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 neuroleptic drug droperidol has been shown to have clinically useful antiarrhythmic activity. Prior reports have resulted in conflicting conclusions regarding actions on ventricular myocardial fibers. The present study was carried out to determine whether droperidol did in fact affect the electrophysiological properties of guinea-pig papillary muscle fibers. By means of microelectrode recordings from preparations mounted in a single sucrose gap, the effects of concentrations from 10(-6) to 4 X 10(-5) M were studied on depolarization-induced automaticity, and on Vmax and its recovery time under several conditions of membrane potential, stimulation rate and external ion concentration. The results showed that at clinically relevant concentrations, droperidol significantly slows ventricular pacemaker activity, a depression reversible by epinephrine. Furthermore, Vmax was decreased and the time constant for Vmax recovery was significantly prolonged under several conditions which pertain to clinical arrhythmias, i.e., reduced membrane potential, elevated extracellular potassium concentrations and increased stimulation rate.
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PMID:Effects of droperidol on depolarization-induced automaticity, maximum upstroke velocity (Vmax) and the kinetics of recovery of Vmax in guinea-pig ventricular myocardium. 63 84

We studied the effect of lowering the extracellular potassium concentration ([K+]o) on the electrophysiological actions of disopyramide phosphate, a new antiarrhythmic drug. At low [K+]o, therapeutic concentrations of disopyramide phosphate caused significantly less depression of action potential amplitude and maximum upstroke velocity of both Purkinje fiber and ventricular muscle action potentials. The drug shifted the membrane responsiveness curve along the voltage axis to more negative membrane potentials regardless of [K+]o. However, a greater shift occurred when [K+]o was normal. Disopyramide phosphate prolonged both action potential duration and effective refractory period in all fibers but there was consistently greater prolongation of these parameters at low [K+]o. More importantly, disopyramide phosphate altered repolarization time course of action potentials in such a way that action potentials with dissimilar durations throughout the ventricular conducting system became more equal. The drug was less effective in decreasing this disparity in action potential durations throughout the ventricles in the presence of low [K+]o. These modifications of the electrophysiological actions of disopyramide by low [K+]o suggest that a therapeutic concentration of disopyramide might have less of an antiarrhythmic effect in the presence of hypokalemia.
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PMID:The electrophysiological effects of disopyramide phosphate on canine ventricular muscle and Purkinje fibers in normal and low potassium. 63 50

Exercise ECGs (bicycle ergometry in recumbency) were obtained in 252 women (aged 20-49 years) without evidence of organic heart disease. In 51 (20%) there was a false-positive change in the ECG with horizontal or descending S-T depression greater than or equal to 1 mm. The frequency of this change increased with increasing age. In group I (20-29 years) it was 5%, in group II (30-39 years) 20%, in group III (40-49 years) 38%. In 34 of the 51 women abnormal repolarisation changes were present even at rest. The S-T depression during exercise in most cases amounted to less than 2 mm and often occurred only on maximum exercise during the first or second minute of the recovery phase. These "ischaemia" changes disappeared in 29 of 41 women after administration of 100 mmol potassium chloride. Nine of 12 women in whom the positive ECG signs persisted after KCl, coronary angiography failed to demonstrate any abnormalities.
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PMID:[False-positive exercise ECG in women without organic heart disease (author's transl)]. 64 56

In rats, a diet depleted of potassium caused a significant hypokalemia and hypermagnesemia, a diuresis and natriuresis, a decrease in urinary and fecal excretion of potassium, a magnesiuria, and a decrease in fecal excretion of magnesium. Balance studies revealed that potassium metabolism was negative in potassium-depleted rats and that magnesium metabolism was positive and higher than in control rats. In potassium-depleted rats, potassium and magnesium contents in muscle were reduced, whereas the sodium level was increased and plasma aldosterone was significantly lower. Therefore, the elevation in plasma concentration of magnesium induced by a diet poor in potassium is the result of a more positive metabolic balance of magnesium and of shifting of magnesium from the tissue into the plasma compartment. Results of additional preliminary studies support the possibility that the hypermagnesemia may be mediated through the depression in mineralocorticoid activity induced by the depletion of potassium.
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PMID:Magnesium metabolism in potassium-depleted rats. 66 73

The effect of hypokalaemia on a neuromuscular blockade induced by pancuronium and its antagonism by neostigmine was studied in the cat anterior tibialis-peroneal nerve preparation using the constant infusion of pancuronium technique. Hypokalaemia was induced by chronic administration of chlorothiazide. The infusion rate of pancuronium required to maintain a 90% depression of twitch tension was reduced from 0.72 +/- 0.06 microgram kg-1 min-1 in the cats with a normal serum concentration of potassium (K+ = 4.4 +/- 0.2 mmol litre-1; n = 7) to 0.41 +/- 0.07 microgram kg-1 min-1 in the hypokalaemic cats (K+ = 2.3 +/- 0.1 mmol litre-1; n = 8). The dose of neostigmine necessary for 50% antagonism of the pancuronium-induced depression of twitch tension (ED50) was 10.0 microgram kg-1 in the cats with a normal potassium concentration and 18.5 microgram kg-1 in hypokalaemic cats. We conclude that hypokalaemia decreases the dose of pancuronium required for neuromuscular blockade and increased the dose of neotigmine required for antagonism of the block.
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PMID:Diuretic-induced hypokalaemia, pancuronium neuromuscular blockade and its antagonism by neostigmine. 66 26

The storage and release of acetylcholine and choline were studied in the isolated superior cervical ganglion of the rat by a radioenzymic method. The acetylcholine and choline contents were 202.2 +/- 5.1 and 624.7 +/- 20.2 pmole/ganglion, respectively. The transmitter tissue store was unaffected during 1 h of superfusion in choline--Krebs solution, while a 20% decrease was exhibited after 2 h and then remained approximately stable. Conversely, choline content declined to 50% within 1 h and further to 37% of the original level by 4 h. About 24% of the choline assayed in the intact preparation is located in the connective sheath. Preganglionic nerve stimulation at 10--20/sec or potassium stimulation (40 mM KCl) invariably decreased the transmitter tissue stores by 25--45%; such a depletion is independent of the presence or absence of external choline. By contrast, the presence of choline proved to be a prerequisite for the efficient release of acetylcholine from eserinized ganglia during continuous 10/sex stimulation. A drastic depression in the acetylcholine release is described which is related to the time of preincubation of the ganglia with eserine prior to stimulation. Indeed, a 30 min exposure to eserine, compared with a 5 min period, resulted in a 4-fold decrease in the steady output rate. Under optimal conditions, the initial volley output at 10/sec was 1.3 X 10(-4) of the releasable transmitter pool and 1.9 X 10(-4) during the steady-state output. These results are discussed in the light of the electrophysiological knowledge of the quantal release process at the ganglionic synapse.
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PMID:Storage and release of acetylcholine in the isolated superior cervical ganglion of the rat. 66 24

The direct effects of potassium-penicillin-G, kanamycin, streptomycin and chloramphenicol on isometric contraction of isolated rat heart muscle were examined. Potassium-penicillin-G did not depress myocardial contractility but rather increased it. Those increases are not due to penicillin itself but due to a small amount of K+ in potassium-penicillin-G. Kanamycin and streptomycin did show not only direct myocardial depressants effects but concentration-dependent depressions. The depression produced by kanamycin could be restored to normal by adding Ca++ to the bath solution. Chloramphenicol did not show any significant concentration-dependent depression in our studies. We conclude that it is important to be aware of the potential depression of cardiac function by antibiotics, particularly in patients who have diminished cardiac reserve and who are undergoing surgical procedures under anesthesia which may also depress cardiac function.
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PMID:Effects of certain antibiotics on isometric contractions of isolated rat heart muscle. 66 71

1. Local stimulus-evoked changes in concentration of extracellular calcium ions, [Ca2+]0, and potassium ions, [K+[0, were measured in the cerebellar cortex of the cat using paired ion-selected micropipettes. 2. Repetitive stimulation of 30 s duration decreased [Ca2+]0 from a base line of 1.2 mM to as low as 0.8 mM and increased [K+]0 from 3 mM to as much as 8 mM. The magnitude of the changes was directly related to stimulus frequency. Laminar analysis showed that the greatest ion changes occurred at the level of maximum parallel fiber-Purkinje cell dendrite stimulation, but that the [Ca2+]0 changes were more localized than the [K+]0 changes. 3. Combining real-time current-source density measurement with [K+]0 determination and local manganese application, showed that the Mn blocked parallel fiber-Purkinje cell synaptic transmission, but that much of the [K+]0 changes persisted. Thus, a large part of the [K+]0 flux most probably originated in the parallel fibers. In contrast, [Ca2+]0 changes were abolished by the Mn, indicating that the decrease in this ion was probably associated with synaptic transmission or dendritic events. 4. In a few cases, spreading depression occurred in the cat cerebellar cortex. This could be accompanied by decreases in [Ca2+]0 to as low as 0.12 mM and increases in [K+]0 in excess of 48 mM. 5. These results show that significant changes in [Ca2+]0 and [K+]0 occur during cerebellar stimulation and indicate possible origins of the ion fluxes in terms of neuronal elements. This work also shows that the cerebellar cortex of the cat can support spreading depression. The present results, together with those of earlier studies on [Ca2+]0 and [K+]0 changes in the presence of aminopyridine in the cat cerebellum, suggest that synaptic or dendritic electroresponsive properties may play a role in the observed [Ca2+]0 and [K+]0 changes.
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PMID:Calcium and potassium changes in extracellular microenvironment of cat cerebellar cortex. 68 86

This study tests the hypothesis that the efficacy of cardioplegic solution depends upon its chemical constituents rather than on its temperature alone. A standard preparation of right heart bypass in the dog was utilized. Left ventricular function curves were inscribed before and after 1 hour of aortic cross-clamping. No deterioration in function was observed in nonischemic control hearts or in hearts protected with cardioplegic solution consisting of potassium chloride (25 mEq. per liter) and mannitol (12.5 Gm. per liter in 5 percent dextrose and 0.2 percent saline at either 4 degrees C or 28 degrees C. Severe myocardial depression was observed in hearts rendered ischemic for 1 hour at 28 degrees C. without protection and also in hearts perfused with 5 percent dextrose and 0.2 percent saline at 28 degrees C. without the potassium chloride and mannitol. The evidence from this study indicates that cardioplegic solution exerts a protective effect beyond that which is afforded by hypothermia.
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PMID:Effect of temperature of cardioplegic solution. 68 67

Potassium-induced cardioplegia was studied in 38 mongrel dogs supported by normothermic cardiopulmonary bypass and subjected to 60 minutes of aortic cross clamping followed by 30 minutes of reperfusion. A study of preischemic and postischemic ventricular function and myocardial high-energy phosphate compounds, lactate, and glycogen showed substantial preservation of high-energy phosphates and ventricular performance when potassium cardioplegia was used. However, the substantial depression in contractility observed following ischemia nad reperfusion suggests that potassium cardioplegia alone does not provide adequate intraoperative protection of the myocardium.
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PMID:Potassium cardioplegia. An alternate method of intraoperative myocardial protection. 68 94


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