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)

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.
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PMID:The electrophysiological effects of ouabain on sinus node and atrium in man. 115 73

Bit-mapped multicomponent CNV complex and reaction time (RT) were recorded and measured in 24 presenile patients with initial symptoms of very mild to moderately severe primary mental deterioration without depression, and in 10 age-matched controls. All patients underwent CT and MRI examinations, EEG spectral analysis and a battery of psychometric test. Significant group differences were obtained for measures of some post-S1 ERP and CNV components, particularly of the post-S1 N1b, P300 and early and late pre-S2 CNV. P300 with increased latency, no significant CNV activity, very prolonged RTs, EEG slowing down and diffuse brain atrophy were observed in the majority of patients with probable presenile Alzheimer's dementia. These results suggest that CNV/RT and EEG activity changes similar to those observed in our patients may constitute a valuable clue for the study of brain dysfunction in the early stage of presenile idiopathic cognitive impairment.
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PMID:Effect of physiological and pathological aging processes on topographic bit-mapped cognitive evoked potentials in presenile subjects. 180 55

Pharmacologic action of antiarrhythmic agents in hypoxia was studied with the microelectrode using the guinea pig papillary muscle. Tyrode solution saturated with 95% O2 and 5% CO2 provided normoxic condition and that with 95% N2 and 5% O2 hypoxic condition. The parameters measured were as follows: 1) Vmax: the maximum rate of rise of the action potential, 2) ERP: effective refractory period, 3) ERP/APD90%: the ratio of effective refractory period to action potential duration at 90% repolarization. [1] When the papillary muscle was perfused more than 15 minutes with the hypoxic solution, irreversible changes ensued inevitably. Accordingly, a perfusion with the hypoxic solution for 15 minutes was succeeded by that with the normoxic solution for 30 minutes. This was then followed by another perfusion with the hypoxic solution. [2] Flecainide was examined in 7 cases. The rate of the depression of Vmax by flecainide was significantly (p less than 0.01) increased in hypoxia (16.3 +/- 4.2%) than in normoxia (7.4 +/- 2.0%). There were no significantly differences in the rate of the change of ERP between both conditions. The rate of ERP/APD90% was significantly (p less than 0.01) increased by flecainide during hypoxia (2.2 +/- 0.8%) than during normoxia (0.1 +/- 2.1%). [3] The depression of Vmax and the increase of ERP/APD90% by flecainide occurred in a dose-dependent manner in normoxia. it was concluded that the depression of Vmax by flecainide over the concentration of 2 micrograms/dl were ascribed to its inhibitory effect on the fast Na channel and that its depressive effects were enhanced during hypoxic condition. This inhibitory action was regarded as the main antiarrhythmic action of flecainide. From the above results, it is expected that flecainide could be effective in the treatment of ventricular arrhythmias in the ischemic heart disease.
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PMID:[A design of the electrophysiological model on the action of antiarrhythmic agent in hypoxic condition and the electrophysiological study of flecainide]. 190 36

Berberine (Ber) 0.1-30 mumol/L decreased the APA, Vmax, maximal depolarization potentials (MDP) and rate of spontaneous impulse initiation in sinoatrial node (SAN) and atrioventricular node (AVN) cells with prolongation of APD50, APD95 and ERP in a dose-dependent manner. The depression of SAN function was shown by increasing sinus cycle length (SCL), sinus recovery time (SRT) as well as corrected sinus recovery time (CSRT). In atria (crista terminalis, CT) higher concentrations of Ber were needed to prolong APD50, APD95, and ERP as compared with SAN and AVN. The effects of Ber on SAN were not antagonized or reversed by atropine (1 mumol/L), alpha 2-receptor agonist BHT-920 (10 mumol/L) or alpha 1-receptor agonist phenylephrine (10 mumol/L), but those effects of Ber on SCL, APA and Vmax could be reversed by norepinephrine (0.1 mumol/L). In calcium free Tyrode's solution, the inhibitory effects of Ber still revealed on SAN but on atria only prolongations of APD50 and APD95 were observed.
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PMID:Electrophysiologic effects of berberine on isolated sinoatrial and atrioventricular nodes of rabbit. 213 May 97

Dauricine (Dau) 1-30 mumol/L produced the concentration-dependent depression of APA, Vmax, MDP, and RP, and prolongations of APD90 of Purkinje fibers (PF) and epicardial ventricular muscles (VM) from both infarcted and non-infarcted zones. The ERP was lengthened only in non-ischemic PF and VM, and APD50 in non-ischemic PF, non- and ischemic VM. The prolonging effects of Dau on APD and ERP of ischemic PF were much less than those of non-ischemic ones, and its depressing effect on the Vmax of ischemic VM was markedly greater than that of non-ischemic VM. The results suggest that Dau exerts its anti-arrhythmic effect through further depressing conduction of ischemic zone.
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PMID:Effects of dauricine on transmembrane potential of ischemic and non-ischemic Purkinje fibers and ventricular muscles from infarcted canine hearts. 213 Jun 14

A few cases of sinus node dysfunction (SND) and AV block (AVB) were described with clonidine therapy. The aim of this study is to evaluate the electrophysiologic properties of clonidine in volunteers with normal electrophysiologic data. Twenty-eight subjects were investigated by endocavitary techniques. The following parameters were measured before and 20 min after intravenous administration of clonidine: systolic and diastolic blood pressure (BP); sinus cycle (SC); PA, AH, and HV intervals; effective (ERP) and functional (FRP) refractory period of right atria (RA); AV node (AVN); His Purkinje system (HP); right ventricle (RV); corrected sinus node recovery time (SNRT); and sinoatrial conduction time (SACT). Blood pressure was reduced from 149/89 to 115/74 mm Hg. Sinus cycle was prolonged by 71 ms (p less than 0.01), corrected SNRT by 81 ms (p less than 0.05), and FRP of AVN by 16 ms (p less than 0.05). SND was more marked when initial SC was longer. Atrioventricular node depression was more marked when the PR interval was longer and when subject was older. Electrophysiologic effects of clonidine are similar to those of beta-blockers. The tensional effects are more marked than electrophysiologic effects. Clonidine in the high risk subject (age, bradycardia, long PR) may be cautiously dosed. Drug association with digitalis antiarrhythmic drugs, beta-blockers, and calcium antagonists may be avoided.
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PMID:Study of the electrophysiologic properties of clonidine administered intravenously. 242 9

1. The preceding paper (Van der Kloot, 1988) described a method for estimating the timing of quantal releases during an end-plate current. This period of elevated quantal release is called the early release period or ERP (Barrett & Stevens, 1972b). In the present paper, this deconvolution method is used to study the effects of varying quantal output by extracellular ions, stimulus patterns and drugs. 2. The data were obtained by voltage clamping end-plates in low-Ca2+ high-Mg2+ solutions, or in solutions containing tubocurarine (measuring the decay of the miniature end-plate currents (MEPCs) before curarization and assuming a value for MEPC amplitude after curarization). Data were also obtained by extracellular recording in Ca2+-free solution, using a recording pipette filled with CaCl2 and regulating Ca2+ release with a bias current. The three approaches led to similar conclusions. 3. Quantal release rose during the ERP along a sigmoid curve and reached a maximum after about 1.4 ms at 10 degrees C. This is called the time to peak. Quantal release then fell, following an exponential time course with a time constant of about 1.2 ms (10 degrees C). This is called the time constant for decline. 4. The ERP was followed by further, elevated quantal release, at a much lower rate, which declined over a longer time course. This is called late release. The magnitude of late release appears to be almost independent of the magnitude of release during the ERP, although the deconvolution method is a poor one for determining late release. The remainder of the results therefore focus on the ERP. 5. Increasing [Ca2+]o increased quantal output, and the rate of quantal output. It did not change the time to peak or the time constant of decline. Similarly, replacing Ca2+ with Sr2+ did not alter the time course of the ERP. 6. Two-pulse facilitation increased quantal output without changing the time to peak or the time constant of decline. 7. Quantal output was enhanced still more following a brief series of repetitive nerve stimulations. There was a lengthening of the time to peak; there was no change in the decline. The depression produced by longer series of repetitive stimulations did not change the time course of the ERP. 8. 4-Aminopyridine (4-AP) and dimethylsulphoxide (DMSO) increased quantal output and lengthened the time to peak, without altering the time constant for decline. 9. Adenosine decreased quantal output without altering the time course of the ERP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The kinetics of quantal releases during end-plate currents at the frog neuromuscular junction. 285 24

Three patients had documented fundus changes conforming to those of the recently described multiple evanescent white dot (MEWD) syndrome. All three patients were unilaterally affected with variously sized, soft, single, and coalescent white lesions at the level of the RPE and the deep retina. Fluorescein angiography demonstrated early staining and hyperfluorescence of the white dots and delayed staining around the optic disc. Some degree of optic disc edema could be seen in all three eyes, two of which had corresponding field defects. In all three eyes, characteristic "stippling," or granularity, of the affected macula developed rapidly and vitreal cells were observed. One eye had signs of previous perivascular inflammation. ERG studies performed on one patient indicated a reduction in the a-wave and depression of the ERP, findings that correlated with the clinical observations of RPE affectation.
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PMID:Multiple evanescent white dot syndrome. 342 Mar 13

Amiodarone, a wide spectrum antiarrhythmic agent, has been associated with hypotensive reactions in man as well as in dogs after intravenous use. This hypotensive effect has been attributed to Tween 80, the diluent in the commercially available form of amiodarone. We studied the electrophysiologic effects of Tween 80 in the cardiac conduction system of the dog. Electrophysiologic studies were conducted in anesthetized adult dogs before and after the administration of 10 and 20 mg/kg of Tween 80, equivalent to the amount of diluent in 5 and 10 mg/kg respectively of commercial intravenous amiodarone. In addition to a drop of 60% in systolic blood pressure and 66% in diastolic blood pressure (p less than 0.005), 10 mg/kg of Tween 80 induced a decrease in heart rate (sinus cycle length increased from 523 +/- 57 msec to 662 +/- 27 msec, p less than 0.025), prolongation of sinus node recovery time (652 +/- 77 msec to 804 +/- 45 msec, p less than 0.05), depression of AV nodal function manifested by induction of Wenckebach at longer cycle length (from 208 +/- 18 msec to 266 +/- 14 msec, p less than 0.005), and increase in atrial ERP (from 138 +/- 7 msec to 176 +/- 14 msec, p less than 0.025) and FRP (from 180 +/- 14 msec to 209 +/- 12 msec, p less than 0.025). No further significant changes were observed after the second Tween 80 dose. The ventricular ERP increased significantly (from 168 +/- 18 msec to 20 +/- 16 msec, p less than 0.025) following the 20 mg/kg dose. It is demonstrated that Tween 80 is a potent depressant of the cardiac conduction system in the dog, capable of causing electrophysiologic changes similar to those produced by amiodarone in humans and dogs.
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PMID:Electrophysiologic effects of Tween 80 in the myocardium and specialized conduction system of the canine heart. 673 37

The syndromes associated with dementia and depression in old age show a considerable overlap and even coincidence, not only for statistical reasons. Starting with a critical evaluation of the term "pseudodementia", possibilities for a differentiation of both types of syndromes by characteristics of clinical features and history and by additional investigations are shown. A critical review of the literature with focus on the differentiating properties of the following methods is given: neuropsychology and rating scales (e.g., "cortical" mediated versus motivational changes), neurophysiology (electroencephalography, EEG; evoked potentials, EP; event-related potentials, ERP), sleep physiology (REM-sleep changes; sleep deprivation results), neuroendocrinology (dexamethasone suppression test), neuroradiology (cranial computed tomography, CCT; magnetic resonance imaging, MRI) and especially the dynamic imaging methods of nuclear medicine (cerebral glucose metabolism with fluorodeoxyglucose and positron emission tomography, FDG-PET; cerebral blood flow (CBF) measurements with PET and single photon emission tomography, SPET). Developments during recent years concerning better imaging of early hippocampal lesions (MRI) or analysis of CBF--changes induced by activation methods may be very helpful. In conclusion, one can say that the diagnosis of dementia and depression remains primarily a clinical one that can be ascertained by means of valuable diagnostic tools.
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PMID:[Early diagnostic differentiation of primary dementia from primary depressive syndromes in the aged--a contribution to the discussion of pseudodementia]. 831 28


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