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)

An interpolated premature ventricular contraction (PVC) may produce either complete block of the next sinus impulse or depression of A-V nodal conduction with a prolonged A-H interval. When a PVC results in partial depression of a A-V nodal conduction, the effect on subsequent premature atrial stimuli is unknown. The authors have recently observed three patients in which the effect of a premature ventricular stimulus with interpolation on the functional refractory period of the A-V node could be measured. In case one an interpolated PVC sufficient to prolong the A-H interval from 80 to 120 msec was followed by programmed premature atrial stimuli which resulted in no additional A-V nodal delay, and the apparent functional refractory period of the A-V node was reduced from 420 to 330 msec when compared with the atrial extrastimulus technique. In case two a programmed ventricular extrastimulus prolonged the A-H interval in the following sinus beat from 120 to 240 msec; atrial extrastimuli then resulted in only minimal increments in A-V nodal delay and the apparent functional refractory period of the A-V node was reduced from 590 msec. A ventricular extrastimulus in case three increased the resting A-H interval from 60 to 115 msec; conduction of atrial extrastimuli then resulted in a reduction in the functional refractory period of the A-V node from 465 to 400 msec. In each case an interpolated premature ventricular stimulus produced (1) depression of A-V nodal conduction in the ensuing sinus beat A1 and (2) relative facilitation of A-V nodal conduction of a subsequent premature atrial stimulus (A2). The functional refractory period of the A-V node was reduced when compared with the atrial extrastimulus technique alone.
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PMID:Dual effects of concealed A-V nodal conduction in man. 6 80

The electrophysiological effects of anti-arrhythmic drugs in man may be classified in three groups: -- Group I: comprising drugs whose characteristic action is on the AV node (beta blockers, verapamil, digitalis) The nodal conduction time (A-H interval) and refractory periods are increased. -- Group II: comprising drugs acting on the His-Purkinje system, the AV nodal conduction staying unchanged. This group has two sub-groups. Sub-group A: these drugs delay the His-Prukinje conduction (increased H-V interval). Examples are quinidine, procainamide, disopyramide, ajmaline, chloro-acetyl-ajmaline. In addition these drugs usually increase the atrial refractory periods and those of accessory pathways. Sub-group B: the His-Purkinje conduction is unchanged but the refractory periods are modified: lengthened (bretylium tosylate) or shortened (diphenylhydantoin, lignocaine, mexiletine). -- Group III: which includes amiodarone and aprindine whose effects are mixed: on the one hand AV nodal depression, and on the other, alteration of the His-Purkinje conduction manifested by an increased H-V internal (aprindine) or refractory periods (amiodarone). These preparations also increase the refractory periods of accessory AV pathways and amiodarone increase the refractory periods of the atria. This type of classification could help towards a more rational clinical approach to the use of anti-arrhythmic drugs.
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PMID:[Electrophysiological effects of anti-arrhythmia agents in man. Attempt at classification]. 10 85

Light and electron microscopic examinations of deer mice (Peromyscus maniculatus) chronically infected with Trypanosoma equiperdum revealed hyperplasia of germinal center lymphocytes (germanocytes) in the lymph follicles of spleen and lymph nodes and infiltration of the splenic red pulp cords and nodal medullary cords with plasma cells. Proliferation and infiltration of plasma cells caused disruption of the B- and T-lymphocyte areas in these organs. Stimulation of splenic lymphocytes in vitro by phytohemagglutinin and concanavalin A revealed marked depression in T-lymphocyte response; stimulation with lipopolysaccharide and pokeweed mitogens showed depression of B-cell response. Deer mice infected with virulent trypanosomes had decreased immunologic response to injection of sheep red blood cells, whereas deer mice given radioattenuated trypanosomes had normal to enhanced immunologic response to injection of sheep red blood cells.
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PMID:Immunosuppression in deer mice with experimentally induced trypanosomiasis. 32 72

Intravenous administration of a single 50-mg bolus of lidocaine in a 67-year-old man resulted in profound depression of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to lidocaine.
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PMID:Lidocaine-induced cardiac asystole. 35 96

A patient is presented who had two paroxysmal supraventricular tachycardias, one slow and incessant and the other fast. Both paroxysmal tachycardias appeared to be atrioventricular (A-V) reentrant, with anterograde conduction by way of a normal A-V pathway. Two pathways conducting in retrograde manner were demonstrated, characterized by different conduction times (fast and slow), identical abnormal atrial activation sequence and A-V nodal-like properties (retrograde Wenckebach periodicity with rapid ventricular pacing, and depression with ouabain and propranolol). Thus, there appeared to be two anomalous A-V bundles with nodal-like properties conducting in retrograde fashion. Whether the paroxysmal tachycardia was fast or slow depended on which of these pathways was utilized. Spontaneous cure of incessant paroxysmal tachycardia was observed and coincided with unexplained total loss of ability for ventriculoatrial conduction.
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PMID:Multiple reentrant tachycardias due to retrograde conduction of dual atrioventricular bundles with atrioventricular nodal-like properties. 45 41

Previous studies have demonstrated that verapamil possess potent anti-arrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Isolated tissue studies performed in rabbit right atrium demonstrated that prompt and prominent slowing of the sinus rate even at a dose of 1 X 10(-7) mol . litre-1. This dose produced significant decrease in action potential amplitude and phase 4 slope, shifted the 'threshold potential' to a less negative value, prolonged action potential duration but did not change maximum diastolic potential. At this dose of verapamil, sinoatrial conduction time prolonged significantly (control: 40.0 +/- 4.8 ms; 1 X 10(-7) mol . litre-1 verapamil: 50.0 +/- 6.4 ms). Purkinje fibre studies demonstrated decreases in dV/dt, resting potential, total amplitude, action potential duration at 75, 95% of recovery and effective refractory period only after exposure to greater than or equal to 1 X 10(-5) mol . litre-1 verapamil. Electrophysiological studies in conscious dogs demonstrated, after bolus administration of verapamil, progressive increases in the A-H interval and heart rate, but no changes in H-V and QRS intervals. Anaesthetised dog studies showed the lack of significant effect on A-H and H-V intervals or QRS duration regardless of the bolus dose of verapamil. However, verapamil produced statistically significant increases in heart rate after 0.025 mg . kg-1. Verapamil administration did not produce a statistically significant change in escape pacemaker rate in vagal stimulation experiments or with spontaneously beating isolated Purkinje fibres. Finally, the effect of increasing intravenous bolus does of verapamil on ischaemic arrhythmias was studied in five conscious dogs 24 h following LAD ligation. Only one dog with ventricular tachycardia and another dog with junctional escape rhythm were converted to sinus rhythm after the 0.05 mg . kg-1 and 0.2 mg . kg-1 doses, respectively. In conclusion, these studies demonstrated that administration of verapamil specifically depresses tissue with electrophysiological dependence on slow channel current. Therefore, sinus and A-V nodal events would be suppressed and slow-channel mediated events in ischaemic ventricle also would be inhibited. Clinically, acute administration of verapamil would lead to depression of sinus and A-V nodal function as well as potentially eliminate slow current mechanisms in ischaemic arrhythmias.
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PMID:Electrophysiological effects of verapamil. 74 94

The incidences of electrocardiographic (ECG) changes during microlaryngoscopy under halothane anaesthesia were compared by using Althesin and thiopentone as induction agents. During the procedure the most common ECG change in both groups was junctional rhythm, which occurred in 37% of the patients in the Althesin group and in 29% of the patients in the thiopentone group. The next most common changes in the Althesin group were: ventricular ectopic beats (22%), ischaemic S-T segment depression (14%), and T wave flattening or inversion (14%); those in the thiopentone group were ventricular ectopic beats (18%) and rapidly ascending S-T segment depression (12%). As well as during the procedures, some ECG changes were registered in both groups during intubation. ECG changes disappeared without any special treatment after manipulation of the vocal cords or after intubation. There was no statistically significant difference in the total incidence of dysrhythmias between the Althesin and thiopentone groups, but the types of dysrhythmias were different in the two groups. There were more lower nodal rhythms, less serious ectopic beats and more ischaemic S-T segment depression in the Althesin group than in the thiopentone group. The results suggest that Althesin is useful and superior to thiopentone in patients with a tendency to develop serious ventricular ectopic beats, whereas in patients with heart and coronary arterial disease, Althesin is inferior to thiopentone and should be used with care.
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PMID:Comparison of electrocardiographic changes during microlaryngoscopy under halothane anaesthesia induced by althesin or thiopentone. 84 73

Studies were performed to determine the chronotropic effect of acetylstrophanthidin during constant infusion through cannulation of the sinus nodal artery. Ten mongrel dogs weighing 13.5 to 18 kg were studied under sodium thiamylal anesthesia. Epicardial atrial and ventricular electrograms were recorded. The sinus nodal artery was cannulated and infused for 20 minutes at a rate of 2 cc/min with a solution containing acetylstrophanthidin, 0.5 microng/cc. Mean results for the group of 10 animals were determined. There was a gradual acceleration of the atrial rate of 45 beats/min after 6 to 8 minutes of infusion. The peak atrial rate of 175 beats/min was achieved by 10 to 12 minutes. This tachycardia persisted for 2 to 4 minutes without atrioventricular block or premature beats. By 12 to 14 minutes, there was a gradual slowing of atrial rate followed by bradycardia, sinus pauses and atrial arrest. Sinus nodal arterial infusion of acetylstrophanthidin produces an initial positive chronotropic effect and, if maintained, a depression of atrial rate and, terminally, atrial arrest. The gradual time course of development and decline of the tachycardia suggests that the "paroxysmal" atrial tachycardia caused by digitalis excess is the result of enhanced pacemaker automatically rather than reentry, and thus is not truly paroxysmal.
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PMID:Chronotropic effect of acetylstrophanthidin infusion into the canine sinus nodal artery. 85 29

Effect of ketamine on the SA node of the dog heart was studied in vivo using a selective perfusion technique of the SA node artery. Injections of ketamine in doses from 100 microgram to 3 mg into the artery produced a depression of the SA nodal activity by a direct action. This depression was followed by the sudden appearance of a stimulatory phase. Bilateral vagotomy and sympathectomy or prior administration of a ganglion blocker failed to inhibit the occurrence of the ketamine-induced tachycardia, while it was completely abolished in the reserpinized dogs or by a prior injection of a beta-blocking agent into the SA node artery. This may indicate that an activation of the peripheral adrenergic mechanism plays an important role in the induction of the excitatory effect of ketamine injected in the SA node artery.
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PMID:Biphasic response of the SA node of the dog heart in vivo to selective administration of ketamine. 92 94

Significant peripheral white blood cell depression was noted in 75% of postmastectomy patients receiving chest wall and nodal irradiation and in 50% of patients receiving only peripheral nodal irradiation. Leukopenia was documented for as long as 36 months following therapy. With the current trend to earlier institution of chemotherapy, the routine use of postoperative irradiation must be reevaluated.
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PMID:Leukopenia after postmastectomy irradiation. 94 94


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