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)

Mice were fed diets deficient in a single essential amino acid, and the primary immune responses to inoculation of allogenic tumor cells was measured by in vitro assay of cellular immunity. Moderate reduction of the amino acids phenylalanine-tyrosine, valine, threonine, methionine-cystine, isoleucine, and tryptophane in the diet produced profound depression of hemagglutinating and blocking antibody responses, although cytotoxic cell-mediated immunity remained intact. These diets had previously been shown to result in a selective depression of tumor growth in mice. Limitation of the amino acids arginine, histidine, and lysine in the diets gave rise to only slight depression of the immune responses. These diets had previously been shown to produce a proportional decrease in both tumor growth and host body weight. Moderate leucine restriction resulted in a paradoxical depression of cytotoxic cell-mediated immunity with little effect on serum blocking activity. Slight increases had previously been noted in the weight of tumors in mice fed leucine-restricted diets. Deficiency or imbalance of essential amino acids in the diet may produce profound depression of immune responses and apparent, marked changes in the immune resistance of the host animal to tumors.
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PMID:Quantitative effects of nutritional essential amino acid deficiency upon immune responses to tumors in mice. 468 18

The administration of beta-receptor blocking drugs and antiarrhythmic drugs in close proximity may result in hemodynamic, electrophysiologic, or pharmacokinetic interactions. We examined the hemodynamic and electrophysiologic effects of 0.20 mg/kg intravenous metoprolol followed by a 15-minute infusion of 0.75 mg/kg/min tocainide. In the six patients sutided, metoprolol produced a fall in cardiac rate and output which was not further altered by tocainide. Both drugs decreased peak left ventricular (LV) dP/dt, ejection fraction, and mean Vcf. There was no change in LV end-diastolic pressure or echo dimension and in clinical ill effects. In eight patients without sinus A-V nodal disease electrophysiologic studies showed mild depression of A-V conduction by metoprolol. Tocainide depressed sinus node function and shortened the functional refractory period of the His-Purkinje system. There were no clinical sequelae. However, three patients with preexisting electrophysiologic abnormalities developed asystole. There was no evidence of pharmacokinetic interaction. It is concluded that metoprolol and tocainide can be given concurrently with reasonable safety to cardiac patients without electrophysiologic abnormalities.
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PMID:Hemodynamic and electrophysiologic interactions between antiarrhythmic drugs and beta blockers, with special reference to tocainide. 610 7

Histidine metabolism was studied in rats fed 10% casein diets supplemented with 1000 IU of retinol/g concurrent with or previous to exposure to high levels of dietary histidine (1% or 2%). When a retinol-supplemented 10% casein + 1% histidine diet was fed ad libitum for 21 days, urinary excretion of formiminoglutamic acid (FIGLU) was decreased by 50-70% over the entire period and plasma histidine was reduced by 30-70% for 16 days compared to rats receiving 10% casein + 1% histidine with normal levels of retinol. Rats pretreated for 10 days with a 10% casein diet supplemented with high levels of retinol oxidized 30% more L-[ring-2-14C]histidine to 14CO2 and excreted 76% less of the administered dose as urinary FIGLU compared to control rats not pretreated with high levels of retinol. Depression in growth due to supplementation of a 10% casein diet with 1% histidine were also partially alleviated in rats that were first pretreated with retinol. Activities of histidase, urocanase, and formiminoglutamic acid formiminotransferase (FIGLU transferase) were unaffected by retinol supplementation. The results suggest that retinol supplementation enhances histidine catabolism by exerting a change on one-carbon metabolism.
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PMID:Enhancement of histidine and one-carbon metabolism in rats fed high levels of retinol. 612 Oct 19

We investigated the effects of histamine applied by microiontophoresis onto serotonin-containing (serotonergic) cells recorded extracellularly in the dorsal raphe nucleus of the rat. Application of histamine at low iontophoretic currents (1-5 nA) produced a rapid depression of the firing of all serotonergic neurons tested. The H1-receptor antagonists mepyramine and diphenhydramine were unable to attenuate the histamine-induced response. Antagonism of the effect of histamine by the iontophoretic application of the H2-receptor antagonists cimetidine and metiamide was not possible to evaluate since both were found to exert potent inhibitory effects by themselves. In contrast, the nonimidazole-derived H2-receptor antagonist ranitidine, which had no effect by itself, selectively antagonized the histamine-induced depression of neuronal activity. Histidine, 3-methylhistamine and a variety of histamine agonists selective for H1- or H2-receptors were unable to mimic the effect of histamine in dorsal raphe. Histamine's effects may, in part, be mediated at a gamma-aminobutyric acid receptor complex as the gamma-aminobutyric acid antagonists bicuculline and picrotoxin rapidly and reversibly antagonized both the histamine- and the cimetidine-induced depression of serotonin cell firing; the glycine antagonist strychnine selectively blocked the inhibitory effect of glycine without altering the histamine-induced response. These data show an inhibitory effect of histamine on serotonin-containing neurons in the dorsal raphe; this effect may be partially mediated at a subtype of H2-receptor. These data further indicate that the inhibitory effects of histamine and cimetidine observed in the dorsal raphe nucleus may result, in part, from an action directly or indirectly at a gamma-aminobutyric acid receptor complex.
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PMID:Effects of histamine, H1- and H2-receptor antagonists on the activity of serotonergic neurons in the dorsal raphe nucleus. 613 28

A 61-year-old man presented with symptomatic 2 degree Mobitz II AV block in association with bifascicular block. Ventricular pacing resulted in temporary depression of AV conduction. The extent of pacing-induced AV block varied directly with the duration and rate of ventricular pacing. Intracardiac recordings proved that the site of spontaneous and pacing-induced AV block was distal to the His bundle. Possible mechanisms by which this phenomenon may arise and several implications of practical importance are discussed.
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PMID:Depression of distal AV conduction following ventricular pacing. 617 98

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

The electrophysiologic basis for the use of amiodarone in the treatment of cardiac arrhythmias is outlined, with reference to studies in isolated cardiac tissues, whole animal, and human studies. Amiodarone appears to have the distinctive property of directly prolonging action potential duration (and hence refractory periods) in nearly all cardiac tissues. Independent of its effects on refractory periods, conduction may also be impaired in the His-Purkinje system, possibly due to depression of phase 0 of the action potential. Sinus node and atrial automaticity, as well as that arising from diseased Purkinje fibers, may be depressed. Normal ventricular escape pacemakers appear relatively unaffected, however. A nonspecific anti-adrenergic action may contribute to its observed effects. These electrophysiological effects are more obvious and predictable after several weeks of oral treatment than after intravenous administration, suggesting a time-dependent mechanism of action. The drug appears well suited to the prevention of enhanced automaticity in the ventricle and re-entry throughout the heart, and its frequent clinical success in a broad spectrum of cardiac arrhythmias attests to this. Unwanted side effects include sinus node depression, His-Purkinje conduction delay or block, and ventricular arrhythmias enhanced by QT prolongation. However, the frequency of clinically significant examples of unwanted arrhythmic effects appears to be acceptably low.
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PMID:The electrophysiologic basis for the use of amiodarone for treatment of cardiac arrhythmias. 619 14

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

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

Mexiletine is a class I antiarrhythmic agent that is active after both oral and intravenous administration and similar in structure and activity to lidocaine. It decreases phase O maximal rate of depolarization (Vmax) by fast sodium channel blockade. The marked rate dependence of Vmax depression may explain mexiletine's lack of effect on normal conduction and its efficacy against ventricular tachyarrhythmias. Mexiletine significantly decreases the relative refractory period in His-Purkinje fibers without changing the sinus rate or atrioventricular and His-Purkinje conduction times. Action potential duration is usually shortened. Mexiletine may aggravate preexisting impairment of impulse generation and conduction. Uptake and distribution of mexiletine are rapid, systemic bioavailability is about 90%, and tissue distribution is extensive. Mexiletine is primarily metabolized in the liver; 10% to 15% is excreted unchanged in the urine. Elimination half-life is 9 to 11 hours after intravenous or oral administration. Microsomal enzyme induction shortens mexiletine's elimination half-life, whereas hepatic disease and acute myocardial infarction prolong it. Renal disease has little effect, although hemodialysis increases mexiletine clearance. Plasma concentrations from 0.75 to 2.0 mg/L are usually associated with a desirable therapeutic response.
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PMID:Pharmacology, electrophysiology, and pharmacokinetics of mexiletine. 632 58


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