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)

The hemodynamic effects of propofol-fentanyl and isoflurane-fentanyl anesthesia during the prebypass period were compared in 42 patients undergoing coronary artery bypass grafting (CABG) and 22 patients undergoing valve replacement (VR) for stenotic lesions. Anesthesia was induced with fentanyl, 25 micrograms/kg, and pancuronium, 0.1 mg/kg, and was maintained with a propofol infusion commenced at 4 mg/kg/h (range 1 to 10 mg/kg/h) or with isoflurane commenced at 1% (range 0 to 2%). Additional fentanyl, 7.5 micrograms/kg, was given before sternotomy. Hemodynamic measurements were made before induction of anesthesia and at various times in the prebypass period. In the VR group, there were no significant differences between the two anesthetics in any hemodynamic variables during the study. Significant decreases (P < 0.05) in mean arterial pressure (MAP 14%), left ventricular stroke work index (LVSWI 29%), and stroke volume index (SVI 24%) occurred after 15 minutes of propofol anesthesia in the CABG group. With isoflurane MAP was well maintained with reductions in LVSWI and SVI of 22% and 20%, respectively. Isoflurane was, however, associated with a significant increase in heart rate (HR) in the CABG group (P < 0.05), whereas no significant change in HR occurred in CABG or VR patients receiving propofol. With both techniques there were no significant changes in right-sided or left-sided filling pressures or in systemic vascular resistance index in the CABG or VR groups, except for a decrease in pulmonary artery occlusion pressure in the propofol VR group and isoflurane CABG group at the time of aortic cannulation. Propofol produced similar hemodynamic changes in the CABG and VR groups. Both anesthetic techniques caused myocardial depression and effectively controlled the autonomic responses to sternotomy in both groups. The study suggests that propofol-fentanyl anesthesia is an acceptable technique for CABG surgery and for VR in patients with stenotic valvular heart disease.
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PMID:Propofol-fentanyl anesthesia: a comparison with isoflurane-fentanyl anesthesia in coronary artery bypass grafting and valve replacement surgery. 806 Dec 62

The purpose of this study was to examine the anaesthetic requirement of intrathecal midazolam in a dose-response fashion in isoflurane-anaesthetized, tracheostomized rats, and to evaluate the apnoeic threshold after each intrathecal midazolam dose. Intrathecal midazolam, 5, 10, 20, and 30 micrograms, was administered to 25 anaesthetized tracheotomized rats. Isoflurane MAC was determined by the tail-clamp method. The effect of intrathecal midazolam on the apnoeic threshold was evaluated, and light and electron microscopy studies were performed on cervical, thoracic and lumbar sections of the spinal cord to investigate possible midazolam-induced neurotoxic effects. Intrathecal midazolam 5, 10, 20 and 30 micrograms decreased isoflurane MAC by 16%, 31%, 42%, and 53% respectively (P < 0.05). The apnoeic threshold was increased by midazolam 5 micrograms (from a PaCO2 of 4.25 +/- 0.55 to 5.28 +/- 0.76 kPa, P < 0.05) when compared with baseline values, but not further by additional doses. Light and electron microscopy studies on sections taken from the spinal cord of four animals did not show any morphological changes suggestive of midazolam-induced neurotoxicity when compared with similar preparations obtained from controls. These data suggest that intrathecal midazolam possesses dose-dependent antinociceptive properties which, associated with the ceiling effect of the apnoeic threshold obtained at the lowest midazolam dose and the lack of neurotoxic effects, may potentiate inhalational anaesthesia without producing marked respiratory depression.
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PMID:Intrathecal midazolam reduces isoflurane MAC and increases the apnoeic threshold in rats. 813 Dec 30

We have studied the cardiovascular effects of 1 MAC end-tidal concentrations of halothane and isoflurane in young (n = 40) and elderly (n = 40) adult patients using non-invasive techniques. Cardiac output was measured by Doppler ultrasonography. Halothane reduced heart rate, systolic, mean and diastolic arterial pressures and cardiac index in both age groups (P < 0.05). Isoflurane reduced systolic, mean and diastolic arterial pressures also, but reduced cardiac index and heart rate only in the older patients (P < 0.05). Halothane depressed cardiovascular state significantly more than isoflurane in the younger adults (P < 0.05), but cardiovascular depression was similar for the two agents in the older age group. The decreases in systolic and diastolic pressures in the older patients were significantly greater with isoflurane compared with halothane (P < 0.05).
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PMID:Cardiovascular effects of isoflurane and halothane in young and elderly adult patients. 825 Dec 83

Hemodynamic changes and left ventricular performance were investigated by simplified mechanocardiography using finger plethysmography instead of carotid artery pulse tracing in patients who received 4 volatile anesthetics with or without nitrous oxide. Systolic blood pressure (Ps), diastolic blood pressure (Pd), heart rate (HR), pre-ejection period (PEP), left ventricular ejection time (LVET), isovolemic contraction time (ICP), PEP/LVET, Pd/ICT, and 1/PEP2 were selected as indices which represent hemodynamics and systolic time intervals. Enflurane 0.6 and 1.2MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT significantly. Addition of nitrous oxide caused more depression. Halothane 0.6MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT. Sevoflurane 1.2MAC shortened only 1/PEP2. Addition of nitrous oxide prolonged PEP and PEP/LVET, and shortened Pd/ICT. Isoflurane 1.2MAC lowered Ps and increased HR. The results indicate that cardiac performance was depressed by volatile anesthetics in the order of enflurane, halothane, sevoflurane and isoflurane.
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PMID:[Volatile anesthetics suppress cardiac function in man; an investigation based on systolic time intervals]. 843 99

Isoflurane anaesthesia was proposed instead of electro-convulsive therapy (ECT) in patients with treatment-refractory depression. This open study compared burst-suppression-isoflurane-anaesthesia (BSIA) and ECT in 12 severely depressed patients. A series of 6 BSIA was administered in every patient. If improvement was insufficient or only temporary, a series of up to 12 ECT was given. A marked improvement of the depression was shown after both BSIA and ECT. Three patients were discharged from hospital after BSIA, nine patients were treated with BSIA and then ECT. The therapeutic effect of both regimens was equal as evidenced by the Hamilton-depression-rating-scale, a visual-analog-scale and the clinical global impression. BSIA requires more time and monitoring than ECT. Our exclusions of coronary, cerebral and peripheral vascular disease, untreated hypertension and focal neurological disease are strongly recommended. Due to the ease of application, ECT remains the standard treatment in depressed patients, but we consider BSIA a valuable alternative at least in patients who object to ECT.
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PMID:Intra-individual open comparison of burst-suppression-isoflurane-anaesthesia versus electroconvulsive therapy in the treatment of severe depression. 846 36

Isoflurane may cause differential effects on different vascular beds of the same animal species. The mechanisms of this action have not been elucidated. Accordingly, we compared in rabbit aorta and femoral artery the effects of isoflurane (1-3.3%) in isolated rings (endothelium denuded) activated by norepinephrine, and isoflurane effects on Ca2+ fluxes from the sarcoplasmic reticulum in skinned strips. When < 30 nM norepinephrine was used to cause ring contraction, isoflurane increased the force of contraction in aortic rings, but decreased force in femoral arterial rings. At 30 nM norepinephrine stimulation, 3.3% isoflurane decreased the force and, in the presence of verapamil, isoflurane actually increased the force in both arterial types. In skinned strips of both arterial types, isoflurane present during Ca2+ uptake decreased the caffeine-induced tension transients, whereas isoflurane present during Ca2+ release enhanced the transients. Isoflurane potentiated the depression of the tension transients by ryanodine. Isoflurane directly caused contracture even in the absence of caffeine. Thus, isoflurane has similar cellular mechanisms of action in the aortic and femoral arterial smooth muscle: inhibiting Ca2+ influx through the sarcolemma, decreasing Ca2+ uptake by the sarcoplasmic reticulum, and enhancing caffeine-induced Ca2+ release from the sarcoplasmic reticulum.
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PMID:Mechanisms of action of isoflurane on contraction of rabbit conduit artery. 861 7

This study primarily examined the effect of three endtidal isoflurane concentrations (0.2, 1.0 and 1.4%) on the isocapnic hypoxic ventilatory response (HVR), as well as the hypercapnic ventilatory response (HCVR), in 18 women (ASA I) who were all in the follicular phase of their menstrual cycle. Capnography was used, together with pulseoximetry to indicate desired levels of hypoxia (SpO2 75-80%). This hypoxic challenge resulted, after 3-4 min, in a stable ventilation, and ventilation measurements were then taken during a 90 s period. The HCVR provocation (inhalation of 4.5% CO2 in air) and measurements were conducted using a similar time frame as for HVR. Isoflurane 0.2% did not affect any ventilatory parameter. Isoflurane 1.0 and 1.4% dose-dependently increased endtidal CO2 and respiratory rate, while tidal volumes decreased. Minute ventilation was not reduced. HVR, as well as HCVR, were both uninfluenced by isoflurane 0.2%. HVR was reduced by 60-70% at isoflurane 1.4% (P < 0.01), and was parallelled by a similar depression of HCVR (P < 0.01). The HVR during anaesthesia was accomplished by a respiratory rate response, while the increase in tidal volume, seen in the awake state, was abolished. The HCVR during anaesthesia was, on the other hand, the result of a dose-dependently depressed tidal volume response, without any increase in respiratory rate. In conclusion, isoflurane 0.2% did not affect the ventilatory response to mild isocapnic hypoxia, nor to mild hypercapnic challenge. During anaesthesia with isoflurane (1.0 and 1.4%), there was a parallel reduction of HVR and HCVR.
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PMID:Hypoxic and hypercapnic ventilatory responses during isoflurane sedation and anaesthesia in women. 884 94

We have assessed the deleterious effects of methylmethacrylate (MMA) on cardiac function and metabolism in the isolated heart-lung preparation with or without volatile anesthetics. Wistar rats were prepared for the heart-lung model. They were randomly divided into 5 groups as follows. (1) Control (C) group. (2) Cement (M) group; they received MMA. (3) Halothane (H) group; they received MMA and 1% halothane. (4) Isoflurane (I) group; they received MMA and 1.5% isoflurane. (5) Sevoflurane (S) group; they received MMA and 2.5% sevoflurane. MMA 1000 micrograms/ml was administered 7 min after the start of perfusion except in the C group. At the end of the experimental period, the hearts were freeze-clamped and then myocardial high energy phosphates, lactate and glycogen were measured. Cardiac output in all groups but C group decreased significantly. PO2 of the perfusion blood in the M, H, I and S groups was significantly lower than that in the C group. Myocardial ATP in the M, H, I and S groups was significantly lower than that in the C group. ADP and AMP in the M, H, I and S groups were higher than those in the C group. There were no significant differences in lactate and glycogen levels between the 5 groups. MMA 1000 micrograms/ml is much higher than the blood level (0.05-31.89 micrograms/ml) which was reported in clinical patients who had femoral prosthesis. Therefore, the direct contribution of MMA itself to cardiac depression may be less than the other factors such as embolism in clinical situations. Volatile anesthetics did not influence the deleterious effects of MMA on cardiac function and metabolism.
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PMID:Cardiac effects of methylmethacrylate in the rat heart-lung preparation with or without volatile anesthetics. 886 19

This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (Q), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentration were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and PACO2 maintained between 38 to 42 mm Hg. Isoflurane caused significant (P < .05) dose-dependent reduction in Q, SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower Q, SV, SAP, and MAP PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in Q, SV, and arterial pressure.
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PMID:Cardiovascular effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane in experimentally induced hypothyroidism in dogs. 892 95

Volatile anesthetics vasodilate in part by direct action on vascular smooth muscle. Isoflurane-induced relaxation of portal vein smooth muscle involves alteration of membrane ionic currents that control cell excitability and contraction. Whole cell voltage clamp technique was used to examine outward Ca(2+)-activated K+ current (IK,Ca) in guinea pig portal vein cells. Isoflurane caused a concentration-dependent reduction in IK,Ca at steady-state conditions but had no significant effect on resting potential. Isoflurane transiently potentiated IK,Ca by a mechanism that may partly involve Ca2+ release from intracellular storage sites. The depression of IK,Ca by isoflurane may occur by direct action on the channel protein or on the lipid environment of the channel to alter conductance or kinetic properties. Since isoflurane reduces IK,Ca coincident with suppression of Ca2+ channel current, it was concluded that the depression of IK,Ca by isoflurane is of secondary importance to reduction in inward Ca2+ channel current. Potentiation of IK,Ca may preclude significant membrane activation during the onset of isoflurane's action.
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PMID:Isoflurane reduces K+ current in single smooth muscle cells of guinea pig portal vein. 894 4


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