002

[Role of atrial stimulation in the treatment of paroxysmal atrial fibrillation].

Preventive treatments for atrial fibrillation by stimulation have been developed for several years now, mainly due to the relative failure of anti-arrhythmic treatments. They are based on the hypothetical effects of stimulation by controlling cardiac frequency, abolishing bradycardia-dependent extrasystoles, by the inhibition of atrial automatic foci with "overdrive", and by the modification of intra- or inter-atrial conduction delays as well as by remodelling the arrhythmogenic substrate. It is clear that an undeniable effect exists for the prevention of atrial fibrillation, even for the risk of cerebral vascular accident, by physiological stimulation (DDD/DDDR) compared to pure ventricular stimulation (VVI/VVIR) in a heterogenous global population of stimulated patients. For the moment, there is not sufficient proof of a positive effect for the emerging sites of cardiac stimulation, either atrial mono-site or double site in the populations at high risk of atrial fibrillation, with or without associated bradycardia. Some new prevention algorithms by "overdrive" are under development but for the moment only a few preliminary studies seem to show a slight benefit. It is clear that at present stimulation should be reserved only for cases of atrial fibrillation associated with a classic indication for implantation. In these patients it is recommended to position the probes in an optimal manner in order to counteract conduction disorders, choosing an adapted double chamber stimulator with prevention algorithms. That said, the patient should be clearly warned that the long term success rate is no more than 50%.

Algorithms↗
PubMed1984

Effects of chlorpromazine on the isolated perfused guinea pig heart.

Chlorpromazine altered the mechanical and electrical activity of the isolated perfused guinea pig heart. While its effects on coronary flow were variable, chlorpromazine increased resting diastolic isometric tension and decreased the isometric systolic tension developed by spontaneously beating hearts. Heart rate was also decreased. The drug depressed conduction through the His-Purkinje system and ventricular muscle to a greater extent than it did atrial conduction time and AV nodal conduction time. From our data, we concluded that the greatest depressant action of chlorpromazine on the electrical activity of the isolated perfused guinea pig heart occurred within the specialized ventricular conduction system and ventricular muscle.

Animals↗
PubMed1980

Wolff-Parkinson-White syndrome type B with tachycardia-dependent (phase 3) block in the accessory pathway and in left bundle-branch coexisting with rate-unrelated right bundle-branch block.

A patient with Wolff-Parkinson-White syndrome type B developed 2:1 atrioventricular block resulting from the association of persistent right bundle-branch block with tachycardia-dependent (phase 3) left bundle-branch block. Electrophysiological studies disclosed the coexistence of a tachycardia-dependent (phase 3) block in the accessory pathway. This conduction disturbance was exposed, not by carotid sinus massage as in previous studies, but by pacing-induced prolongation of the interval between two consecutively conducted atrial impulses. Furthermore, the surface electrocardiogram showed, at different times, ventricular complexes resulting from: (1) exclusive atrioventricular conduction through the normal pathway without bundle-branch block; (2) predominant, or exclusive, atrioventricular conduction through a right-sided accessory pathway; (3) exclusive atrioventricular conduction through the normal pathway with right bundle-branch block; (4) exclusive conduction through the normal pathway, with left bundle-branch block; (5) fusion between (1) and (2); and finally, (6) fusion between (2) and (3) However, QRS complexes resulting from simultaneously occurring Wolff-Parkinson-White syndrome type B and left bundle-branch block could not be identified. Future electrophysiological investigations should re-evaluate the criteria used to diffrentiate between true and false patterns of Wolff-Parkinson-White syndrome type B coexisting with left bundle-branch block.

Bundle-Branch Block↗
PubMed1988

Acute effects of cocaine on catecholamines and cardiac electrophysiology in the conscious dog.

To evaluate the electrophysiologic and neurohumoral effects of cocaine on the sinus node, atrium, atrioventricular node, and His-Purkinje system, 14 conscious dogs were studied before and after an infusion titrated to maximum tolerance or to increase the systolic blood pressure by at least 15%. Plasma cocaine and catecholamine levels, blood pressure, surface and intracardiac electrograms were recorded. Programmed electrical stimulation was performed from the right atrium. The sinoatrial conduction time, paced PR interval, atrioventricular nodal conduction time, atrioventricular nodal effective refractory period and blood pressure increased. Plasma noradrenaline, adrenaline and dopamine increased and remained at two to three times control levels throughout the study although plasma cocaine levels declined. Adrenaline levels were strongly correlated with the hemodynamic response while plasma cocaine levels were not. No sustained spontaneous atrial or ventricular arrhythmias were recorded after cocaine infusion. Atrial fibrillation with a slow ventricular response was induced by pacing after cocaine in only three dogs. There were no significant changes in pacing threshold, right intra-atrial conduction time, infranodal conduction time, heart rate, QRS or QT. No pacing induced infranodal block occurred. The cocaine dose rate infused was 2.8 +/- 1.2 mg/kg; cocaine plasma levels were 1402 +/- 885 ng/mL immediately after the initial infusion and 525 +/- 321 ng/mL at the end of the study. It is concluded that in normal canine heart cocaine increases blood pressure, sinoatrial conduction time, atrioventricular nodal effective refractory period, paced PR interval, atrioventricular nodal conduction time, plasma catecholamines and susceptibility to atrial fibrillation. These findings cannot be explained solely by increased sympathetic nervous system activity and suggest participation of the parasympathetic nervous system.

Animals↗
PubMed1979

[Chronic idiopathic binodal block. Occurrence, course and pathogenesis].

The incidence of binodal, sinoatrial (SA) and atrioventricular (AV), block was determined in a series of 362 patients, 90 of whom had chronic sinoatrial block (group I), 162 suprahisian, infrahisian or diffuse AV block (group II), 38 with paroxysmal supraventricular tachycardia (group III), and 70 with slow atrial fibrillation, 54 of whom were studied in sinus rhythm (group IV). Electrophysiological investigation revealed: overt or latent AV block in 71% of group I, 48% of group III, and 100% of group IV; overt or latent SA block in 40 to 61% of group II, 87% of group III and 78% of group IV; paroxysmal atrial fibrillation in 61% of group I, 25% of group II and 50% of group IV; intra-atrial block in 26% of group I, 20% of group II, 16% of group III and 31% group IV. An ECG syndrome associating binodal block and disturbances or atrial conduction and excitability is suggested. The pathogenesis and anatomical basis are discussed, the prime lesion of which may be fibrosis of the atrial tissues which may ultimately result in partial or total atrial standstill.

Adult↗
PubMed1987

[Function of the heart conduction system in patients with progressive muscular dystrophy].

Intracardiac electrophysiologic studies were carried out in 9 patients with progressive muscular dystrophy. Diagnostic stimulation of the heart demonstrated no sinus mode dysfunction. The intra-atrial conduction time increased to 72 +/- 7.1 ms (p less than 0.05), and the interatrial conduction time, to 97 +/- 12.5 ms (p greater than 0.05) in response to shortened testing stimulus delay in 3 patients. All 9 patients showed great variation in the duration of effective refractory atrial and atrioventricular periods (97.0 +/- 12.5 ms). The H-V interval increased from 43.9 +/- 4.3 to 73.9 +/- 7.6 ms (p less than 0.01) in response to shortened delay in 7 of 9 patients. Atrial pre-excitation resulted in a block of the right and left limbs of the His bundle in 5 of 7 patients. Third-degree atrioventricular block was recorded by continuous ECG monitoring in 7 patient. It is suggested that an apparent or latent intraventricular conductivity disorder may be present in most cases of progressive muscular dystrophy.

Adolescent↗
PubMed1997

Effects of 2,3-butanedione monoxime on atrial-atrioventricular nodal conduction in isolated rabbit heart.

INTRODUCTION: 2,3-Butanedione monoxime (BDM) has been found to reversibly block cardiac contraction, without blocking electrical conduction. This study characterizes the dose-dependent effects of BDM on the conduction through the atrioventricular node (AVN) of rabbit heart. METHODS AND RESULTS: Thirteen isolated atrial-AVN preparations were used in control, during and after exposure to 5, 10, and 20 mM BDM. Anterograde and retrograde pacing protocols were used to obtain the Wenckebach cycle length, effective and functional refractory periods of the AVN, index of AVN conduction delay (the area under the AVN conduction curve), as well as index of intra-atrial conduction delay between the AVN inputs. Compared to control, 5 and 10 mM BDM produced either shortening or no effect on all of the above parameters except a slight (6% and 14%, respectively) increase in the intra-atrial delay. At 20 mM, BDM produced a further increase in the intra-atrial delay (up to 50%) as well as in the retrograde AVN conduction delay (up to 16%), while the characteristics of the anterograde conduction were still improved. The effects of perfusion with BDM on these parameters were reversible after washout. CONCLUSIONS: Aside from its known effect as an electromechanical uncoupler, BDM reversibly altered some of the electrical responses of the AVN. Most of these alterations, however, did not impede but rather improved AVN conduction. Since a dose of 10 mM is sufficient to fully eliminate undesirable motion, BDM should be considered a safe and valuable tool in AVN studies in vitro requiring a mechanically quiescent preparation.

Action Potentials↗