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At least 19 recordsLinked to original sources
PubMedDate not supplied

Time couse of the blockade effect of propranolol on sinus node and atrioventricular node.

The time course of the blockade effect of propranolol on the sinus node (SN) and the atrioventricular node (AVN) was studied in six normal volunteers. Serial isoproterenol infusions were done before and after oral propranolol administration, 160 mg daily for two days. The inhibition by propranolol of the heart rate increases due to isoproterenol was used to assess the blockade of the sinus node, and the diminution by propranolol of the shortening in the PR interval due to isoproterenol was used to assess the blockade of the atrioventricular node. The blockade effects on the sinus node and the atrioventricular node were identical and persisted more than 24 hours. There was no good relationship between plasma propranolol and blockade effect on sinus node and/or atrioventricular node as propranolol was no longer detectable in the plasma 24 hours after the last dose. A transient hypersensitivity to isoproterenol was present 36 to 48 hours after propranolol withdrawal. The explanation of these phenomena most likely lies in the peculiar nature of beta-adrenergic receptors.

Adult↗
PubMed1979

Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart.

We used intracellular microelectrodes to study the effects of hypoxia on the isolated, superfused sinoatrial (SA) node, atrium, and atrioventricular (AV) node of the rabbit heart. Hypoxia decreased the rate of spontaneous impulse initiation in SA nodal fibers by decreasing the slope of diastolic depolarization. With gradually decreasing Po2, the sinus rate was reduced; concomitantly, the corrected sinus node recovery time after rapid atrial stimulation was much less affected demonstrating marked prolongation only under severe anoxic conditions. Hypoxia decreased the amplitude of action potentials of the SA node and of the AV node but not of the atrium. SA and AV nodal conduction were slowed by hypoxia; intraatrial conduction was not significantly affected. AV nodal conduction block occurred at lower atrial rates, and the effective refractory period of the AV node was prolonged. Inhomogeneity of SA and AV nodal impulse propagation often was observed in the presence of hypoxia. This was associated with concealed reentry within both nodal areas. The extracellular K+ concentration of the atrial tissue was measured with ion-sensitive microelectrodes. [K+]o remained unchanged even after prolonged periods of severe hypoxia. These results are consistent with the hypothesis that acute hypoxia predominantly inhibits slow response activity but has only little effect on the fast inward sodium current.

Action Potentials↗
PubMed1979

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).

Adult↗
PubMed1979

Morphology of the atrioventricular node, bundle and proximal bundle branches: a study employing computerized reconstruction.

The morphology of the human atrioventricular node, atrioventricular bundle and bundle branches is described. A block of tissue bounded by the ostium of the coronary sinus, the pars membranacea, the septal leaflet of the tricuspid valve and the atrial and ventricular septa is removed. The block is then sectioned serially from the right endocardial surface in the frontal plane of the heart. Sectioning in this way produces fewer sections than from techniques previously described. Outlines of the atrioventricular node, atrioventricular bundle and proximal bundle branches are digitally registered and stored in a computer. Three dimensional reconstructions of the structures are then generated by computer and displayed on an oscilloscope so that the entire three dimensional image can be rotated in any plane. Stereoscopic image pairs are produced to assist perception of the shape of the atrioventricular node, bundle and branching patterns of the bundles. This technique is unique in that it describes a method from which a relatively small number of histologic sections are generated permitting not only a complete histologic examination, but also a study of the morphology of the area.

Adult↗
PubMed1978

Dissociation of the atrioventricular node in acute inferior wall myocardial infarction. 2. Longitudinal dissociation (dual atrioventricular nodal pathways).

Four cases of longitudinal dissociation of the atrioventricular node, with dual pathways developing during the acute phase of an inferior wall myocardial infarction (three cases) or during acute ischemia (one case), are presented. In all four cases, two grossly different P-R intervals were recorded, and in two cases, studies of the His bundle confirmed the location of the dissociation within the atrioventrcular node. In one case, premature atrial depolarization caused a bidirectional shifting of P-R intervals, while in the remaining three cases, premature ventricular depolarization (spontaneous or pacemaker-induced) was responsible for this phenomenon. In all cases, evidence of longitudinal dissociation of the atrioventricular node appeared during the acute phase of the infarction or ischemia, and in all of them the phenomenon was transient. This favors the assumption that this phenomenon is of a functional nature, most probably related to the ischemic lesion of the atrioventricular node.

Acute Disease↗
PubMed1979

Reentry within the atrioventricular node: surgical cure with preservation of atrioventricular conduction.

Paroxysmal supraventricular tachycardia (PSVT) is commonly caused by reentry within the atrioventricular (AV) node. This arrhythmia was abolished by operative dissection of the AV junction in a patient with disabling tachycardia that was not controlled by drugs. The operation was intended to create complete AV block, but AV conduction persisted after surgery. An electrophysiologic study 1 year after the operation revealed that the operation changed AV conduction in both the antegrade and retrograde directions, which may explain the absence of tachycardia. The patient has been free of arrhythmias for 18 months.

Atrioventricular Node↗
PubMed1979

Multilevel block in the atrioventricular node during atrial tachycardia and flutter alternating with Wenckebach phenomenon.

The electrocardiograms of 100 patients with rapid and regular PP intervals during atrial arrhythmias (because of atrial tachycardia or flutter, or pacing) were examined for periods of irregular atrioventricular conduction. This irregular conduction corresponds to an alternating Wenckebach phenomenon, of a type that can be determined from simple rules. The different types of conduction encountered in different patients and the changes seen in the same patient suggest that the atrioventricular node functions physiologically with 3 levels of sequential block. The different prevalence of the 2 types of alternating Wenckebach block may reflect functional differences at the level of the atrioventricular node.

Atrial Flutter↗
PubMed1978

Dissociation of the atrioventricular node in acute inferior wall myocardial infarction. 1. Transverse dissociation (alternate Wenckebach periods).

Two cases of alternate Wenckebach periods developing during the acute phase of inferior wall myocardial infarction are presented. In both cases, syncope occurred and severe bradyarrhythmia was recorded on the day of admission. Electrophysiologic study performed in one patient and a narrow QRS complex in the other patient during the alternate Wenckebach periods confirmed the atrioventricular node as the level of block. Transverse dissociation of the atrioventricular node with two (or more) levels of block is the most acceptable explanation for this phenomenon. We suggest that alternate Wenckebach periods occurring during the acute phase of inferior wall myocardial infarction is a severe bradyarrhythmia, and prophylactic temporary pacing is recommended.

Acute Disease↗
PubMed1977

Positive dromotropic effect of dibutyryl cyclic adenosine 3',5'-monophosphate on the atrioventricular node.

The effect of atrioventricular (A-V) conduction of N6-2'-0-dibutyryl cyclic 3',5'-adenosine monophosphate (dibutyryl cyclic AMP) was investigated in comparison with those of norepinephrine, cyclic 3',5'-adenosine monophosphate (cyclic AMP), adenosine-5'-monophosphate (5'-AMP), and adenosine by the use of the isolated, blood-perfused A-V node preparation of the dog. Single injections of dibutyryl cyclic AMP (3-300 micronmol) and norepinephrine (0.1-1 nmol) into the posterior septal artery of the preparation (the upper part of the A-V node is mainly perfused through this artery) produced a dose-dependent decrease in the A-V conduction time. The time to the peak effect and the duration of the effect of dibutyryl cyclic AMP were much longer than with norepinephrine. The positive dromotropic effect of dibutyryl cyclic AMP was resistant to the beta-adrenoceptor blocking action of propranolol. Unlike dibutyryl cyclic AMP, cyclic AMP (above 30 nmol), 5'-AMP and adenosine (above 1 nmol) injected into the posterior septal artery prolonged the A-V conduction time in a dose-dependent manner. The results indicate that dibutyryl cyclic AMP has a mode of action on A-V nodal cells which differs distinctly from that of either norepinephrine or cyclic AMP, 5'-AMP, and adenosine.

Adenosine↗
PubMed1979

Ultrastructure of the atrioventricular node of the big brown bat, Eptesicus fucus.

This investigation describes the ultrastructure of the atrioventricular node of Eptesicus fuscus. Two conducting cells types (nodal and transitional) are indentified which differ in location, myofibrillar content, and types of intercellular junctions. Centrally located nodal cells display variable staining intensity and contain disorganized myofibrils which rarely form sarcomeres. Desmosomes and nexus-like junctions connect the nodal cells. Transitional cells, situated peripherally, exhibit distinct sarcomeres and are attached to the adjacent cells through desmosomes and underdeveloped intercalated discs. Longitudinal arrangement of the mitochondrial cristae is frequently seen in both cells types. In the connective tissue stroma, numerous capillaries (with micropinocytotic vesicles), axons, and possibly axonal terminals, some filled with vesicles, are observed. A large ganglionated nerve trunk is present on the nodal periphery. True nexuses and neuromuscular junctions are not observed. It is suggested that nodal cell types previously reported in different vertebrates under various names are merely simple variations of the two basic types of conducting cell--nodal and transitional. No interspecific differences are observed between these cells of the big brown bat compared with those in other vertebrates.

Animals↗
PubMed1978

[Electrophysiological demonstration of more structures in the atrioventricular node (author's transl)].

Three types of atrioventricular nodal conduction curves, relating A1A2 to H1H2, generated with atrial extrastimulus technique, are known. The first type is smooth, suggesting the homogeneous structure of A-V node. The second type, with abrupt increase in H1H2 response over a critical range of A1A2 coupling intervals, suggests the presence of fast and slow A-V nodal pathways. We have found in five patients the third tipe of A-V conduction curve, giving evidence of an intranodal final common pathway, distal to the fast and slow A-V nodal pathways. The thyrd type of curve enables us to know also some alectrophysiological properties of final common pathway. Indeed we have defined effective and functional refractory periods of fast, slow and final common pathways as far as we can in this type of curve. Paced heart rate variations and atropine medications have led the third type of A-V conduction curve to change into the second type in three cases, into first type in one case. These changes of A-V nodal conduction curves are related to different influence of cardiac cycle lenghts and autonomic nervous system on refractory periods and conduction velocity of the outlined intranodal structures.

Adolescent↗
PubMed1978

Corpora amylacea in mesothelioma of the atrioventricular node.

Rounded or polyhedral, acellular, dense lamellated structures were seen within gland-like spaces in a case of atrioventricular mesothelioma. These structures exhibited many of the histochemical characteristics of amyloid, viz., pink colour with green birefringence and bright red fluorescence with alkaline Congo red; ortochromasia and red birefringence with standardised toluidine blue; positive DMAB-nitrite and diazotisation coupling reactions and spontaneous autofluorescence. It is suggested that these bodies are derived from spontaneous assembly or polymerisation of microfibrils of desquamated cells lining the cystic spaces of the tumour as occurs in prostatic corpora amylacea. The peculiar intramyofibre proliferation of tumour cells in the peripheral part of the tumour suggests that viable tumour cells can penetrate, survive and proliferate within atrial or nodal myofibres leaving an intact sarcolemmal sheath. The slow tumour cell growth and the successive degeneration of central tumour cells may explain the tubular and/or glandular pattern constantly seen in this tumour.

Aged↗
PubMed1978

The effect of nifedipine on the sinus and atrioventricular node of the dog heart after beta-adrenergic receptor blockade.

The effect of nifedipine (BAY 1040), a calcium-antagonistic inhibitor of the electromechanical coupling process was tested on atrioventricular conduction and refractoriness of the dog heart in situ by means of His-bundle electrography and programmed electrical stimulation. The animals were anaesthetized with sodium pentobarbital. As the basic effects of the compound can be altered by release of catecholamines from sympathetic nerves of heart and vessels, the dogs were pretreated with acebutolol, a beta-adrenergic receptor blocking agent, which decreased heart rate and prolonged atrioventricular conduction and refractoriness. Nifedipine 1,6 and particularly 30 microgram/kg body weight increased the heart rate and decreased atrioventricular conduction time during atrial pacing, whereas atrioventricular conduction time during sinus rhythm and atrioventricular refractoriness were only affected by nifedipine 30 microgram/kg. In this respect, nifedipine differs distinctly from another calcium antagonistic compound, verapamil.

Acebutolol↗