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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recurring substernal chest pain is an important clinical problem, causing anxiety for patients and their physicians because of the fear of possible cardiac disease. The differential diagnosis includes coronary artery disease, oesophageal disorders such as acid reflux disease and motility disturbances, musculoskeletal problems, psychological disorders including panic attacks, and a new 'fly in the ointment'--microvascular angina. History alone usually cannot distinguish cardiac from non-cardiac chest pain. After exclusion of significant coronary artery disease, attention must be turned to oesophageal disorders, which may be seen in as many as 50% of these patients. Oesophageal motility disorders, particularly the nutcracker oesophagus, are common, but the relationship between pain and abnormal contraction pressures is not well established. Provocative tests such as edrophonium (Tensilon) and balloon distension help to identify the oesophagus as the source of chest pain but do not direct therapy. Recent studies with ambulatory oesophageal monitoring suggest that gastro-oesophageal reflux may be a more common cause of chest pain than motility disorders. This is an important finding as acid reflux is a treatable problem, while therapies for motility disorders may only worsen reflux disease. The recent observation that oesophageal disorders are frequently associated and interact with psychological disorders such as anxiety, depression, somatization and panic attacks complicates the evaluation and understanding of chest pain. How these various abnormalities may be linked is an unresolved issue. Increased central nervous system stimulation and altered visceral and/or central pain sensitivity could be the common factors. It is hoped that further research into these areas will lead to new understandings of and possible solutions to the complex problem of non-cardiac chest pain.
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PMID:Investigation and management of non-cardiac chest pain. 191 53

The effects and interactions of nifedipine and diltiazem with tubocurarine, gallamine and pancuronium and their reversal by edrophonium and neostigmine were studied on isolated skeletal muscle of the chick. The nerve-muscle preparation of the chick biventer cervicis was set up in an organ bath containing Krebs-Henseleit solution and the mechanical responses produced either by motor nerve stimulation or by drug application were recorded isometrically. The results showed that nifedipine (29-1015 microM) and diltiazem (22-572 microM) reduced, in a dose-dependent manner, the amplitude of indirectly-elicited twitch tension, evoked at 0.2 Hz with 5-10 V and 0.2 msec pulse duration, and increased the neuromuscular blockade produced by d-tubocurarine (1-254 microM), gallamine (0.01-2.0 microM) and pancuronium (0.01-7.0 microM). Edrophonium (250 nM) and neostigmine (150 nM) completely reversed the neuromuscular blockade produced by the muscle relaxants, alone and in combination with nifedipine or diltiazem. The mean IC50 values (concentrations to produce 50% of maximum inhibition) of nifedipine and diltiazem-induced depression of twitch response were 324 +/- 16 microM and 143 +/- 11 microM respectively (means +/- S.E., n = 6). Nifedipine, in high concentrations, produced small contractions (0.4 +/- 0.1 g of tension, n = 6), in the chick muscle. In contrast, diltiazem produced no such contractions in the muscle. However, in concentrations which had little effect on twitch response, diltiazem (20 microM) and nifedipine (50 microM) both increased the neuromuscular blockade produced by tubocurarine, gallamine and pancuronium by about 2-fold. Increasing the external calcium concentration, by a 2-fold, did not reverse or antagonize the inhibitory effects of diltiazem or nifedipine. It was concluded that diltiazem and nifedipine inhibit indirectly-elicited twitch tension and intensify neuromuscular blockade produced by muscle relaxants. These effects of nifedipine and diltiazem may be due to blocking influx of calcium and on release of acetylcholine from presynaptic nerve terminals.
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PMID:Interactions of nifedipine and diltiazem with muscle relaxants and reversal of neuromuscular blockade with edrophonium and neostigmine. 379 69

The extent of cholinergic-sympathetic interaction in the heart was examined in the resting control state and after isoproterenol stimulation in eight conscious dogs. Sonomicrometer crystals and solid-state pressure transducers were implanted in the left atrium and the left ventricle to evaluate mechanical function while heart rate was held constant by atrial pacing. Edrophonium (0.5 mg/kg i.v.) was given as a single dose at rest and during increased sympathetic tone produced by continuous infusion of isoproterenol (0.08 micrograms/kg/min). In the control state, edrophonium administration caused no change in left ventricular dP/dt, fractional shortening or velocity of contraction, but produced significant (P less than .001) decreases in left atrial fractional shortening and contraction velocity. During isoproterenol infusion there were significant increases in dP/dt, the velocity of contraction and fractional shortening in both left atrium and ventricle (P less than .001). Administration of edrophonium during this increase in inotropic state produced significant (P less than .01) decreases in left ventricular dP/dt, fractional shortening and contraction velocity. Moreover, after edrophonium, left atrial fractional shortening and velocity of contraction were decreased to values that were significantly (P less than .001) less than control. Thus, cholinergic stimulation caused selective depression of left atrial systolic function at rest and depression of both left atrial and ventricular function during sympathetic stimulation.
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PMID:Cholinergic-sympathetic interactions in the left atrium and left ventricle of conscious dogs. 683 73

Edrophonium's onset and duration of antagonism (n = 26) and atropine requirement (n = 24) were determined under conditions of d-tubocurarine (dTc) neuromuscular blockade and halothane, nitrous oxide anesthesia. Results are compared with previous work in our laboratory on neostigmine and pyridostigmine under similar conditions. dTc was administered by continuous infusion to maintain a 90% depression of muscle twitch tension. Edrophonium (0.03-1.0 mg/kg) was injected as an iv bolus in combination with atropine (0.5 mg). dTc infusion was continued until a stable 90% depression of muscle twitch tension was reestablished. Time-to-peak effect (onset of action), duration, and magnitude of antagonism were recorded. The atropine requirement was determined during spontaneous recovery from dTc (0.3 mg/kg) and stable halothane, nitrous oxide anesthesia. Edrophonium (0.5 mg/kg) was mixed with 7, 15, or 30 micrograms/kg of atropine and compared to neostigmine (0.043 mg/kg) and atropine (15 micrograms/kg). Blood pressure, heart rate, and rhythm were recorded for 60 min following edrophonium administration. The time-to-peak antagonism for edrophonium (0.8-2.0 min) was far more rapid than neostigmine (7-11 min) or pyridostigmine (12-16 min). The ED50 for edrophonium was 0.125 mg/kg, however, the dose-response curve was not parallel to those for neostigmine or pyridostigmine. In equiantagonistic doses, the duration of antagonism by edrophonium (66 min) did not differ from neostigmine (76 min), but was shorter than pyridostigmine. Edrophonium required one-half the amount of atropine as did neostigmine to prevent bradycardia. The authors concluded that edrophonium has a more rapid onset than neostigmine and an equivalent duration of antagonism, and requires less atropine to prevent bradycardia.
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PMID:Edrophonium: duration of action and atropine requirement in humans during halothane anesthesia. 712 61

We have compared the antagonism of neuromuscular block produced by pipecuronium with pancuronium in 80 anaesthetized surgical patients using mechanomyography and electromyography. Pancuronium 0.1 mg kg-1 or pipecuronium 0.07 mg kg-1 was given after induction of anaesthesia and neuromuscular block was adjusted to 75% twitch depression at the time of antagonism. The following regimens were used: edrophonium 0.5 and 1.0 mg kg-1, neostigmine 0.04 mg kg-1, pyridostigmine 0.3 mg kg-1 and edrophonium 0.25 mg kg-1 with pyridostigmine 0.15 mg kg-1. Antagonism was evaluated also by the head lift test. There was no difference between the reversibility of neuromuscular block produced by pancuronium or pipecuronium. Edrophonium produced a significantly faster antagonism than neostigmine or pyridostigmine but onset of action was not significantly faster than that of edrophonium with pyridostigmine. All regimens produced 100% (or near 100%) antagonism of twitch response within 15 min. However, TOF fade antagonism was more complete with pyridostigmine, neostigmine and edrophonium 1.0 mg kg-1 than with edrophonium 0.5 mg kg-1. The head lift test indicated somewhat less antagonism with edrophonium 0.5 and 1.0 mg kg-1. Using five monitoring methods, the rank order of reversal potency was: pyridostigmine approximately neostigmine > edrophonium 1.0 mg kg-1 > edrophonium+pyridostigmine > edrophonium 0.5 mg kg-1.
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PMID:Antagonism of pancuronium- and pipecuronium-induced neuromuscular block. 773 60

This longitudinal study utilized a community sample of children (N=91, 45% female, 8-11 years at time 1) to investigate physiological responses (heart rate reactivity [HRR] and electrodermal responding [EDR]) during delay of gratification in relation to emotionality, self-regulation, and adjustment problems. Cluster analyses identified three profiles among children who successfully delayed: children who waited easily with low EDR and moderate HRR, children who had difficulty waiting with high EDR and moderate HRR, and children who had difficulty waiting with low EDR and low HRR. The 3 clusters and children who did not wait were compared. Children with low EDR-low HRR had the lowest self-regulation, and like the no-wait group, demonstrated the greatest baseline adjustment problems. The high EDR-moderate HRR group demonstrated highest self-regulation and increases in depression across one year. Distinct profiles among children in delay contexts point to children who are over- and under-regulated with implications for adjustment problems.
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PMID:Physiological Profiles During Delay of Gratification: Associations with Emotionality, Self-regulation, and Adjustment Problems. 2004 98