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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using His bundle recording techniques, we examined direct and autonomically mediated conduction system effects of quinidine in five cardiac transplant recipients who have anatomically denervated hearts. We made control conduction interval and refractory period measurements, and then infused 10 mg/kg quinidine gluconate over a 20-min period. At 30 min, we determined the electrophysiologic changes induced by quinidine. Quinidine significantly increased the atrial-His (AH) interval (from 97+/-9 [SEM] to 108+/-7 ms, P less than 0.001), the His-ventricular (HV) inteval (from 43.9 +/- 1 to 52.8 +/- 3 ms, P less than 0.01), the donor heart sinus cycle length (from 599 +/- 38 to 630 +/- 56 ms, P less than 0.08), and the atrial effective refractory period (from 214 +/- 14 to 241 +/- 11 ms, P less than 0.01). Quinidine significantly decreased the innervated, remnant atrial sinus cycle length (from 847 +/- 104 to 660 +/- 96 ms, P less than 0.01) and the blood pressure. The mean plasma concentration of quinidine at the time that electrophysiologic measurements were repeated was 4.37 +/- 0.449 micrograms/ml. We conclude that quinidine's predominant sinus nodal and atrioventricular nodal effects in man are autonomically mediated and opposite to its direct actions upon these structures. On the other hand, quinidine's prevailing effect on atrial refractoriness and His-Purkinje conduction in man is direct.
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PMID:The electrophysiologic effects of quinidine in the transplanted human heart. 32 Feb 27

Despite the prevalence of digitalis usage in children, the electrophysiologic effects of digitalis on sinoatrial (S-A) nodal function is unknown in this age group. The purpose of this study was to determine the effect of digitalis on sinoatrial conduction time as well as on S-A nodal automatically. Ten subjects (mean age 10.5 years) underwent electrophysiologic assessment of S-A nodal function before and 30 minutes after administration of ouabain (0.01 mg/kg). Total S-A conduction time increased in each subject and the mean value after ouabain (182 msec +/- 13 standard errors of the mean [SEM]) was significantly higher (P less than 0.01) than before (149 msec +/- 11). The sinus cycle length was variable after ouabain (P greater than 0.1). The corrected sinus nodal recovery time also was variable (P greater than 0.1), decreasing substantially in three subjects. Mechanisms of the effect of digitalis on the S-A node and atrium are proposed and discussed. It is concluded that digitalis prolongs the S-A conduction time in children with normal S-A nodal function. By prolonging the S-A conduction time, digitalis may artifactually shorten corrected S-A nodal recovery time in some patients.
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PMID:Electrophysiologic effect of digitalis on sinoatrial nodal function in children. 50 38

In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (Ae), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no Ae. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 +/- 32 msec (mean +/- SEM; 10 pts). In contrast, all 21 patients with Ae had intact V-A conduction with mean VABCL of 382 +/- 21 msec (14 pts) (P less than 0.05). Repetitive re-entrance occurred only when Ae conducted to the ventricles. Seven patients had only single Ae. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 +/- 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 +/- 18 msec (8 pts) (P less than 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.
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PMID:The determinants of atrioventricular nodal re-entrance with premature atrial stimulation in patients with dual A-V nodal pathways. 87 18

Transmembrane recordings and surface electrograms were used to evaluate the influence of propafenone on the cellular electrophysiology of isolated neonatal and adult rabbit atrioventricular node (AVN) preparations. An automatic interval of 863 +/- 82 ms (mean +/- SEM, n = 14) in neonates was found to be significantly shorter than the 1510- +/- 205-ms (n = 12) automatic interval observed in adults. Propafenone in a concentration of 5 x 10(-6) M significantly increased the automatic interval of neonatal pacemakers but not that of the adult preparations. These changes in automaticity produced by propafenone were not dependent on the adrenergic receptor-blocking action of the drug. The pacemaker escape time after overdrive pacing was also shorter in the neonate than in the adult. Propafenone prolonged the escape time of the neonatal tissues but not those of the adult. AVN refractory period, A-H interval, and antegrade Wenckebach rate were comparably increased in a concentration-dependent manner in both age groups. The maximum diastolic potential was decreased by propafenone in the neonatal atrionodal tissue but not in other regions of the AVN and not in any region of the adult AVN. Action-potential duration was increased in all regions of the AVN in both age groups. Action-potential amplitude and maximum upstroke velocity were decreased by propafenone in both age groups. Unlike other excitable tissues of the heart, the action-potential duration of AVN nodal cells increased with decreasing pacing intervals as the pacing interval approached the Wenckebach interval.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Developmental cellular electrophysiologic effects of propafenone on the rabbit atrioventricular node. 128 55

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.
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PMID:Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties. 134 76

The subcellular mechanism of cell-to-cell communication in the natural pacemaker region of the mammalian heart was studied using electrophysiological and immunofluorescence techniques in isolated pairs of rabbit sinus nodal cells. By measuring whole-cell currents using a double patch-clamp approach, it was demonstrated that communication in the sinus node is mediated through gap junctional channels similar to those in other types of adult cardiac cell pairs. Macroscopic sinus nodal junctional resistance had a mean value of 387.9 +/- 97.1 M omega (mean +/- SEM, n = 10) and was greatly increased by superfusion with alkanols. Single-channel junctional conductance could be resolved in three cell pairs. Given their high membrane resistance (1.16 +/- 0.32 G omega, n = 12), the electrical coupling provided by as few as three gap junctional channels between nodal cells will allow for pacemaker synchronization. Further evidence for the presence of the channels was obtained from immunofluorescent double-labeling of desmin and the gap junction protein (connexin43) in sinus nodal tissue as well as in cultured sinus nodal cells. Using antisera against residues 243-257 of the connexin43 protein, a specific staining at the site of cell-to-cell apposition was demonstrated. These data provide direct evidence in favor of electronic coupling as the means for achieving pacemaker synchronization in the rabbit sinus node.
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PMID:Gap junctional channels in adult mammalian sinus nodal cells. Immunolocalization and electrophysiology. 137 58

To evaluate and compare the pathogenesis of pseudo-intimal hyperplasia (PH) of venous and arterial prostheses, a segment of the inferior vena cava (n = 16) or abdominal aorta (n = 16) was substituted by a 3 mm internal diameter polytetrafluoroethylene tube graft (PTFE, 3 cm long, 30 microns in nodal distance) in albino rabbits. At designated time intervals (3-28 days) after the replacement, graft patency was examined and the dry weights of the intraluminal deposits measured as an indicator of the degree of PH. The harvested grafts were then subjected to an ultrastructural analysis by means of light microscopy (LM), and scanning electron and transmission electron microscopy (SEM, TEM). All the grafts remained patent during the entire observation period. The PH judged by the dry weight was significantly more extensive in the venous than in the arterial prostheses. The PH on day 28, observed by light microscopes was apparently most extensive in the mid-portion of venous prostheses but in the arteria prostheses it was mostly seen at the anastomotic sites. The lining of the intraluminal surface of the prostheses with endothelial-like cells observed by SEM was faster and more extensive in venous than in arterial prostheses. The process of PH in venous prostheses observed by TEM may be divided into the following steps: early thrombosis, phagocytosis of the thrombus, appearance of fibroblasts, growth of endothelial-like cells, appearance of smooth muscle cells, and pseudointimal thickening and proliferation of fibroblasts producing collagen fibrils. The process in arterial prostheses was essentially identical to that in venous prostheses but was much slower and less extensive. From these observations, it was concluded that the formation of PH occurs much faster in venous than in arterial prostheses, although the mechanism of PH is mostly identical in venous and arterial prostheses.
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PMID:Ultrastructural analysis of pseudo-intimal hyperplasia of polytetrafluoroethylene prostheses implanted into the venous and arterial systems. 149 39

The effects of selective cardiopulmonary receptor unloading on atrioventricular (AV) conduction were examined in 7 patients undergoing electrophysiologic testing. During -35 mmHg lower body negative pressure (LBNP) before autonomic blockade with propranolol and atropine, the AV-nodal conduction time (AH interval), the effective and functional refractory periods of AV node decreased at paced cycle length, when systemic arterial and central venous pressures decreased and heart rate increased. These responses to -35 mmHg LBNP except reductions in systemic arterial and central venous pressures disappeared after autonomic blockade. During -10 mmHg LBNP before autonomic blockade, both effective and functional refractory periods of AV node at paced cycle length decreased by 11 +/- 3% (mean +/- SEM) and 6 +/- 1% respectively with the reduction of central venous pressure while AH interval, systemic arterial pressure and heart rate remained unchanged. After autonomic blockade, -10 mmHg LBNP reduced central venous pressure but all the other parameters remained unchanged. These results suggest that cardiopulmonary baroreceptors participate in the reflex control of AV nodal refractoriness in humans.
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PMID:Reflex control of atrioventricular nodal refractory periods by cardiopulmonary receptors in humans. 157 2

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.
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PMID:Vagal modulation of the rate-dependent properties of the atrioventricular node. 217 1

The effects of indecainide, previously shown to be a class 1c antiarrhythmic drug restricting fast inward current, have been studied on rabbit sinoatrial (SA) node and atrioventricular (AV) node. Indecainide at concentrations up to 2.9 mumol/L in 5 preparations did not produce a sinus bradycardia, nor reduce the maximum rate of rise of the intracellular action potential of sinus node cells, but it did antagonize the tachycardia induced by increasing the extracellular calcium concentration. Indecainide slightly prolonged AV conduction time [from 49.07 +/- 4.43 ms to 57.37 +/- 0.90 ms at 2.9 mumol/L (means +/- SEM in four preparations)], but this small delay could be attributed to slowing of conduction in atrial fibres leading to the node, rather than to an effect on the AV nodal cells themselves. It is concluded that indecainide does not block channels carrying inward calcium current in nodal tissues.
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PMID:The effects of indecainide, a new antidysrhythmic drug, on nodal tissues in the isolated rabbit heart. 241 71


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