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)

Apart from sufficient experience on the part of the examining physician and adequate technical apparatus, proper premedication can facilitate the procedures for both patient and physician considerably. The paper reports on experience gained in 500 laparoscopies carried out under conditions which were deviated slightly from those hitherto recommended in the literature. The analgesic employed was Tilidine (in Germany: Valoron), and Diazepam was used as a sedative; both of these substances were given intravenously, the vein was kept open for the entire course of the examination. The Tilidine dose was normally 50-100 mg, but under exceptional circumstances as much as 150 mg. Tilidine showed good analgesic effectiveness and tolerance; no case or nausea or vomiting and no sign of respiratory depression of effects on smooth muscle were observed under the conditions stated. The fact that Tilidine is not subject to the restrictions imposed by the German narcotics law is also seen as an advantage. The Diazepam dose was 5-30 mg. Apart from its sedative effect Diazepam also diminishes the tonus of skeletal muscle (important in laparoscopy) and has a relatively long time of elimination (20-48 h). In addition to these two substances, 10-20 ccm of 1% Lidocaine solution with Epinephrine additive was given as a local anaesthetic. The investigators' experience with the above premedication procedure was found to be convincingly positive.
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PMID:[Premedication with valoron (Tilidin) in internal laparoscopy]. 13 78

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.
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PMID:Polymorphous ventricular tachycardia: clinical features and treatment. 46 73

Local anesthetics administered intrathecally seen more effective when in hypobaric solution than when in hyperbaric solution. To test whether an unrecognized osmotic effect might be playing a part in this, sheathed vagus nerves of rabbit were incubated in electrolyte-deficient or electrolyte-free media of various degrees of hypo-osmolarity. The nerves gained weight over a period of 15 min. They lost nearly half their sodium, but very little potassium, within 5 min. Electrolyte depletion by incubation in sucrose solutions depressed the amplitude of the C-fiber component of the compound action potential more rapidly in hypo-osmotic than in iso-osmotic solutions. In iso-osmotic sucrose, 50 per cent depression developed in 61 +/- 12 min (mean +/- SD, n = 5), but in 0.6 iso-osmotic sucrose, 50 per cent depression was reached in 17 +/- 3 min (n = 5). Lidocaine, 100 microM (approximately 0.003 g/100 ml) in iso-osmotic sucrose was without observed effect; lidocaine, 100 microM in 0.6 iso-osmotic sucrose produced 50 per cent depression in 7 +/- 2 min (n = 4). Thus, osmotic swelling plus electrolyte depletion, but not electrolyte depletion alone, markedly intensified inhibition of conduction by lidocaine. All effects were reversible by returning the nerves to isotonic physiologic incubation medium. The results suggest that intrathecal osmotic swelling of neural tissue may contribute to the conduction block in hypobaric spinal anesthesia.
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PMID:Osmotic swelling effects on neural conduction. 49 57

The effects of lidocaine and its primary metabolite monoethylglycinexylidide (MEGX) on isolated human muscle strips from non-gravid and gravid uteri were evaluated. No differences between the effects of lidocaine and those of MEGX on gravid and non-gravid muscle strips were observed. Lidocaine produced significant (P less than 0.01) dose-related depression of uterine contractility, although significant pharamacologic depression occurred only at lidocaine concentrations in excess of 25 microgram/ml. MEGX produced no consistent changes in any of the responses measured.
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PMID:Lidocaine, monoethylglycinexylidide, and isolated human uterine muscle. 62 23

We compared the effects of a therapeutic concentration of disopyramide with those of quinidine and lidocaine on the action potential characteristics and on the steady-state relationship between membrane potential and the maximum rate of rise of the action potential in the same normal Purkinje fiber in which constant impalement was maintained for more than 7 h. All the drugs depressed the steady-state upstroke velocity in the following order of magnitude: quinidine greater than disopyramide greater than lidocaine. Both lidocaine and disopyramide shifted the normalized steady-state curve to more negative membrane potentials indicating a greater depression of upstroke velocity at lower membrane potentials. Quinidine did not shift this curve. Lidocaine abbreviated all phases of repolarization while both disopyramide and quinidine shortened the plateau phase and lengthened the terminal phase of the action potential. The results suggest that the actions of disopyramide on upstroke velocity resemble those of lidocaine, while its effects on action potential duration resemble those of quinidine. The actions of this drug are therefore more complex than previously assumed.
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PMID:Disopyramide phosphate: is it just another quinidine. 63 88

The antiarrhythmic effects of the quinoline derivative, quinetholate, on ouabain-induced tachycardia were compared with those of lidocaine and procainamide in dogs. In addition, the effects of these three agents on cardiac function were compared. Quabain was injected intravenously until ventricular ectopic beats accounted for at least 60% of the heart rate. Then one of the above antiarrhythmic agents was infused until sinus rhythm was reestablished for a minimum of 3 min or until it became evident that successful reversion would not occur. All three agents effectively reversed ouabain-induced ventricular tachycardia in most instances. Quinetholate was especially consistent, causing 16 reversions out of a total of 17 experiments. The relative molar antiarrhythmic potencies of the three agents in responding animals were as follows: lidocaine = 1.0, procainamide = 1.5, and quinetholate = 3.1. Quinetholate caused the longest lasting reversions, i.e. usually lasting at least 30 min after infusion was stopped. The degree of cardiac depression caused by the three agents at their mean effective antiarrhythmic doses was determined using the left ventricular function curve method. Lidocaine produced a significant depression of the ventricular function curve at the antiarrhythmic dose while procainamide and quinetholate did not.
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PMID:A comparison of the effects of quinetholate, lidocaine and procainamide on ouabain-induced ventricular tachycardia and cardiac function. 67 62

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.
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PMID:Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs. 79 79

Regional myocardial function following occlusions of the circumflex coronary artery was studied in unanesthetized dogs using minature ultrasonic crystal pairs implanted subendocardially within the left ventricle for measurement of control, marginal, and ischemic lengths. As early as five beats after coronary occlusion, reduced function was apparent in ischemic zones, and an increase in heart rate occurred (78 to 115 beats/min) at an average of 25 sec. In the control zones, shortening initially increased from a constant end-diastolic length, but later end-diastolic length also increased by 7.5%. Shortening in the marginal zones was reduced by 50% at 90 sec as holosystolic expansion developed in the ischemic zones. On reperfusion, systolic function returned to normal within a few minutes while protodiastolic abnormalities persisted for up to 45 min. With coronary occlusions longer than two minutes most dogs exhibited arousal and further tachycardia; this reaction was prevented by morphine. During two minute occlusions morphine also decreased the heart rate increase by 37%, and marginal segment shortening was improved by 40%. Prior administration of propranolol also decreased heart rate during coronary occlusion and produced similar improvement in marginal segment function; however, in contrast to morphine, there was depression of contraction in the control segments. Nitroglycerin given during coronary occlusion caused decreases in end-diastolic length of all segments and increased shortening in the marginal segment by 28%. Lidocaine administered during coronary occlusion produced a mild depression of myocardial function in all regions of the heart.
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PMID:Regional Myocardial function in the conscious dog during acute coronary occlusion and responses to morphine, propranolol, nitroglycerin, and lidocaine. 81 13

The effect of various local anesthetics and other substances known to modify calcium fluxes in cells, on submaximal responses of guinea-pig ileum to substance P, acetylcholine, histamine and barium chloride was determined. Procaine caused a dose-related depression of the response to all the agonists but the response to substance P was far less susceptible to this depression. Lidocaine, bupivacaine, pramoxine and W 6211 also caused a lower degree of attenuation of the response to substance P than the responses to acetylcholine, histamine and barium chloride. Verapamil caused a dose-related depression of responses to all the agonists equally. The use of calcium-free solutions abolished responses to substance P, acetylcholine and histamine. The response to barium chloride was less affected by calcium withdrawal but was reduced markedly. In the presence of 10 mM lanthanum chloride, the response to all the agonists was abolished. The relative resistance of the substance P responses to antagonism by local anesthetics suggests that different and more efficient channels for calcium entry into the smooth muscle cell are involved.
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PMID:Interactions between local anesthetics and spasmogens on the guinea-pig ileum. 93 95

A new lidocaine derivative (Astra, GEA 968) depresses excitability of myelinated frog nerve in a manner which depends upon the rate of use of the nerve. This phenomenon has been shown, under voltage clamp conditions, to involve "frequency-" or "use-dependent" inhibition of the transient inward sodium currents at the node of Ranvier. With 0.6 mM GEA 968 in the solution bathing the node, the inward sodium currents produced by 5-msec depolarizing pulses to -20 mV are reduced to 40% of control values if the node is rested for a few hundred seconds prior to the test pulse. Repetitive opening of the sodium channels by depolarizing pulses enhances this inhibition, for example, currents are eventually reduced to 10 to 20% of control with repetitive depolarization at 2 sec-1. If the preparation is then allowed to rest, this use-dependent increment in inhibition gradually declines with a time constant of about 10 seconds. Repetitive opening of the sodium channels by depolarizing pulses preceded by large hyperpolarizing prepulses reverses the inhibition caused by application of depolarizing pulses alone. It is hypothesized that the GEA 968 molecule binds to open sodium channels and, in doing so, simultaneously blocks the channel and shifts the curve relating sodium inactivation to membrane potential by 20 to 40 mV in the hyperpolarizing direction. Several kinds of evidence supporting this molecular hypothesis are presented. Lidocaine, procaine, procaine amide and a quaternary lidocaine derivative QX-314 also cause use-dependent depression of sodium currents in this preparation. This common mode of action of tertiary and quaternary anesthetics implies that the cationic form of tertiary anesthetics is active.
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PMID:Mechanism of frequency-dependent inhibition of sodium currents in frog myelinated nerve by the lidocaine derivative GEA. 108 Nov 38


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