Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of amrinone on conduction in the intact canine heart were studied. Intracardiac His-electrode catheter recordings were used to measure the functional refractory period (FRP) of the AV node and conduction time through the AV node (A2H2 interval) and in the His-Purkinje system (H2V2 interval). Amrinone (2.5 to 10 mg/kg) shortened the FRP and A2H2 in a dose-dependent manner but had no significant effect on H2V2. In hearts where AV conduction was depressed by treatment with verapamil, propranolol, or ouabain, amrinone partially reversed this depression. Amrinone also shortened the recovery time of spontaneous sinoatrial (SA) node activity following a train of rapid atrial stimulation. This effect was also observed after depression of SA nodal recovery with verapamil, propranolol, or ouabain. These results indicate that amrinone enhances AV conduction and SA nodal activity in the normal heart and may favorably influence depressed AV conduction and SA nodal activity induced by a variety of cardioactive agents.
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PMID:Effects of amrinone on atrioventricular conduction in the intact canine heart. 688 27

Ninety-three rapid atrial pacing studies were performed in 38 children to compare preoperative and early postoperative function of the sinus and atrioventricular (AV) nodes. The interval between the preoperative and postoperative studies was under 6 months in the majority of patients. Postoperative studies were performed within 48 hours of operation and between 4 and 8 days after operation. Sinus nodal function as measured by sinus nodal recovery time (SNRT) was an unreliable index in determining depression since the number who improved postoperatively (10/55) was nearly equal to the number that worsened (12/55). The majority who had abnormal function postoperatively demonstrated a junctional rather than sinus recovery focus. This finding appears a more definitive and more reproducible indicator of sinus node depression in the postoperative patient. Postoperative AV nodal function was decreased (as measured by the cycle length [CL] at which Wenckebach periodicity occurred) in 15 of 55 studies (27%) of the entire group. There was nearly an equal chance for improvement (24%) in function. This also applied to those patients who had sequential studies. Therefore, this method of assessment for AV nodal function was unreliable, or else the operation did not affect the node significantly. The latter is unlikely in view of late postoperative data. The greatest utility of this test was to determine the capability for AV conduction in certain patients with slow escape rhythms in the absence of surface P waves, and to differentiate complete heart block from AV dissociation when atrial activity was absent. Despite the variability of effects on the sinus and AV nodes in these patients, those who demonstrated depression had a significantly higher incidence of dysrhythmias (80% of patients with sinus nodal depression and 100% of patients with AV nodal depression).
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PMID:Sinus and atrioventricular nodal function: Preoperative and early postoperative assessment in children. 705 9

1 Melperone, a butyrophenone tranquillizer, caused bradycardia in vivo and in vitro. 2 Although Melperone had alpha-adrenoceptor antagonist activity in the pithed rat, it was not a beta-adrenoceptor antagonist, nor was it a cholinoceptor agonist. 3 The bradycardic action could be attributed almost entirely to a prolongation by Melperone of action potential duration (APD) in sinus node cells, with little effect on the slow diastolic depolarization. 4 APD was prolonged by Melperone in atrial and ventricular muscle, and most of all in the bundle of His, but only moderately in the terminal Purkinje cells. 5 In all cardiac tissues depolarized by fast inward current. Melperone caused a dose-related reduction in the maximum rate of depolarization and conduction velocity. On desheathed frog nerve Melperone had a local anaesthetic potency equal to that of procaine. 6 There was no negative inotropic effect in cardiac muscle, nor interference with A-V nodal conduction, from which it was inferred that Melperone did not restrict slow inward current. 7 Melperone did not reduce hypoxic shortening of APD relative to the initial value at the start of hypoxia, but because APD was already lengthened by Melperone in normoxic conditions, APD90 during hypoxia remained close to normal values. There was no protection against hypoxic depression of contractions. 8 It was concluded that Melperone had class 1 and class 3 antiarrythmic actions and merited trial as an antiarrhythmic drug.
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PMID:Differential actions on rabbit nodal, atrial, Purkinje cell and ventricular potentials of melperone, a bradycardic agent delaying repolarization: effects of hypoxia. 707 78

We evaluated efficacy and mechanisms of the antiarrhythmic action of verapamil in 20 patients with sustained supraventricular tachycardia. Two patients had sinus nodal re-entrant tachycardia, nine atrioventricular (AV) nodal re-entrant tachycardia, and nine AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. The study design comprised a double-blind, randomized, cross-over phase using a 0.075 mg/kg dose of verapamil versus placebo and an open-label phase using a 0.15 mg/kg dose of verapamil. The overall results of both phases showed that 15 of 19 patients converted to sinus rhythm with verapamil while only one of 16 converted to sinus rhythm with placebo. The effective plasma verapamil concentration measured 123 +/- 40 ng/mL (mean +/- SD). Verapamil suppressed sinus nodal and AV nodal re-entry but exerted no selective depression between fast and slow AV nodal pathways. It had no significant effect on accessory AV bypass tract but was effective in terminating AV reciprocating tachycardia by its depressive action on the AV node.
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PMID:Intravenous verapamil for termination of re-entrant supraventricular tachycardias: intracardiac studies correlated with plasma verapamil concentrations. 721 75

Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1:1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na (108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.
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PMID:Peculiarities of AV nodal conduction and the role of slow Na current. 721 99

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.
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PMID:Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia. 723 16

In 36 patients sinoatrial conduction time (SACT) was calculated by the continuous-atrial-pacing technique, first described by Narula et al. (9). Using three different stimulation frequencies, it could be shown that the return cycles A2A3 and the postreturn cycles A3A4 both were linearly correlated with rising stimulation frequency. Thus, if the formula given by Narula et al. was used [SACT = (A2A3 - A1A1) : 2] the calculated SACT-values linearly rose, too, which was caused by a stimulation frequency dependent progressive depression of the sinus nodal automaticity. This interfering influence of sinus nodal depression could be corrected by applying a modified formula for calculation of the SACT, i.e. SACTM = (A2A3 - A3A4) : 2. Thus calculation of sinuatrial conduction time by the modified continuous-atrial-pacing technique represents a method widely applicable in routine electrophysiological testing.
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PMID:[Depression of sinus nodal automaticity during permanent atrial pacing for the determination of the sinoatrial conduction time (author's transl)]. 726 28

Electrophysiologic studies were performed in 14 patients with atrioventricular nodal reentrant paroxysmal tachycardia (PSVT) before and after oral administration of 1.2-1.6 g quinidine sulfate over a 24-hour period (0.3-0.4 g every 6 hours). Studies were performed after 0.5-1 mg i.v. atropine before and after quinidine. All 14 patients had induction of sustained PSVT before quinidine, with or without atropine. After quinidine, 11 patients lost the ability to induce echoes or sustain PSVT, reflecting depression of the retrograde pathway with either absence of atrial echoes (six patients) or induction of nonsustained PSVT, with termination of echoes or PSVT occurring after QRS (block in retrograde pathway) (five patients). In only one of these 11 patients was sustained PSVT inducible after addition of atropine. All 11 were discharged on the same dose of quinidine. In three patients, quinidine was discontinued because of side effects. Follow-up in the remaining eight patients for 8 +/- 2 months showed no recurrence of sustained PSVT. Three of the 14 patients had induction of sustained PSVT after quinidine. Ventricular paced cycle length producing ventriculoatrial block was 314 +/- 7 msec (mean +/- SEM) before and 392 +/- 13 msec after quinidine (p less than 0.01) in the 14 patients, suggesting depression of the retrograde pathway with quinidine. In summary, quinidine inhibited induction of sustained atrioventricular nodal reentrant tachycardia with depression of the retrograde pathway. It is very effective in preventing recurrence of PSVT in most patients.
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PMID:Effects of quinidine on atrioventricular nodal reentrant paroxysmal tachycardia. 727 82

Effects of local anesthetics (procaine, lidocaine, prilocaine, mepivacaine and bupivacaine) on AV conductivity were studied using a direct perfusion technique of the canine AV node artery in situ. The agents induced dose-dependent depression of AV conductivity in doses between 100 microgram and 3 mg. The depression was assumed to have resulted from their direct action on the AV node, since it was not affected by prior administration of atropine or tetrodotoxin into the AV node artery. The order of potency to suppress AV nodal conductivity evaluated from ED50 for causing first to third degrees of AV block was bupivacaine greater than mepivacaine = prilocaine = lidocaine greater than procaine with a relative potency ratio of 5 : 2--2.5 : 1.
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PMID:Comparative study of the action of local anesthetics on AV conductivity of dog heart in situ. 728 50

By means of intracardiac recordings and programmed electrical stimulation of the heart, the combination effect of verapamil and disopyramide on induction of circus movement tachycardia was studied in 8 patients with anomalous extranodal atrioventricular (A-V) pathway. In 4 of 6 patients who manifested reproducible circus movement tachycardia, verapamil, 0.2 mg/kg intravenously administered, prevented the induction of tachycardia by increasing the A-V nodal refractoriness. Disopyramide in a dose of 2 mg/kg was injected 30 minutes after the start of verapamil administration, when prolongation of the A-V nodal conduction time (A-H interval) had continued in most of the patients. Disopyramide lengthened the effective refractory period of the anomalous pathway in all patients in whom this could be determined. The A-H interval, which had been prolonged by verapamil, was shortened in 4 patients and about unchanged in the remaining 4. After addition of disopyramide, sustained tachycardia could be induced in 2 patients who had lost the ability of initiating circus movement tachycardia after verapamil administration. Thus, disopyramide, when administered together with verapamil, may block the effect of verapamil on the A-V node by its anticholinergic action. A concomitant prescription of disopyramide with verapamil in expectation of the depression of both the anomalous pathway and the A-V node may have an untoward outcome.
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PMID:Combined effect of verapamil and disopyramide on induction of circus movement tachycardia in patients with pre-excitation. 729 93


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