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)

Twitch contractions of the isolated guinea-pig vas deferens induced by sympathetic nerve stimulation were augmented by acetaldehyde (0.1-10 mM). With high concentrations (5-10 mM), acetaldehyde produced a biphasic response consisting of an initial brief depression and a subsequent potentiation of the contraction. The late effect was associated with repetitive contractions that were not prevented by tetrodotoxin. A low concentration of phentolamine (27 microM) increased and a high concentration (1.3 mM) suppressed the potentiating action of acetaldehyde. Acetaldehyde did not induce contractions in surgically sympathectomized vasa or vasa pretreated with reserpine. Acetaldehyde caused a dose-dependent increase in noradrenaline release into the bathing fluid. The study shows that acetaldehyde has a dual effect on sympathetic neuroeffector transmission, and that an increase in noradrenaline secretion appears to contribute to the late facilitatory effect in the isolated vas deferens.
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PMID:Effects of acetaldehyde on contractile response to nerve stimulation in guinea-pig vas deferens. 196 46

With the aid of a contact K(+)-sensitive electrode, potassium levels were measured near the surface of the frog resting and twitching isolated m. gastrocnemius. Increasing extracellular K+ in case of indirect repetitive stimulation of the muscle or the blocking of K(+)-Na(+) pump can lead to a depression of the muscle twitches. Transition from repetitive to single-shock stimulation of the muscle restored the twitches. Elevated extracellular potassium seems to be able to cause a presynaptic blockade in the motor axons.
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PMID:[The potassium ion yield from the frog muscle studied using a contact ion-selective electrode]. 196 25

One hundred seventeen adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-narcotic (BAL, n = 45) nitrous oxide-halothane (HAL, n = 27) and nitrous oxide-isoflurane (ISF, n = 45) anesthesia. Anesthesia was maintained with nitrous oxide (60%-70%) and oxygen (30%-40%) with end-tidal concentrations of halothane or isoflurane to yield a total MAC of approximately 1.25, or with supplemental fentanyl and thiopental as clinically indicated. Twitch response of the adductor pollicis muscle was elicited by supramaximal square wave pulses of 0.2 msec duration at a frequency of 0.15 Hz (Grass S44 stimulator) to the ulnar nerve and quantitated by a Grass FT10 transducer. Nine patients in each of the HAL and ISF groups received one of four doses of mivacurium (0.03, 0.05, 0.10 or 0.15 mg/kg). Ninety patients in the balanced anesthesia group received one of seven doses of mivacurium (0.03, 0.04, 0.05, 0.08, 0.15, 0.20, 0.25 mg/kg). The ED50, ED75 and ED95 of mivacurium in each group were estimated from linear regression plots of log dose versus probit of maximum percentage depression of twitch height. The ED50, ED75 and ED95 for halothane and isoflurane are 0.040, 0.053 and 0.081 and 0.037, 0.043 and 0.053, respectively. The ED50, ED75, and ED95 for the balanced group are 0.039, 0.050, and 0.073 mg/kg respectively. There was no significant difference between the slopes of the HAL and BAL inhalation anesthetic dose-response curves. The slope of the ISF group was significantly than the slope of the BAL group. Intercepts of the HAL and BAL curves were not different. The isoflurane curve's intercept was significantly less than the other groups' intercepts, lying above the halothane curve, but below the BAL curve. For the 0.05 mg/kg dose, maximum block was greater in the ISF group (89.1 +/- 2.7%, n = 9) than in the HAL (70.3 +/- 7.6%, n = 9) or BAL (67.7 +/- 6.4%, n = 9) groups. At higher doses of mivacurium, isoflurane produces a greater potentiation of neuromuscular block than halothane or balanced anesthesia. There were no significant cardiovascular changes seen in any group following mivacurium doses up to 0.15 mg/kg (approximately 2xED95).
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PMID:Neuromuscular and cardiovascular effects of mivacurium chloride (BW B109OU) during nitrous oxide-narcotic, nitrous oxide-halothane and nitrous oxide-isoflurane anesthesia in surgical patients. 214 82

The response of the neuromuscular junction to expansion of the motor unit after partial denervation (section of L5 root) was compared in soleus muscles from young (5-8 month) and old (25-30 month) mice. The object was to determine the relative capacity of young and old motor neurons to adapt to an enlarged functional field of innervation, and to delineate physiological parameters that are compromised under these conditions. Neuromuscular function was studied at 30, 60, and 120 d after partial denervation. The initial (18-23) and postoperative number (5-8) of motor units was the same in both age groups. Twitch strength declined in proportion to loss of motor units at 30 d but returned completely (young) or nearly completely (old) by 60 d. In old but not young muscle, the safety factor (assayed by twitch depression in low calcium) was decreased even before functional sprouting had occurred, indicating a reduced safety factor in nondenervated junctions. The proportion of fibers with "long" latencies (delay between stimulation and endplate potential) increased transiently (at 30 d) in young muscle but persisted without recovery at 120 d in regenerated junctions in old muscle. After partial denervation, decline in miniature endplate potential (mepp) amplitude, in mepp frequency, and in estimated quantal content of evoked release was relatively more pronounced in old than in young mice, and in the case of mepp amplitude and frequency, more persistent. Mepp amplitude was also decreased in presumed nondenervated junctions of old muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of age on neuromuscular transmission in partially denervated mouse muscle. 215 58

We studied the effect of aminophylline on twitch tension (TT) and intracellular pH (pHi) in isolated rat diaphragm strips that were fatigued, hypercapnic, or hypoxic. Superfused muscles were directly stimulated at 0.5 Hz. The pHi was measured from distribution volumes of dimethyl-oxazolidinedione. Fatigue was induced by intermittent tetanic stimulation. Hypercapnia and hypoxia were produced by altering superfusate carbon dioxide tension (PCO2) or oxygen tension (PO2). Aminophylline (1.0 mmol.l-1) reversed the twitch decay seen during fatigue or hypercapnic acidosis, and caused partial recovery of twitch depression during hypoxia. Muscle fatigue was not due to an intracellular acidosis. Both hypercapnia and hypoxia lowered pHi. Aminophylline did not alter pHi in unstimulated muscles, but caused a significant fall in pHi in stimulated muscles that were fatigued or hypoxic. High dose aminophylline improved twitch tension in diaphragm strips that were fatigued, acidotic, or hypoxic. Twitch potentiation was not due to an intracellular alkalosis. Aminophylline lowered pHi in stimulated muscle, and thus, theoretically, could sometimes be harmful in the treatment of muscle fatigue.
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PMID:The effect of aminophylline on function and intracellular pH of the rat diaphragm. 228 69

We developed a two-compartment model to simulate neuromuscular function and heart rate following the administration of four nondepolarizing neuromuscular blocking agents (atracurium, vecuronium, pancuronium, and d-tubocurarine), three neuromuscular block reversal agents (edrophonium, neostigmine, and pyridostigmine), and two anticholinergic agents (atropine and glycopyrrolate). Twitch depression, train-of-four ratio, and heart rate were modeled during fentanyl, halothane, enflurane, or isoflurane anesthesia, optionally supplemented with nitrous oxide. Simulation results, compared with published values for each drug, fell within the clinical accuracy range (onset time 6.1 +/- 3.9% [mean +/- SEM]; duration, 1.7 +/- 3.5%, 50% effective dose, 0.5 +/- 5.7%; and 95% effective dose, 2.1 +/- 1.1%). The simulation graphically demonstrates the pharmacokinetics, pharmacodynamics, and interactions between neuromuscular blocking agents, reversal agents, and anticholinergic agents. During a simulation, the need for frequent monitoring and repeated delivery of a neuromuscular blocking agent to keep neuromuscular blockade stable becomes apparent, especially with the intermediate-acting neuromuscular blocking agents. When inhalational agents are given concomitantly, the task becomes even more difficult, since potentiation changes with anesthetic uptake. Recurarization, tachycardia, or bradycardia may be seen with the simulation if an improper drug regimen is followed. Concurrent simulation of two identical patients allows comparison of different modes of administration, choice of anesthetic agents, and drug doses.
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PMID:A simulation of neuromuscular function and heart rate during induction, maintenance, and reversal of neuromuscular blockade. 240 85

The discovery of insulin in 1922 aroused immediate clinical interest in its use in heart disease. In severe heart failure, insulin release is suppressed by the combined effect of poor pancreatic perfusion and by increased sympathetic activity. In these circumstances, myocardial metabolism of glucose may break down through the deficiency of insulin. Because of this, glucose, insulin and potassium solution (GIK solution) has been used in cardiopulmonary resuscitation. However, its mechanism is not yet fully known. This study was designed to determine the effect of insulin on cardiac muscle at various temperatures. The mechanical response of papillary muscle isolated from guinea pig ventricle was observed under various thermal conditions (23-37 degrees C). Twitch tension was increased by the administration of 0.2 I.U./ml insulin under each thermal condition. In all circumstances, the increase in contractile force was noted about 2 min after the administration of insulin. The effect of insulin on 20 preparations demonstrated the mean maximum contractile force was 226% ( +/- 34 S.D., n = 5) in 37 degrees C, 194% ( +/- 36 S.D., n = 5) in 30 degrees C, 190% ( +/- 30 S.D., n = 5) in 27 degrees C and 200% ( +/- 36 S.D., n = 5) in in 23 degrees C. The differences between different temperatures was not significant. The effect of insulin during depression Na-K pump by high concentration of ouabain (g-strophanthin, 10(-5) M) was also observed. Insulin (0.2 I.U./ml) was administered when the papillary muscle showed no response to electrical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of isolated guinea pig myocardium to insulin therapy during normothermia and graded hypothermia. 242 78

1. Twitches, tetanic contractions and potassium contractures were recorded isometrically from small bundles of rat soleus muscle fibres. 2. Solutions with reduced calcium concentrations (low-calcium solutions), whether buffered with EGTA (85 and 3 microM-Ca2+) or not (15 microM-Ca2+), caused an initial potentiation of contraction followed by depression. 3. The decay of potassium contractures (200 mM-potassium) was more rapid than normal in low-calcium solutions. 4. Recovery from the inactivation produced by a 200 mM-potassium contracture was slowed in low-calcium solutions but full recovery was seen within 10-15 min after return to a solution containing 2.5 mM-Ca2+. 5. Nifedipine (50 microM) in solutions containing 2.5 mM-Ca2+ potentiated contraction whereas, in low-calcium solutions, contraction was depressed and the depression was more pronounced the lower the Ca2+ concentration. 6. As with low-calcium solutions, potassium contractures decayed more rapidly in solutions containing nifedipine. Nifedipine slowed still further the rate of recovery from inactivation in low-calcium solutions. 7. (-) Bay K 8644 (50 microM) depressed contraction, increased the rate of decay of potassium contractures and slowed recovery from inactivation, like nifedipine. The racemate of Bay K 8644 was less effective. 8. In explanation of these and other observations, it is proposed that there is a dihydropyridine-binding molecule in the walls of the transverse tubular system that normally exists predominantly in a 'precursor' form at the resting membrane potential and is converted by membrane depolarization to an 'activator' form essential for excitation-contraction coupling. Conversion of the precursor to activator involves both conformational change and dissociation of calcium. Prolonged depolarization converts activator to an inactivated form by inducing further conformational change and dissociation of calcium. Recovery from inactivation requires reverse conformational changes and rebinding of calcium. The dihydropyridines affect contraction by reducing the affinity of the molecule for calcium.
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PMID:Effects of extracellular calcium concentration and dihydropyridines on contraction in mammalian skeletal muscle. 245 97

The effects of sodium selenite on the neuromuscular junction of the phrenic nerve-diaphragm of the mouse were studied. Nerve-evoked twitches of the diaphragm of the mouse, the frequency of miniature endplate potentials, the quantal content of endplate potentials and the compound action potentials of the axon were measured. Sodium selenite induced a slight increase of the amplitude of the twitch, followed by twitch depression. The amplitude of the twitch, increased by selenite, became more prominent after the suppression of the twitch induced by cadmium ions, d-tubocurarine or magnesium ions. It appeared that the increased amplitude of twitch was due to the facilitation of transmitter release, since selenite significantly increased the frequency of miniature endplate potentials, and the amplitude and quantal content of endplate potentials; the amplitude and half decay time of miniature endplate potentials were unaffected. Twitch depression induced by selenite was enhanced by ammonium ions, high potassium and low magnesium and attenuated by high calcium. During the period of gradual depression of the twitch, selenite decreased the amplitude of compound action potentials of the phrenic nerve axon and caused the disappearance of endplate potentials. Ammonium ions enhanced the blockade of axonal conduction induced by selenite. Moreover, the depolarizing agents, ammonium and high potassium also induced an initial increase of twitch amplitude followed by depression of the twitch. These findings indicate that selenite probably alters the release of the transmitter by depolarizing the nerve membrane. The effects of selenite were antagonized by glutathione and cyanide, suggesting that the binding of selenite to sulfhydryl groups of the membrane was essential for inducing its pharmacological actions.
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PMID:Effects of sodium selenite on neuromuscular junction of the mouse phrenic nerve-diaphragm preparation. 247 66

The sedative effects of medetomidine at doses of 20 and 40 micrograms/kg im given alone or followed 16-18 min later by fentanyl (2 micrograms/kg iv) was investigated in 6 bitches of mixed breeds. The higher dose of medetomidine alone caused the greater degree of sedation, but two bitches were only lightly sedated with either dose. Side effects noted in some cases included apparent pain on injection, vomiting on induction of sedation, bradycardia, slowing of respiratory rate, cyanosis and muscular twitching. The intravenous injection of fentanyl caused a marked increase in depth of sedation in all animals, inducing a condition similar to neuroleptanaesthesia in which the eyes were rotated downward and the pedal reflex abolished. Slight twitching and sensitivity to sound occurred immediately after fentanyl injection, but this was transient. The cardiopulmonary effects of medetomidine (40 micrograms/kg im) followed 20 min later by either fentanyl (2 micrograms/kg iv) or a saline placebo were investigated in 4 beagle dogs. Medetomidine caused bradycardia, hypotension and reduced respiratory rate, inducing an intermittent respiratory pattern. The iv injection of fentanyl did not further alter the heart or respiratory rate or blood pressure. However there was a small but significant decrease in arterial oxygen tension and rise in arterial carbon dioxide tension. indicating some respiratory depression. We conclude that the use of intravenous fentanyl to dogs already sedated with medetomidine could prove useful in clinical cases where the initial sedation with medetomidine has proved inadequate.
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PMID:The use of medetomidine/fentanyl combinations in dogs. 257 Dec 71


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