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)

Membrane hyperpolarization (increase in resting potential) together with a conductance increase has been suggested as a common mechanism of anesthetic action. The current study compared the effects of halothane, enflurane, and isoflurane on resting membrane potential and conductance of hippocampal CA1 neurons in vitro. At 1 MAC, halothane produced significant (P less than 0.01) hyperpolarization (-2.8 +/- 1.3 mV, mean +/- SD) accompanied by a conductance increase (6.2 +/- 2.7%). Enflurane also produced a significant (P less than 0.001) hyperpolarization (-3.15 +/- 1.2 mV); however, this was accompanied by a conductance decrease (-4.5 +/- 1.5%). Isoflurane produced variable effects. Anesthetic-induced hyperpolarization was maximal in neurons with more negative initial resting potentials and was reduced by depolarization. Across agents, these relatively small changes in resting potential were not correlated with decreases in excitability as measured by synaptically evoked population spike depression. The results are not consistent with a common action of the three agents on a single ionic channel.
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PMID:Anesthetic effects on resting membrane potential are voltage-dependent and agent-specific. 198 63

We have studied the EEG analysed with the cerebral function analysing monitor (CFAM) during trimetaphan (TMP)-induced hypotension to a mean arterial pressure (MAP) of 40 mm Hg in 20 normocapnic patients anaesthetized with either 1% end-tidal isoflurane or 0.5% halothane. During the acute reduction in MAP, the average reduction in mean EEG amplitude with halothane was 14%, two patients showing short periods of EEG suppression; the decline in EEG amplitude correlated with declining MAP in four patients. In contrast, the average reduction in mean EEG amplitude with isoflurane was only 0.3% and there were neither periods of suppression nor any correlation between EEG amplitude and MAP. No significant changes in EEG frequency occurred in either group. Isoflurane prevented EEG amplitude depression during TMP-induced hypotension.
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PMID:Isoflurane prevents EEG depression during trimetaphan-induced hypotension in man. 222 59

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

Depressant effects of halothane and isoflurane on isolated right ventricular guinea pig papillary muscle bathed in Tyrode's solution at 37 degrees C were examined. Contractions were elicited by stimulation through external field electrodes while tension was recorded continuously and the intracellular cardiac action potential (AP) was monitored simultaneously by microelectrodes. The time differential of tension (dT/dt) and of membrane potential (V) was determined electronically and recorded also. Contractions after rest and at stimulation rates of 0.1, 0.25, 0.5, 1, 2, and 3 Hz were studied. With normal APs, isoflurane (1.3 and 2.5%) depressed peak tension significantly less at high frequencies than did equivalent doses of halothane (0.75 or 1.5%). Isoflurane depressed dT/dt max less than halothane at all frequencies. At 0.3 Hz stimulation, isoflurane (1-4%) significantly increased the normal AP duration by 7-11%. Slow calcium-dependent APs and accompanying contractions were studied in partially depolarized muscles (-40 to -45 mV resting potential in 26 mM K+ Tyrode's solution) stimulated with 0.1 microM isoproterenol. Following rest and at 0.1, 0.25, 0.5, 1, 2, and 3 Hz, both isoflurane (1.3% or 2.5%) and enflurane (1.7% or 3.5%) markedly depressed the late-peaking slow AP contraction observed with low-frequency stimulation. Halothane (0.75% or 1.5%) caused a similar contractile depression (40-60%) at all frequencies. In contrast, isoflurane depressed early peaking tension and the dT/dt max at frequencies greater than 1 Hz significantly less than did halothane or enflurane. At 0.3 Hz, 2% and 4% isoflurane caused 9% and 17% depression of slow AP maximum rate of depolarization (Vmax), but significantly prolonged the AP duration. Isoflurane altered the pattern of tension development in a different manner than halothane, suggesting differing mechanisms of myocardial depression by these anesthetics.
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PMID:Differential depression of myocardial contractility by halothane and isoflurane in vitro. 242 14

Haemodynamic changes and catecholamine responses were measured during anaesthesia with sufentanil (total dose 7 micrograms kg-1) supplemented with isoflurane in 14 patients undergoing coronary artery surgery. Isoflurane was used to control systolic arterial pressure, which was allowed to decrease to 100 mm Hg. Mean inspired isoflurane concentration was 0.22 (SD 0.19)% (induction), 0.34 (0.18)% (pre-bypass) and 0.22 (0.17)% (post-bypass). During cardiopulmonary bypass 0.22 (0.13)% isoflurane was administered to control mean perfusion pressure. During induction and the pre-bypass period, significant decreases in systolic and diastolic arterial pressure, systemic vascular resistance and left ventricular stroke work index (LVSWI) (P less than 0.01) were noted. The decrease in LVSWI with unchanged filling pressures indicated myocardial depression. Serum catecholamine concentrations remained at the pre-induction value until cardiopulmonary bypass, when a significant increase was noted. Tracheal intubation, sternotomy and sternal spread were not associated with hypertension or tachycardia. Clinical signs that could reflect myocardial ischaemia were not observed peroperatively. After operation, cardiac enzymes were within the normal clinical range and ECG was unchanged.
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PMID:Low-dose sufentanil-isoflurane anaesthesia for coronary artery surgery. 252 26

alpha 2-Adrenergic agonists have been used as potent adjuncts to anesthesia and have anesthetic properties themselves. For this reason, we studied the effects of medetomidine, and isoflurane (1 MAC) on ventilatory drive in dogs. Six chronically tracheotomized mongrel dogs were studied during spontaneous ventilation. Arterial blood samples were analyzed for pH, PaCO2, and PaO2. Airway O2, CO2, N2, and isoflurane were continuously monitored using a mass spectrometer; respiratory rate was determined. The hypercapnic ventilatory response was assessed using the Read rebreathing technique. Control measurements were made under isoflurane anesthesia. Fifteen minutes after the medetomidine (20 ug/kg) was given and the isoflurane discontinued, all measurements were repeated. Isoflurane levels were 1.38 volume % during the isoflurane test period and had declined to 0.3 volume % by the time the medetomidine measurements were obtained. The slope of the CO2 response curve was significantly steeper after medetomidine (0.582 vs 0.269 1.min-1.mmHg), suggesting less respiratory depression when compared to the measurements under isoflurane. PaCO2 and endtidal CO2 were significantly lower in the medetomidine group. No other significant differences were found. Under these conditions, medetomidine (20 ug/kg) resulted in normal blood gas values with less depression of the hypercapnic response curve than under isoflurane anesthesia.
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PMID:The effects of medetomidine, an alpha 2-adrenergic agonist, on ventilatory drive in the dog. 257 Dec 80

Actions of halothane were investigated under voltage-clamp conditions in single cells from guinea-pig ventricular muscle. Contraction (measured by an optical method) evoked by step depolarization to 0 mV was consistently reduced by halothane. At positive membrane potentials (+60 mV) 2% halothane did not cause a consistent depression of peak contraction, and in the majority of cells contraction was enhanced. Two per cent halothane increased the time-to-peak contraction at +60 mV. However, when a pre-pulse to 0 mV was applied to inactive calcium current through L-channels, any effect of 2% halothane on the time-to-peak of contraction was reduced or abolished. A halothane-induced increase in time-to-peak contraction was also observed at membrane potentials in the range of the action potential plateau (+20 and +40 mV). In double-pulse experiments contraction during a 'test' depolarization to +60 was measured following a 'conditioning' depolarization to 0 mV. Contraction at +60 mV was slightly reduced at brief interpulse intervals (less than 400 ms) following the 'conditioning' depolarization to 0 mV, and recovered as the interval was prolonged; in cells exposed to halothane contraction at +60 mV was no longer influenced by the interval between the pulses. Isoflurane (3.2%) had qualitatively similar but less potent effects than halothane on contraction at +60 mV. These observations are consistent with the suggestion that mechanisms for calcium entry may vary with the membrane potential: at 0 mV, the major pathway for calcium entry may be through halothane-sensitive L-type calcium channels, while at +60 mV entry may be through additional pathways which are relatively resistant to halothane. Actions of halothane on the time-to-peak of contraction may be accounted for by its influence on the sarcoplasmic reticulum to decrease net uptake and release of calcium. These actions of halothane might be of importance during the action potential plateau.
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PMID:Influence of halothane on contraction at positive membrane potentials in single cells isolated from guinea-pig ventricular muscle. 272 44

This study examined global hemodynamic responses to increasing concentrations of halothane and isoflurane in pigs with an acute critical coronary stenosis (CCS) on the left anterior descending coronary artery (LAD). The CCS was caused by graded inflation of an hydraulic occluder to the point where no hyperemic response was observed following a 10 sec. total LAD-occlusion. A minute, piezoelectric epicardial Doppler probe applied without dissection was used to monitor the stenosis. Previously reported minimum alveolar concentrations (MAC) were used as endtidal concentrations ([ Et]). The [Et] was increased stepwise until each animal died. Recordings obtained in this study were compared to recordings obtained during similar stepwise increments of these anesthetics in pig preparations without CCS. Isoflurane had a significantly less depressant effect on global hemodynamics compared to halothane and caused death at higher MAC than halothane in either case. A critical LAD-stenosis caused no major changes in the general dose-response pattern of isoflurane but further aggravated the depression of cardiac output and stroke volume induced by increasing concentrations of halothane.
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PMID:Hemodynamic dose-responses to halothane and isoflurane are different in swine with and without critical coronary artery stenosis. 273 40

It has been postulated that inhalation anaesthetics may interfere with calcium movement across cell membranes. We have evaluated the interaction between diltiazem and the inhalation anaesthetics halothane and isoflurane on sinus automaticity in the isolated right atrium (SAIRA). Isoflurane significantly reduced atrial rate at all concentrations tested. However, halothane produced only a small but significant decrease at the higher concentrations used (1-2 v/v%). Diltiazem modified the maximal negative chronotropic response to inhalation anaesthetics. Maximum depression of SAIRA was significantly greater in the presence of two different doses of diltiazem compared with exposure to halothane and isoflurane alone. These results suggest that inhalation anaesthetics may block the influx of extracellular calcium through voltage-dependent calcium channels inhibited by diltiazem.
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PMID:Interactions between diltiazem and inhalation anaesthetics in the isolated heart. 280 89

We examined the feasibility of administering nearly 100% oxygen throughout the induction-delivery period of general anaesthesia for 113 Caesarean sections. Isoflurane 1.25% was compared with 1.5% enflurane for maintenance of anaesthesia. The level of anaesthesia was monitored by use of the isolated forearm technique. There was a greater amount of isolated forearm movement when enflurane was used. The three main criteria for a satisfactory general anaesthetic technique for Caesarean section were fulfilled, namely no maternal awareness, no undue depression of the fetus and no adverse effect on uterine contractility. Isoflurane and enflurane appear to be suitable anaesthetic agents for facilitating hyperoxygenation during Caesarean section.
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PMID:Comparison of 1.5% enflurane with 1.25% isoflurane in oxygen for caesarean section: avoidance of awareness without nitrous oxide. 292 65


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