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 a number of vasoactive and neurotransmitter substances on lymphocyte traffic were studied by assessing their effects on the release of lymphocytes into primary peripheral (popliteal) nodal efferent lymph of sheep following acute infusion into cannulated afferent nodal lymphatics. In a total of 23 experiments, the output of lymphocytes, small and blast, was increased by serotonin, substance P, bombesin, [met]enkephalin, isoprenaline and phenylephrine and was decreased by vasoactive intestinal peptide (VIP), neurotensin and carbachol. Substances whose actions are modulated by prostaglandins and enhanced by prostaglandin synthesis inhibitors and which elevate blood monocyte and nervous tissue levels of cyclic GMP tended to increase lymphocyte traffic through peripheral lymph nodes in sheep in vivo. The opposite effect tended to be produced by substances whose actions require or are associated with prostaglandins or histamine, and which affect blood monocytic cyclic nucleotide levels by elevation of cyclic AMP or depression of cyclic GMP. Pain and inflammation tended to increase lymphocyte traffic, while analgesics and immunomodulators tended to decrease it.
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PMID:Modification of lymphocyte traffic by vasoactive neurotransmitter substances. 614 65

The implications of the minor ECG abnormalities that I have dealt with may be categorized as follows. Innocent: 1. Sinus arrhythmia, with or without nodal escape beats 2. Atrial extrasystoles 3. Incomplete right bundle-branch block 4. Parabolic depression of the ST segment in association with a rapid heart rate 5. Elevation of the ST segment in the right precordial leads 6. Positive/negative T waves in the transitional zone. Not necessarily indicating disease: 1. Ventricular indicating disease: 1. Ventricular extrasystoles 2. Complete right bundle-branch block 3. Left anterior or posterior hemiblock 4. Abnormally directed T-wave vectors. Probably indicating disease: 1. Plane or downward-sloping ST depression, at rest or on exercise, of more than 1 mm 2. Pyramidal arrowhead T waves, with or without an abnormally directed T-wave vector 3. Negative/positive T waves in leads facing the left ventricle 4. Inverted U waves. It is clear that careful assessment must be made before minor ECG abnormalities in presumptively normal individuals are accepted as indicators of the presence of heart disease.
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PMID:Symptomless abnormalities. Minor ECG abnormalities. 618 Jul 89

We compared the cardiac and coronary vasodilator actions of a new calcium-antagonistic vasodilator, KB-944, in isolated, blood-perfused heart preparations of dogs. In all preparations KB-944 injected intra-arterially produced an increase in blood flow. In sinoatrial (SA) node preparations KB-944 decreased sinus rate and in large doses produced atrial standstill. In atrioventricular (AV) node preparations KB-944 increased AV conduction time and in large doses produced second- or third-degree AV block only when injected into the artery supplying the AV node. In the same preparations KB-944 had virtually no effect on AV conduction when injected into the artery supplying the His-Purkinje-ventricular system. In papillary muscle preparations KB-944 in medium and large doses depressed force of contraction, the depressant action being greater at high rates of contraction. In the same kind of preparations KB-944 affected automaticity slightly and inconsistently. Depression by KB-944 of SA nodal automaticity and AV nodal conduction occurred pari passu with coronary vasodilation, whereas force of contraction was depressed to a lesser extent in coronary vasodilator doses. In these respects, KB-944 resembles verapamil and diltiazem rather than nifedipine and nicardipine.
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PMID:Cardiac versus coronary vasodilator actions of KB-944, a new calcium antagonist, assessed in isolated, blood-perfused heart preparations of dogs. 619 Nov 31

We compared the effects of the calcium channel blocking drugs verapamil and nifedipine on atrioventricular (AV) nodal function by His bundle electrocardiography in 24 pigs. AV nodal conduction time was decreased 16% by nifedipine (0.1 mg/kg + 3 micrograms/kg/min; p less than 0.05) and increased 20% by verapamil (0.2 mg/kg + 10 micrograms/kg/min; p less than 0.05). Pretreatment with a beta-adrenoceptor blocking agent (metoprolol, 0.4 mg/kg) prevented the decrease in AV nodal conduction time by nifedipine. Vasodilatation alone (nitroprusside, 20 micrograms/kg/min) produced a 16% decrease in AV nodal conduction time and a 19% decrease in cycle length. Before any of the drugs was given, AV nodal conduction time correlated negatively with the heart rate (rho = -0.65; p less than 0.001; n = 24). beta-Adrenoceptor blockade (metoprolol, 0.4 mg/kg) resulted in a 13% increase in cycle length and an 8% increase in AV nodal conduction time. These results indicate that, even with high concentrations, the effect of nifedipine on the AV node in vivo is primarily a facilitation caused by a baroreceptor reflex. In contrast, verapamil causes a depression of the AV node without such an increase in sympathetic tone.
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PMID:Heart rate-dependent atrioventricular nodal conduction and the effects of calcium channel blocking drugs: comparison of verapamil and nifedipine. 620 Jul 15

Electrophysiologic studies were performed in 10 patients with atrioventricular (A-V) nodal reentrant paroxysmal supraventricular tachycardias (PSVT), before and after intravenous administration of propafenone (1.5 mg/kg). All patients utilized an A-V nodal slow pathway for anterograde conduction and an A-V nodal fast pathway for retrograde conduction of the reentrant impulse. Propafenone depressed retrograde fast pathway conduction which was manifested by: 1) complete V-A block at all ventricular paced cycle lengths after propafenone in 3 cases; 2) increase in mean +/- SD of ventricular paced cycle length producing V-A block from less than 308 +/- 37 ms to 432 +/- 63 ms in the remaining 7 patients. Nine of the 10 patients had induction of sustained PSVT before propafenone. In 7 of the 9, PSVT could not be induced or sustained after propafenone, reflecting depression of the retrograde fast pathway conduction with either absence of atrial echoes (5 patients) or induction of nonsustained PSVT, with termination occurring after the QRS (2 patients). In 1 patient, single atrial echoes were induced before propafenone but none were noted after the drug. In only 2 patients was a sustained PSVT inducible after propafenone. In conclusion, propafenone inhibited induction of sustained A-V nodal reentrant PSVT in most patients, reflecting depression of retrograde A-V nodal fast pathway conduction.
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PMID:Effects of propafenone on induction and maintenance of atrioventricular nodal reentrant tachycardia. 620 64

Effects of electrolyte concentrations on atrioventricular (AV) conduction were studied in isolated, perfused rabbit hearts by recording the His bundle electrogram. Initial calcium (Ca++), sodium (Na+), and potassium (K+) concentrations were 2.4, 144.8, and 4.5 mM, respectively. Lowering of Ca++ to 0.8 mM slightly prolonged the AH interval, whereas elevation of Ca++ to 4.8 or 7.2 mM more markedly prolonged this interval, often causing intranodal block. High Ca++-induced depression of intranodal conduction was antagonized by high K+ (7.5 mM). Verapamil (0.5 to 1.0 mg/L) produced second-degree intranodal block. High Na+ (172 mM) restored 1:1 conduction, whereas high Ca++ did not. These results suggest that: (1) an optimal Ca++ concentration for intranodal conduction exists; (2) high K+ counteracts high Ca++-induced intranodal block; (3) verapamil effect on AV node is antagonized by high Na+; and (4) slow Na+ current may play a role in AV nodal action potentials.
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PMID:Effects of calcium and sodium concentrations on atrioventricular conduction: experimental study in rabbit hearts with clinical implications on heart block and slow calcium channel blocking agent usage. 627 62

The action of nifedipine given first intravenously and then orally was studied in nine patients undergoing investigation for angina pectoris who were already receiving atenolol (100-200 mg/daily) and who had been shown to be fully beta blocked (reduction in maximal heart rate by greater than 25%). Intravenous nifedipine 7.5 micrograms/kg reduced both systolic blood pressure and left ventricular pressure (dP/dt) transiently; both values were significantly lower five and 10 minutes after the infusion of nifedipine but were not significantly different from control values at 20 minutes. There was minimal but pronounced depression of atrioventricular nodal function after giving intravenous nifedipine, though this was detected only when sensitive tests of atrioventricular nodal function were used. These effects were also transient, showing no significant change from control values at 20 minutes. Atrioventricular nodal conduction time and sinus rate were unchanged. Radionuclide angiography of patients taking the oral combination of atenolol and nifedipine for chronic angina showed no change in ejection fraction compared with those taking atenolol alone, but there was a small increase in peak ejection rate. Resting blood pressure and heart rate were unchanged and the PR interval did not lengthen. Peak heart rate and systolic blood pressure showed no alteration on exercise testing when the drugs were combined compared with the response with atenolol alone. Despite the negative inotropic influence when nifedipine was given intravenously, the absence of haemodynamic deterioration when oral nifedipine is combined with atenolol has confirmed that this combination can be used safely in patients with normal left ventricular function. The minimal changes in atrioventricular nodal function cannot be detected on the surface electrocardiogram and are not of clinical importance in patients with normal conduction.
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PMID:Acute and chronic haemodynamic and electrophysiological effects of nifedipine in patients receiving atenolol. 635 28

Electrophysiologic studies were performed in 11 patients with atrioventricular (AV) nodal reentrant tachycardia (SVT) before and after intravenous administration of 1.5 to 2 mg/kg ethmozin. Initially, 9 of 11 patients had induction of sustained SVT, and two remaining patients had nonsustained SVT and atrial echoes, respectively. Ethmozin terminated induced SVT in six of nine patients. In six of nine patients ethmozin prevented the development of sustained SVT, indicating that ethmozin depressed retrograde fast pathway AV nodal conduction. In four of these patients atrial echoes were abolished. In the two remaining cases ethmozin prevented the induction of nonsustained SVT. In only three of these nine patients was sustained SVT induced. Anterograde fast and slow pathway properties did not significantly change with ethmozin administration. Effective refractory period (ERP) of the ventriculoatrial (VA) conduction system and ventricular paced cycle length producing VA block was 305 +/- 40 (mean +/- SEM) and 347 +/- 38 msec before and 424 +/- 105 and 475 +/- 71 msec after ethmozin administration, respectively (p less than 0.01, n = 8), suggesting depression of retrograde pathway with ethmozin administration. Ethmozin significantly (p less than 0.05) lengthened PA, AH, HV, and PR intervals (36 +/- 11 to 45 +/- 14 msec, 84 +/- 21 to 93 +/- 17 msec, 42 +/- 8 to 50 +/- 7 msec, and 163 +/- 23 to 190 +/- 31 msec, respectively). No significant change was observed in sinus rate, QRS and QT intervals, or ERP of atrium and ventricle. Thus, a single intravenous dose of ethmozin terminated induced SVT and prevented induction of sustained SVT in most patients, reflecting depression of retrograde fast pathway conduction.
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PMID:Ethmozin. II. Effects of intravenous drug administration on atrioventricular nodal reentrant tachycardia. 638 89

25 females (57.7 +/- 11.1 years) and 1 male (71 years) with histologically verified metastasizing breast cancer were submitted to mitoxantrone therapy. Secondary tumours were found in following organ systems: bone: 19 cases; lung: 13 cases; liver: 6 cases; skin: 5 cases; locoregional and nodal: 5 cases; brain: 1 case. All patients showed normal bone marrow and heart function before commencement of treatment. Mitoxantrone was given in form of a 30-minute infusion at a dosage of 14 mg/m2. In 4 patients dosage was increased to 20 mg/m2. Treatment cycles were repeated every 3 weeks according to peripheral blood counts. All patients were cardiologically monitored throughout the study by means of electrocardiogram, systolic time interval measurement and radionuclide angiography. The mean observation period was 169 +/- 98 days. The response of the patients was as follows: 1 complete remission, 5 partial remissions, 4 unchanged disease and 16 progressive disease. Side effects were normally mild; only nausea, leucopenia and moderate hair loss were of clinical relevance. Cardiac decompensation was not observed. No significant electrocardiographic alterations were found throughout the study. Results of systolic time interval measurements (PEPI, PEP:LVET) and radionuclide angiography (LVEF) gave evidence of moderate depression of heart function. In view of the optimal benefit/risk ratio of mitoxantrone this drug could be used in combined modality treatment schedules in metastasizing breast cancer.
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PMID:[Mitoxantrone in the primary treatment of metastasizing breast cancer]. 647 82

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through the autonomic nervous system.
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PMID:Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade. 649 84


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