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 purpose this study was to examine the effects of halothane on baroreflex control of heart rate in developing swine. Serial tests of baroreflex function were performed over the first 2 months of life in eight piglets in the conscious state and during anesthesia with 0.45, 0.9, and 1.35% halothane. Systemic blood pressure was increased with phenylephrine (pressor test) and decreased with nitroprusside (depressor test), and stimulus-response curves relating mean blood pressure to heart rate were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Halothane markedly depressed baroreflex sensitivity at all ages in a dose-dependent manner (conscious greater than 0.45% greater than 0.9%, 1.35%). Increasing age was accompanied by decreasing baroreflex sensitivity in both the conscious and the anesthetized states. The difference in baroreflex sensitivity between conscious and anesthetized states did not change with age for the depressor test (tachycardia response), but it did change with age for the pressor test (bradycardia response). For this test, conscious values converged toward anesthetized values at higher ages; therefore, there was relatively less depression by halothane at older ages. Halothane also decreased resting heart rate and decreased the limits and narrowed the range of the baroreflex heart rate response. Increasing age was accompanied by a decreasing resting heart rate and by decreasing limits and a narrowing range of the baroreflex response. The effect of halothane on heart rate variables was similar at all ages. Halothane decreased resting blood pressure and decreased the lower limit and widened the span of the baroreflex blood pressure range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Depression of baroreflex control of heart rate by halothane in growing piglets. 188 57

Whether the major action of anesthetics is to depress the central nervous system (CNS) by reducing excitation or enhancing inhibition remains unknown. Using whole cell patch-clamp recording in hippocampal slices, halothane and pentobarbital were found to prolong the decay time constant (TAU(D)) of GABAA-mediated spontaneous inhibitory postsynaptic currents (sIPSCs). Intracellular administration of the Ca2+ chelator BAPTA or the Ca2+ release inhibitor dantrolene significantly (ANOVA, P less than 0.005) reduced halothane's effect; in contrast, the pentobarbital effect was unchanged. Halothane induced depression of population spike amplitude was blocked by the GABAA antagonist bicuculline. Together, these findings suggest that a major depressant effect of halothane involves enhancement of GABAA-mediated inhibition through release of intraneuronally stored Ca2+.
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PMID:Halothane enhances tonic neuronal inhibition by elevating intracellular calcium. 190 6

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.
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PMID:Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver. 198 65

Alterations in Purkinje-to-muscle conduction may play a role in the development of cardiac arrhythmias. We compared the effects of halothane on impulse propagation in Purkinje fibers with its effects on impulse propagation across the Purkinje-muscle (P-M) junction. In canine Purkinje fibers, halothane (3%) significantly depressed conduction (P less than 0.05). Exposure to halothane altered conduction velocity (theta) in a manner predicted by cable theory; a significant correlation was noted between depression of Vmax and depression of the square of conduction velocity (theta 2) in Purkinje fibers exposed to 3% halothane (n = 11, r = 0.78, P less than 0.01). Halothane (3%) significantly slowed impulse propagation across the P-M junction (P less than 0.05). Vmax and the square of apparent P-M conduction velocity were not significantly correlated (n = 7, r = 0.34, P = 0.45). The data demonstrate that alteration of active membrane properties can account for halothane's slowing of conduction in Purkinje fibers but not for its slowing of conduction across the P-M junction. The data also suggest that a reduction in cell-to-cell coupling may contribute to depression of Purkinje-to-muscle conduction by halothane.
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PMID:Effects of halothane on impulse propagation in Purkinje fibers and at Purkinje-muscle junctions: relationship of Vmax to conduction velocity. 167 May 95

Volatile anesthetics produce their negative inotropic effect on the heart mainly by interference with calcium homeostasis in the myocardial cell. In order to elucidate the mechanism of the depression, we have evaluated the effect of the volatile anesthetics on the binding of the calcium channel blocker [3H]nitrendipine to purified bovine cardiac sarcolemma. The radioligand binding studies were carried out at 25 degrees C, with increasing concentrations of [3H]nitrendipine (0.01-1 nM), in the presence or absence of unlabeled nitrendipine to determine specific binding, and with or without 1.9% halothane, 2.3% isoflurane, and 4.8% enflurane. Separately, [3H]nitrendipine was measured in the presence of increasing doses of halothane (0.78, 1.33, 1.90, and 2.57%). Kinetic studies of association and dissociation rate were performed with 1.90% halothane and 1 nM [3H]nitrendipine at different time intervals. All three volatile anesthetics produced depression of [3H]nitrendipine binding to the isolated cardiac sarcolemma. Only halothane produced a significant depression in binding, ranging between 59 and 66% (P less than 0.05), depending on the concentration of [3H]nitrendipine used. Isoflurane produced 29-38% depression, and enflurane produced 5-22% depression. Halothane also produced a significant (P less than 0.01) dose-dependent decrease in [3H]nitrendipine-specific binding. The kinetic binding experiments demonstrated that the time course for halothane's effect on association and dissociation of [3H]nitrendipine was 5 min for the half-maximum effect; the maximal reduction in binding capacity was at 15-30 min (P less than 0.05). Scatchard analysis revealed that all three volatile anesthetics produced reduction in the maximal number of binding sites; however, they varied in their effect on binding affinity. Only halothane produced a homogenous increase in the dissociation constant, signifying reduced affinity of the Ca2+ blocker to the channel. We suggest that the volatile anesthetics produce conformational changes in these channels consistent with their ability to depress channel-mediated Ca2+ influx into myocytes.
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PMID:Volatile anesthetics depress calcium channel blocker binding to bovine cardiac sarcolemma. 198 41

Amiodarone may cause serious complications in patients receiving general anesthetics. Potentially adverse electrophysiologic interactions between amiodarone and halothane were studied with the use of standard microelectrode techniques to record intracellular action potentials (APs) from excised canine Purkinje fibers. A second dog (support dog) was anesthetized and a femoral arteriovenous bypass circuit created in which arterial blood from the support dog superfused the Purkinje fiber in a tissue bath. The applicability of this model was established by first comparing the AP effects of halothane during blood perfusion with those in Tyrode's solution. Halothane reduced AP duration (APD; P less than 0.05) during Tyrode's solution superfusion and blood cross-perfusion. After the blood perfusion-Purkinje fiber model was validated, the interaction between halothane and amiodarone was studied using Purkinje fibers from dogs chronically treated with oral amiodarone, superfused with blood from chronically amiodarone-treated support dogs. Amiodarone reduced resting membrane potential and prolonged APD. Depression of AP amplitude and reduction of the maximum rate of increase of phase 0 of the AP (Vmax) by halothane (both P less than 0.05) suggested risk of conduction defects if halothane is administered to patients receiving chronic amiodarone therapy.
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PMID:The electrophysiologic effects of amiodarone and halothane on canine Purkinje fibers. 206 34

Impedance dispersion in liposomes measures the lateral charge transfer of lipid membrane surfaces. Depending on the choice of frequency between 1 kHz and 100 GHz, relaxation of the counterions at the interface, orientation of the head group, and relaxation of the bound and free water are revealed. This study measured the impedance dispersion in dipalmitoylphosphatidylcholine (DPPC) liposomes at 10 kHz. The surface conductance and capacitance showed breaks at pre- and main transition temperatures. Below the pre-transition temperature, the activation energy of the ion movement was 18.1 kJ.mol-1, which corresponded to that of the spin-lattice relaxation time of water (18.0 kJ.mol-1). At temperatures between pre- and main transition it increased to 51.3 kJ.mol-1, and agreed with 46.2-58.0 kJ.mol-1 of the activation energy of the dielectric relaxation of ice. Because the present system was salt-free, the ions were H3O+ and OH-, hence, their behavior represents that of water. The above results show that below the pre-transition temperature, the conductance is regulated by the mobility of free ions, or the number of free water molecules near the interface. On the other hand when the temperature exceeded pre-transition, melting of the surface-bound water crystals became the rate-limiting step for the proton flow. Halothane did not show any effect on the ion movement when the temperature was below pre-transition. When the temperature exceeded pre-transition, 0.35 mM halothane (equilibrium concentration) decreased the activation energy of the ion movement to 29.3 kJ.mol-1. This decrease indicates that halothane enhanced the release of the surface-bound water molecules at pre-transition. The surface-disordering effect of halothane was also shown by depression of the pre-transition temperature and decrease of the association energy among head groups from 9.7 kJ.mol-1 of the control to 5.2 kJ.mol-1 at 0.35 mM.
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PMID:Proton flow along lipid bilayer surfaces: effect of halothane on the lateral surface conductance and membrane hydration. 216 83

The study was carried out to assess the effects of atracurium neuromuscular blockade in children anaesthetized with N2O:O2: halothane vs N2O:O2: isoflurane. Thirty-two ASA I-II children, age 1-13 yr, undergoing elective surgery, were divided into two groups according to age and the mode of anaesthesia induction. Anaesthesia was induced in the younger children (group 1: 1-6 yr) with nitrous oxide and inspired halothane or isoflurane in oxygen via a face mask. Intravenous thiopental (6-7 mg/kg-1) was used to induce anaesthesia in older children (group 2: 7-13 yr). Each group of patients was randomly allocated to two groups each receiving halothane (group A: n = 8) or isoflurane (group I: n = 8). Halothane 0.8% end-tidal and isoflurane 1% end-tidal as anaesthesia maintenance. A bolus dose of atracurium 0.35 mg/kg-1 was administered. Premedication consisted of oral flunitrazepam (0.04 mg/kg-1) and bellafoline (0.02 mg/kg-1). Heart rate (by electrocardiography), arterial pressure (by auscultation) were monitored. Then end-expired carbon dioxide concentration was maintained at 30-40 mmHg. Neuromuscular transmission was evaluated by response to indirect stimulation (TOF) of the ulnar nerve at the wrist via surface electrodes. Conditions for endotracheal intubation were excellent in 25 of the children, good in 6 and poor in 1. The intubation was carried out within 112 s (group 1A), 130 s (group 1 I), 112 s (group 2A) and 135 s (group 2 I) following the administration of atracurium. The maximum twitch depression was recorded in the isoflurane groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atracurium with halothane and isoflurane in pediatric anesthesia]. 221 86

The authors investigated the effects of halothane (HAL) and isoflurane (ISO) on cardiac depression produced by global hypoxia and the recovery of function following reoxygenation is isolated guinea pig hearts perfused with Krebs' solution at constant pressure. Isovolumetric left ventricular systolic (LVSP) and end-diastolic pressures (LVEDP) were measured by placing a saline filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurements of heart rate (HR), atrioventricular conduction time (AVCT), and determination of the incidence and severity of dysrhythmias occurring during hypoxia and reoxygenation. Hearts were divided into three groups: control (n = 20), halothane (n = 12), and isoflurane (n = 13). All hearts were exposed in sequence to oxygenated perfusate (PO2, 530 mmHg), moderately hypoxic perfusate (PO2, 91 mmHg) for 30 min, and then to oxygenated perfusate for 40 min. Halothane (1%, 0.4 mM) or isoflurane (1.5%, 0.5 mM) were administered 10 min before hypoxia, during hypoxia, and during the first 10 min of reoxygenation. Exposure to halothane and isoflurane before hypoxia produced a 14 and 11% decrease in heart rate, a 32 and 23% increase in AVCT, and a 47 and 28% decrease in LVSP (all P less than or equal to 0.001) for halothane and isoflurane, respectively, and no significant change in LVEDP. During hypoxia, HR decreased and AVCT increased similarly in both groups. Left ventricular systolic pressure (LVSP) decreased sharply with a narrowing of the prehypoxic differences among the groups. In the control and isoflurane groups, LVEDP increased during hypoxia but remained unchanged in the halothane group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential protective effects of halothane and isoflurane against hypoxic and reoxygenation injury in the isolated guinea pig heart. 224 Jun 87

Short periods of coronary artery occlusion are known to produce prolonged periods of ventricular dysfunction. The effects of halothane or isoflurane on contractility and metabolism in postischemic "stunned" myocardium were studied in an open-chest canine model in which the left anterior descending artery (LAD) was occluded for 15 min and then reperfused. Regional function in the LAD and circumflex artery (CIRC) areas were measured with sonomicrometry, and metabolic data were determined from simultaneous arterial and venous measurements of oxygen and lactate. Halothane and isoflurane produced equivalent decreases in systolic shortening in both normal (CIRC) and stunned (LAD) areas of the heart. Furthermore, the amount of depression was similar with either halothane or isoflurane. Halothane 0.75 MAC significantly decreased systolic shortening in both the LAD region (from 38.8 +/- 25.9% to 11.0 +/- 21.8%) and in the CIRC region (from 116.7 +/- 24.7% to 87.5 +/- 23.3%). At equivalent MAC concentrations of isoflurane, the values were 42.5 +/- 45.7 to -7.0 +/- 49.9% in the LAD region and 91.5 +/- 11.9% to 66.9 +/- 23.9% in the CIRC area. At 1.5-MAC halothane, systolic shortening in the LAD region decreased from 47.9 +/- 47.2% to -0.6 +/- 20.3% and in the CIRC area from 114.6 +/- 16.8% to 76.0 +/- 18.7%. Isoflurane at 1.5 MAC produced significant decreases, from 23.4 +/- 54.5% to -15.6 +/- 27.1% in the LAD region and from 94.4 +/- 33.2% to 61.3 +/- 28.2 in the CIRC area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of halothane and isoflurane on postischemic "stunned" myocardium in the dog. 224 1

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