Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 fatal anaesthetic ratio (FAR) has been determined for halothane-diethyl-ether (HE) in pigs, and the central circulation during hypovolaemia has been investigated using a well-documented agent such as isoflurane as a standard. The fatal anaesthetic ratio for HE in pigs was (3.21/1.03) = 3.12. This is high compared to the FAR for halothane of 1.7. The central circulation was investigated in 12 pigs which were randomly allocated to either HE or isoflurance anaesthesia, respectively. Baseline values were recorded when they were stable at 1.3 MAC of the volatile anaesthetic used. The pigs were bled 30% of their blood volume, and measurements were made at 5 and 30 min. There was one significant difference between these groups in central circulation: the blood pressure was higher at baseline measurement in the HE group. At 5 min and 30 min, there were no significant differences between these groups. There was a general depression of central circulation without any sign of decreased contractility. HE anaesthesia is well tolerated during hypovolaemia in pigs.
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PMID:Central circulation during halothane-diethyl-ether azeotrope and isoflurane anaesthesia in the pig. 176 92

To determine if learning occurs during general anaesthesia, 72 women undergoing surgery were given postoperative implicit memory tests in which performance could be influenced by auditory information presented during general anaesthesia. Two methods of anaesthesia were used: nitrous oxide and opioids (n = 24) or nitrous oxide and isoflurane (1, 1.3 and 1.5 MAC for n = 12, 24 and 12, respectively). Three tests showed some retention, apparently unconscious, of information presented during anaesthesia: in Behavioural Suggestions tests, patients who were instructed during anaesthesia to touch a particular body part (ear or nose) during later questioning touched the "correct" (suggested) body part longer than the "incorrect" (not suggested) body part during a postoperative interview on the day of surgery (means 2.5 vs 0.2 s); in World Completion tests, patients shown a page containing the first three letters of words and asked to give words beginning with those letters gave more words from a list that had been played during anaesthesia than from a list not played (means 0.48 vs 0.27 words); in Nonsense Word tests, patients who were played different nonsense words between two and 16 times during anaesthesia preferred and guessed more accurately those that had been played most often (16 times) relative to those played less often in subsequent preference and recognition tests (means 56% vs 46% for preference and 62% vs 48% for recognition), while showing no such patterns in additional control tests. Learning did not vary with the method of anaesthesia, as might have been expected if learning was a monotonic function of brain depression. Some information processing functions of the brain evidently continue to function during adequate general anaesthesia.
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PMID:Human learning during general anaesthesia and surgery. 181 16

Using respiratory inductive plethysmography, we have measured rib cage and abdominal motion during isoflurane anaesthesia in 16 healthy day-surgery patients. Anaesthesia was induced with propofol and maintained with 1 MAC isoflurane in air-oxygen via a laryngeal mask. Measurements were taken during both resting ventilation and hyperpnoea induced by rebreathing carbon dioxide. For resting ventilation, the rib cage contributed a mean (SD) of 33 (15)% of the total ventilation whilst awake, and 39 (12)% during anaesthesia (ns). With increasing end-tidal carbon dioxide whilst awake, the subjects showed a mean increase in the percentage rib cage contribution of 7.1 (12.5)%/kPa of carbon dioxide. With isoflurane anaesthesia, there was significant depression of this rib cage recruitment with the mean contribution decreasing by 3.6 (7.4)% kPa-1 (P less than 0.05). These results indicate that 1 MAC of isoflurane does not selectively depress rib cage motion, except during carbon dioxide stimulated hyperpnoea.
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PMID:Rib cage contribution to resting and carbon dioxide stimulated ventilation during 1 MAC isoflurane anaesthesia. 183 70

The effects of halothane, enflurane, and isoflurane on voltage-dependent Ca2+ channel current (ICa) were compared in canine ventricular cells by the whole-cell voltage-clamp technique. ICa was elicited in each cell by progressively depolarizing pulses, from -80 or -40 mV to more positive membrane potentials. The peak amplitude and inactivation rate of the inward current were analyzed before, during, and after the external application of equianesthetic concentrations (0.5, 1.0, and 2.0 MAC) of halothane, enflurane, or isoflurane. The concentrations of these agents in the Krebs' solution were as follows (percentage in the gas phase): halothane 0.36, 0.68, and 1.50%; isoflurane 0.50, 1.00, and 1.90%; and enflurane 0.66, 1.36, and 2.39%. Halothane, enflurane, and isoflurane rapidly reduced peak ICa amplitude at all voltages studied, resulting in a depression of the entire current-voltage relationship for ICa activation. This depression was concentration-dependent and completely reversible upon wash-out of the anesthetic agents. Quantitatively, the three anesthetic agents produced a similar inhibition of peak ICa at approximately equianesthetic concentrations. Inactivation of ICa during 200-ms depolarizing pulses was not affected by two lower concentrations of the anesthetic agents, but was accelerated by the highest concentration of enflurane used. These findings suggest that the negative inotropic and chronotropic actions of halothane, enflurane, and isoflurane on the ventricular myocardium are related, at least in part, to their inhibition of ICa at the sarcolemma. However, since all three anesthetic agents depressed ICa amplitude similarly, their quantitatively different effects on cardiac performance are due most likely to differences in actions at other cellular sites.
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PMID:The effects of halothane, enflurane, and isoflurane on calcium current in isolated canine ventricular cells. 184 26

The cardiovascular actions of three concentrations of desflurane (formerly I-653), a new inhalation anesthetic, were examined in 12 unmedicated normocapnic, normothermic male volunteers. We compared the effects of 0.83, 1.24, and 1.66 MAC desflurane with measurements obtained while the same men were conscious. Desflurane caused a dose-dependent increase in right-heart filling pressure and a decrease in systemic vascular resistance and mean systemic arterial blood pressure. As measured by echocardiography, left ventricular end-diastolic area did not change except for a small increase at 1.66 MAC desflurane, and systolic wall stress was less at all concentrations of desflurane than during the conscious state. Desflurane did not change cardiac index or left ventricular ejection fraction. Heart rate did not change at 0.83 MAC, but progressively increased with deeper desflurane anesthesia. Stroke volume index was less at all concentrations of desflurane than while the men were conscious, but desflurane did not alter the velocity of ventricular circumferential fiber shortening. Mixed venous blood PO2 and oxyhemoglobin saturation were higher during all concentrations of desflurane anesthesia than during the conscious state. No volunteer developed a metabolic acidosis. We conclude that desflurane with controlled ventilation and constant PaCO2 causes cardiovascular depression, as indicated by the increased cardiac filling pressure and decreased stroke volume index and by no change in the velocity of circumferential fiber shortening in the presence of decreased systolic wall stress. However, cardiac output is well maintained, and heart rate does not increase at light levels of anesthesia. The cardiovascular actions of 0.83 and 1.66 MAC desflurane were also reexamined in 6 of the 12 men during the seventh hour of anesthesia. Prolonged desflurane anesthesia resulted in lesser cardiovascular depression than was evidenced during the first 90 min. The measures of cardiac filling (central venous pressure and left ventricular end-diastolic cross-sectional area) did not differ between the early and late periods of anesthesia. Systemic vascular resistance decreased further during the late period, but systolic wall stress did not differ between the two time periods. During the seventh hour of desflurane anesthesia, heart rate and cardiac index were higher at both anesthetic concentrations than during the first 90 min of anesthesia. Left ventricular ejection fraction and velocity of fiber shortening did not change with duration of desflurane anesthesia. Oxygen consumption, oxygen transport, the ratio of the two, mixed venous PO2, and mixed venous oxyhemoglobin saturation (SO2) increased late in the anesthetic in comparison with the first 90 min.
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PMID:Cardiovascular actions of desflurane in normocarbic volunteers. 185 29

We determined the cardiovascular effects of 0.91, 1.34, and 1.74 MAC of desflurane/nitrous oxide anesthesia (60% inspired nitrous oxide contributed 0.5 MAC at each level) in 12 healthy, normocapnic male volunteers. Desflurane/nitrous oxide anesthesia decreased systemic blood pressures, cardiac index, stroke volume index, systemic vascular resistance, and left ventricular stroke work index, and increased pulmonary arterial pressures and central venous pressure in a dose-dependent fashion, while heart rate was 10%-12% and mixed venous oxygen tension was 2-4 mm Hg higher at all MAC levels than at baseline (awake). Desflurane/nitrous oxide anesthesia modestly increased left ventricular end-diastolic cross-sectional area (preload) and decreased velocity of left ventricular circumferential fiber shortening, systolic wall stress (afterload), and area ejection fraction; this combination of changes indicates myocardial depression. At approximately comparable MAC levels, heart rate was lower and systemic blood pressures, central venous pressure, left ventricular stroke work index, and systemic vascular resistance usually were significantly higher during anesthesia with desflurane and nitrous oxide than during desflurane anesthesia alone (same volunteers, data collected in crossover design). After 7 h of anesthesia, regardless of the background gas, somewhat less cardiovascular depression and/or modest stimulation was apparent: cardiac index, area ejection fraction, and velocity of left ventricular circumferential fiber shortening recovered to or toward awake values, whereas heart rate was further increased. Evidence of circulatory insufficiency did not develop in any volunteers during the study. Segmental left ventricular function was normal at baseline, and no segmental wall-motion abnormalities, ST-segment change, or dysrhythmias developed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of desflurane/nitrous oxide anesthesia in volunteers. 185 30

Use of the benzodiazepine antagonist flumazenil may inhibit the effects of benzodiazepines in a competitive manner. The only known partially agonistic effect of flumazenil is a weak anticonvulsive action at high doses. However, reports have claimed that flumazenil reduces the MAC of isoflurane in animal studies. Other reports have found that antagonizing midazolam-induced sedation or anesthesia by flumazenil led to an increase in respiratory depression. The aim of this study was to examine whether flumazenil i.v. increases fentanyl-induced respiratory depression. METHODS. In two separate sessions, ten healthy young volunteers were given either 0.0027 mg/kg fentanyl alone or 0.0027 mg/kg and 1 mg flumazenil i.v. over 4 min each time. The CO2 rebreathing method was used to determine the ventilatory response. RESULTS. Fentanyl alone brought about a significant reduction in CO2 response, characterized by a shift to the right and a decrease in the slope of the rebreathing curve (from 1.95 +/- 0.76 l.min-1.mmHg-1 to 0.86 +/- 0.53 l.min-1.mmHg-1). The infusion of additional flumazenil caused similarly significant respiratory depression (from 2.21 +/- 1.0 l.min-1.mmHg-1 to 0.77 +/- 0.38 l.min-1.mmHg-1). In both groups changes persisted for at least 120 min. No statistically significant differences between the two groups could be detected. CONCLUSION. Flumazenil does not enhance fentanyl-induced respiratory depression. Flumazenil's weak, partially agonistic action is therefore of no clinical importance.
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PMID:[The effect of flumazenil on alfentanyl-induced respiratory depression]. 186 67

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.
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PMID:Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs. 188 90

The relationship of memory self-report to self-rated depression and to actual performance on computer-simulated everyday memory tasks was investigated in 125 normal adults. Canonical correlation analyses demonstrated that self-rated memory performance and objective computer-simulated everyday memory performance shared from 27.9% to 29.4% of common variance. These data provide initial concurrent validity for a new memory self-report scale, the MAC-S. Results are discussed in relation to psychometric factors important in the design and validation of self-report memory scales.
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PMID:The association of memory complaint with computer-simulated everyday memory performance. 191 80

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


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