UMLS:C0011570 - FACTA Search

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

The effects of increasing rest periods on rest contractions and rest potentiation were analysed on isometric contractions of guinea pig papillary muscles at room temperature. Rest contraction amplitude is dependent on pause duration and potentiated for short pauses, which decreases as the rest period increases. their inotropic state is also dependent on the inotropic state of steady state control contractions. This statement is validated by the interdependence between control contractions and rest contractions amplitude and also because positive (5.0 mM CaCl2) and negative (0.5 mM NiCl2)inotropic interventions do not change the time course of dF/dt pause duration curves. They also show a slow activation characterized by a prolonged TTP that depends on pause duration being observed even in contractions occurring after short pauses. Rest contractions can be elicited under depolarized conditions produced by TKBa (Tyrode with high potassium and barium) and TKAdr (Tyrode with high potassium and adrenaline), showing that they are dependent on calcium influx occurring during the slow response of the cardiac action potential. The present study, carried out under depolarized conditions and in low extracellular Na+, shows that Na+ entry during the Na-dependent fast component of the action potential is necessary for the occurrence of rest potentiation. These findings suggest that the intracellular Na+, that can be exchanged by external calcium with the Na/Ca exchange mechanism, is necessary for the occurrence of the rest potentiation and to avoid the accelerated depression of the rest contractions with increasing pause duration.
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PMID:Mechanical behavior of rest contractions in cardiac muscle. 320 99

1. To study the origin of ischaemic myocardial depolarization, the diastolic surface potential - T-Q depression-was correlated with subepicardial extracellular K+ accumulation during serial episodes of widespread ischaemia in open-chest dogs, and in isolated, blood-perfused canine hearts. Placement of the reference electrode on a small island of non-ischaemic myocardium simplified the interpretation of the T-Q potentials. 2. In some experiments, changes in resting potential in the ischaemic zone were recorded using a 'contact' monophasic action potential (MAP) electrode. The change in MAP resting potential was linearly related to T-Q depression for a wide range of experimental conditions (R greater than 0.98). T-Q depression is therefore a linear index of depolarization in superficial myocardial cells. 3. The validity of T-Q depression as a 'measure' of local cellular depolarization was further tested by infiltration of isotonic KCl into the superficial myocardium subjacent to the ischaemic zone electrode. Resulting T-Q depression was 2- to 3-fold larger than the maximum values obtained in ischaemia; and the ratio of T-Q depression to the amplitude of the accompanying monophasic potential was consistent with the assumption that KCl had fully depolarized the underlying myocardium (delta Vm = 89 mV). KCl prevented (i.e. occluded) further changes in the T-Q potential during ischaemia. KCl did not have these effects if it was introduced at sites more remote from the electrode (greater than 4 mm). 4. Ischaemic T-Q depression was drastically accelerated by increasing the heart rate from 90 to 180 beats/min and was further accelerated by arterial infusion of CaCl2. These effects were most striking during the first minute of ischaemia. 5. In contrast, the above manoeuvres produced little acceleration of subepicardial K+ accumulation. After CaCl2 infusion, large ischaemic potentials, severe conduction impairment, and arrhythmias could be observed when K+ activity was almost normal (aK = 4.0-4.5 mM). 6. T-Q depression was larger in vivo than in isolated hearts, both absolutely and relative to K+ accumulation. 7. Based on the reproducible amplitude of ischaemic epicardial potential-estimates of cellular depolarization (delta Vm) could be obtained, which were compared with the concurrent change in K+ electrode potential (delta EK) for each experimental condition. 8. Estimated depolarization was nearly identical to delta EK in isolated hearts under basal conditions. However, depolarization significantly exceeded delta EK during rapid pacing, CaCl2 infusion, or during paced occlusions performed in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanism of depolarization in the ischaemic dog heart: discrepancy between T-Q potentials and potassium accumulation. 341 9

The use of end-plate current (e.p.c.) latency measurements to estimate the time course of the stochastic probabilistic process governing evoked release was investigated in the sciatic nerve-sartorius muscle preparation of the frog, Rana pipiens. We also examined the possibility that the release of a quantum depresses or enhances the subsequent release of additional quanta. Muscle end-plates were voltage clamped at 3-4 degrees C. Quantal release was restricted to a short, or localized, region of the nerve terminal using Ca2+-free, EGTA Ringer solution and a Ca2+-filled micropipette. The number of e.p.c.s containing 0, 1, 2, etc. quanta were totalled and compared to numbers predicted using Poisson's theorem. The differences between the actual and predicted numbers of events were not significant at the nineteen junctions studied (P less than 0.05). The latency of the first quantum observed in several hundred e.p.c.s was measured and used to calculate an estimate, alpha 1(t), of the time-dependent, probabilistic process, alpha (t), governing all evoked quantal release (Barrett & Stevens, 1972b). In three experiments, all quantal latencies were measured to obtain the actual alpha (t). The alpha 1(t) function gave an excellent approximation of alpha (t) (P greater than 0.2), in real and simulated latency data. The latency of the second quantum in the e.p.c.s was measured and used to provide another estimate, alpha 2(t), of alpha (t). The alpha 2(t) function was lower (depressed) during the first few milliseconds of the evoked release period, relative to alpha 1(t). The difference was significant (P greater than 0.01) in all experiments. Our measurement procedures were tested using computer-generated 'e.p.c.s' containing randomly occurring 'quanta'. These tests showed that the early depression was due to inadequate detection of the second quantum in the e.p.c.s. The effect of Sr2+ on evoked release was examined using double-barrelled pipettes containing 1 M-SrCl2 and CaCl2 solutions. The major result was that the durations of alpha 1(t) and alpha 2(t) were equally lengthened in Sr2+, relative to Ca2+.
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PMID:Estimating the time course of evoked quantal release at the frog neuromuscular junction using end-plate current latencies. 348 94

Cardiovascular function, serum ionized calcium (Ca+2), and serum citrate were measured intraoperatively in patients (n = 9) undergoing orthotopic hepatic homotransplantation. Serum citrate increased 20-fold (P less than 0.0006) following transfusion of citrated blood products in the absence of a functional liver. Serum ionized calcium decreased (P less than 0.003) with concomitant decreases in cardiac index (P less than 0.005), stroke index (P less than 0.004), and left ventricular stroke work index (P less than 0.001). Hemodynamic depression and ionic hypocalcemia were reversed following the administration of CaCl2. In contrast to patients with normal hepatic function, who may tolerate large amounts of citrated blood, patients with end-stage liver disease demonstrate acute ionic hypocalcemia with concomitant hemodynamic depression when receiving citrated blood products during the course of hepatic transplantation.
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PMID:Cardiovascular depression secondary to ionic hypocalcemia during hepatic transplantation in humans. 353 71

The effect of calcium (0.5-6 mM) and neomycin (0.1-0.2 mM) on the maximum post-tetanic twitch tension (MTT) and post-tetanic depression (PTD) of the indirectly elicited twitch tension was studied on the mouse isolated phrenic nerve-diaphragm preparation. The effect of neomycin on MTT of directly stimulated twitch tension was also tested in (+)-tubocurarine pretreated preparations. Three-dimensional plots between MTT and frequency and duration of indirect tetanic stimulation revealed that the frequencies and durations inducing maximal MTT were 500 Hz for 20 s in 0.5 mM CaCl2, 100 Hz for 5 s in 2 mM CaCl2 and 100 Hz for 10 s in 6 mM CaCl2. The frequency and duration inducing maximal PTD was 100 Hz for 20 s in 0.5 mM CaCl2, but there was no PTD in 2 mM or 6 mM CaCl2. Neomycin was associated with significantly greater MTT than in control if the duration of tetanic stimulation was 1 or 2 s, while it was associated with less MTT if the duration of tetanic stimulation was 10 or 20 s. Neomycin caused PTD in 2 mM CaCl2; sometimes the depressive effect was so severe that twitch tension was abolished. The maximal depression effect was found after 100 Hz tetanic stimulation for 20 s. Increasing the extracellular calcium concentration to 6 mM antagonized the effects of neomycin on MTT and PTD, whereas neostigmine (1.6 microM) antagonized the effect partially. Neomycin had no effect on the MTT or PTD of the directly stimulated twitch tension. It is concluded that neomycin alters the conditions of tetanic stimulation inducing MTT.
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PMID:Effect of neomycin on post-tetanic twitch tension of the mouse diaphragm preparation. 358 Jul 2

Intracellular recordings were performed in Cs-loaded sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus, identified by antidromic stimulation, in the slice of the T2 or T3 segment of the cat spinal cord. Loading the neurons with Cs resulted in broadening of the action potential, depression of the fast component of the afterhyperpolarization (AHP), and appearance of an afterdepolarization (ADP). A typical ADP in a Cs-loaded neuron had time to peak of 45-110 ms, half-decay time of 70-250 ms, and amplitude of 2-10 mV at membrane potentials between -60 and -70 mV and at a Ca and K concentration of 2.5 and 3.6 mM, respectively, in the superfusion medium. The ADP was associated with a decrease in neuron input resistance and increased in magnitude with hyperpolarization of the cell membrane. The relation between peak ADP amplitude and membrane potential was linear within the range of membrane potentials from -60 to -100 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM) or by low Ca Krebs solution (0.25 mM). Superfusion with BaCl2 (1.0 mM) or tetraethylammonium (TEA) (10-20 mM) caused an increase in amplitude of the ADP and an increase in action potential duration. Hyperpolarizing pulses, delivered during the course of the spike shoulder, resulted in a decrease of spike duration and ADP amplitude. The ADP was not affected by tetrodotoxin, at a dose blocking the Na-spike, and was enhanced, in association with an increase in action potential duration, when NaCl in the Krebs solution was replaced with choline chloride. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. Changes in external K concentration from 3.6 to 10 or 0.36 mM increased and decreased, respectively, the amplitude of the ADP. In the absence of Cs, and ADP, with similar time course to that recorded in Cs-loaded SPNs, was recorded when CaCl2 was replaced by BaCl or NaCl was replaced by TEAC1. It is concluded that the SPN afterpotential includes a Ca-dependent inward current, in addition to the already described fast and slow outward K currents of the AHP.
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PMID:Afterdepolarization mechanism in the in vitro, cesium-loaded, sympathetic preganglionic neuron of the cat. 358 70

Effects of isepamicin sulfate (HAPA-B), a new aminoglycoside antibiotic, on the neuromuscular transmission were studied in rats and compared with those of amikacin (AMK) or other aminoglycoside antibiotics. The HAPA-B, as well as other aminoglycoside antibiotics, depressed the twitch response of diaphragm to phrenic nerve stimulation in vitro. The depression effects of different drugs were compared and graded in the order of strengths of blocking action as: netilmicin (NTL) greater than gentamicin (GM) greater than streptomycin (SM) greater than kanamycin (KM) greater than AMK greater than HAPA-B. The IC50 (concentration which inhibited the response by 50%) of HAPA-B was 3.6 X 10(-3) g/ml. The neuromuscular blockade produced by HAPA-B was reversed by CaCl2, KCl or caffeine but not by neostigmine. D-Tubocurarine or MgCl2 augmented the neuromuscular effects of HAPA-B. Intramuscular (400 mg/kg) and intravenous (100 mg/kg) injections of HAPA-B did not affect the twitch response of gastrocnemius muscle to sciatic nerve stimulation in situ. Intravenous injection of 200 mg/kg caused death in some rats and depression of the twitch response in others. Intravenous AMK produced no significant effect on the twitch response at 50 mg/kg and caused death at 100 mg/kg. GM and SM caused death or significant degree of depression of the twitch response at intravenous doses of 50 mg/kg. In experiments of intravenous drug infusion for 60 minutes, the twitch response was depressed by HAPA-B at 400 mg/kg/hr and by AMK at 200 and 400 mg/kg/hr. In conclusion, HAPA-B has a neuromuscular blocking action presumably at the nerve terminal. However, its action was the weakest among the aminoglycoside antibiotics tested.
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PMID:[The neuromuscular blocking activity of isepamicin sulfate (HAPA-B) compared with other aminoglycoside antibiotics]. 358 26

In order to evaluate the effects of the combination of halothane and verapamil on left ventricular function and coronary blood flow (CBF), six sheep were anaesthetized with halothane (1.2% inspired) and given increasing cumulative doses of intravenous verapamil. Regional myocardial function was assessed by sonomicrometry in the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (LC). Changes in global haemodynamics, atrioventricular conduction, LV relaxation and systolic shortening after 0.32 mg X kg-1 intravenous verapamil indicated impaired left ventricular function. Significant myocardial dysfunction (post-systolic shortening) occurred in the LAD territory, accompanied by a 64% decrease (42 +/- 6 to 15 +/- 3, P less than 0.01) in coronary perfusion pressure (CPP). Coronary blood flow in the LC segment decreased 83% (102 +/- 15 to 17 +/- 13, P less than 0.01) as coronary reserve was exhausted with the decrease in CPP. Calcium chloride reversed the impairment of global and regional myocardial function observed with verapamil, improved the impaired left ventricular relaxation, but did not significantly alter atrioventricular conduction. Thus the combination halothane-verapamil can cause significant left ventricular depression and myocardial dysfunction, possibly by inducing subendocardial ischaemia or by direct pharmacologic effect. Calcium chloride reverses this regional myocardial dysfunction as well as the deleterious global haemodynamic changes caused by halothane-verapamil; however, the changes in atrioventricular conduction are not corrected by calcium.
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PMID:Calcium reverses global and regional myocardial dysfunction caused by the combination of verapamil and halothane. 363 May 88

To investigate the potential risk of regional anaesthesia in a verapamil-treated patient, the cardiovascular effects of a combined intravenous infusion of bupivacaine and verapamil were studied in seven conscious and chronically instrumented dogs and were compared to those obtained when each drug was infused separately in the same animals. During verapamil infusion, the decrease in arterial pressure and myocardial contractile force, and the increase in heart rate were constant during the infusion. The lengthening of PR interval correlated with the plasma level of verapamil. During infusion of bupivacaine alone, there was an increase in heart rate and arterial pressure at the end of infusion, whereas the initial depression of myocardial contractile force was compensated. PR interval remained unchanged throughout the infusion of bupivacaine. During combined infusion of bupivacaine and verapamil, there was a time-dependent decrease in heart rate, arterial pressure and myocardial contractile force. A further increase in PR interval correlated with verapamil plasma concentrations which were higher than when verapamil was infused alone; bupivacaine plasma levels were in the same range as during bupivacaine infusion alone. Short periods of second-degree atrioventricular block developed in three out of the seven dogs but no relation was found between QT interval and heart rate in the whole group. Calcium chloride during bupivacaine-verapamil returned heart rate, arterial pressure and myocardial contractile force to their control values within 5 min. Atrioventricular block disappeared and PR interval was shortened following administration of calcium. Bupivacaine and verapamil have additive cardiovascular effects which lead to atrioventricular conduction dysfunction. The effects, at these doses, are reversed by calcium chloride.
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PMID:Bupivacaine accentuates the cardiovascular depressant effects of verapamil in conscious dogs. 365 84

Primary pharmacological and electrophysiological screening procedures were carried out on the aromatic polycyclic amine 3-hydroxy-4-benzyl-4-azahexacyclo[5.4.1.0(2,6).0(3,10).0(5,9).0(8, 11]- dodecane (NGP 1-01). Effects observed in the isolated guinea-pig atria and ileum were, respectively, reversal of CaCl2 induced positive chronotropy and inotropy and papaverine-like depression of the dose-response curve induced by acetyl choline. Electrophysiological studies using isolated guinea-pig papillary muscle showed a reduction in the action potential (AP) plateau potential and an increase in AP duration with accompanying negative inotropic effects. The calcium-mediated (slow response) AP was completely, but reversibly blocked by NGP 1-01 at concentrations of 5 X 10(-5) M and higher. Experiments on sheep Purkinje fibres strongly supported the finding that NGP 1-01 blocks the slow inward (calcium dependent) current Isi, but also suggested a decrease brought about in an outward current, most probably the background potassium current, IK1.
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PMID:Characterization of NGP 1-01, an aromatic polycyclic amine, as a calcium antagonist. 373 54

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