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 cardiocirculatory responses to equianaesthetic concentrations (MAC 0.5 and MAC 1.0 plus 67% N2O) of halothane, methoxyflurane, enflurane and isoflurane were studied in a total of 35 closed-chest dogs during ventilation controlled to produce normocapnia. Each anaesthetic produced a dose-related decrease in mean arterial pressure and in values reflecting cardiac function. These included cardiac output, stroke volume, left ventricular max dp/dt and ejection fraction. Isoflurane seemed slightly less depressant to the heart than the other 3 anaesthetics. Total peripheral resistance remained nearly unaffected during halothane and methoxyflurane anaesthesia but decreased significantly with MAC 1.0 enflurane and isoflurane. There was no change in heart rate at low anaesthetic concentrations. The deeper levels of anaesthesia were associated with moderate increases in heart rate. In spite of the obvious depression of myocardial contractility there was a fall in pulmonary artery and left ventricular end-diastolic pressures and in left ventricular end-diastolic volumes with each of the agents. We take this as an expression of decreased ventricular filling resulted from pooling of blood in peripheral capacitive vessels. With the exception of isoflurane, each of the other three anaesthetics reduced coronary blood flow. Coronary vascular resistance was not substantially influenced by halothane and methoxyflurane, but decreased with MAC 1.0 enflurane and isoflurane. Myocardial oxygen availability was always found to be adequate. Isoflurane even produced a significant rise in coronary venous oxygen saturation indicating coronary vasodilation. Parallel with the depression in cardiac performance and blood pressure as two of the main predictors of energy demand, myocardial oxygen consumption was found to be significantly reduced by each of the anaesthetics. The ratio of the external work of the left ventricle to its oxygen consumption indicated that myocardial efficiency deterioated. The clinical implications are discussed.
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PMID:[Influence of modern inhalation anaesthetics on haemodynamics, myocardial contractility, left ventricular volumes and myocardial oxygen supply (author's transl)]. 87 90

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
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PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

Tracheal mucociliary flow rates in dogs were measured with a radioactive droplet technique during thiopental anesthesia, and subseqently during halothane anesthesia. Body temperature and inspired gas temperature and humidity were held constant. Ventilation was controlled with 25 per cent oxygen in nitrogen to produce PaCO2 30 torr. Mucociliary flow rate remained constant when halothane concentration was held constant at 1.2 MAC halothane. Mucociliary flow rates at 0.6 MAC halothane were comparable to those after thiopental, 25 mg/kg. Increases in concentration from 0.6 to 1.2 to 1.8 to 2.4 MAC halothane progressively depressed mucociliary flow. Flow at 2.4 MAC halothane was 27 per cent of the control (thiopental) value. Flow returned to previous values as end-tidal halothane concentration was reduced. The depression produced by halothane may represent impairment of an important pulmonary defense mechanism.
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PMID:Halothane depresses mucociliary flow in the trachea. 93 52

Serial invasive and noninvasive (systolic time interval) measurements of left ventricular performance were obtained in six healthy volunteers during general anesthesia employing the following sequence: thiopental induction, succinylcholine (prior to endotracheal intubation), and halothane--100 per cent oxygen at 1.25 and 1.75 MAC. Heart rate (HR), mean pulmonary arterial "wedge" pressure (PAW) and mean systemic arterial pressure (MAP) were measured continuously; cardiac index and systolic time intervals (STI's) were measured during each intervention. At both levels of halothane, MAP and stroke work index decreased (both P less than 0.02), while HR and systemic vascular resistance did not change. At 1.25 MAC halothane PAW was unchanged, but at 1.75 MAC PAW increased from 8 +/- 4 (SD) to 11 +/- 5 torr (P less than 0.02). Preload was altered at 1.25 MAC by administration of 600-1,000 ml lactated Ringer's solution; PAW increased from 9 +/- 4 to 17 +/- 3 torr (P less than 0.01). At 1.75 MAC halothane, volume expansion increased PAW in a similar manner, but the resultant ventricular function curve was depressed compared with 1.25 MAC halothane. In additon, at each level of halothane anesthesia, the ventricular function curve was depressed compared with results obtained in awake normal subjects. Afterload was altered at 1.25 MAC halothane by infusion of phenylephrine sufficient to raise MAP by 30 per cent. This intervention resulted in a greater depression of cardiac performance than that observed at 1.75 MAC halothane alone. Although alterations in STI's were directionally similar to changes observed in invasive hemodynamic measurements, STI's were sensitive to acute alternations in loading conditions. It is concluded that the levels of halothane commonly employed for general anesthesia significantly depress left ventricular performance in normal subjects, as evidenced by abnormal responses to alterations in preload and afterload, and that STI's should not be employed for routine measurement of left ventricular performance during anesthesia unless both the afterload and the preload on the myocardium are known.
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PMID:Alterations of normal left ventricular performance by general anesthesia. 98 77

The neuromuscular effects of d-tubocurarine (dTc), pacuronium, and succinylcholien (SCh) were studied in 37 unpremedicated adult surgical patients anesthetized with 1.25 MAC enflurance in oxygen. The relaxant doses that produced 50 per cent depression of twitch height (ED50) were 1.57, 0.29, and 4.9 mg/m2 for dTc, pancuronium, and SCh, respectively. These doses are approximately 3.1, 1.7, and 1.0 times less than the amount of dTc, pancuronium, and SCh required to produce 50 per cent depression of twitch height during halothane anesthesia but are the same as ED50 values during isoflurane anesthesia. In eight additional unpremedicated patients anesthesia was maintained at 0.71 MAC enflurane in oxygen (five patients) or 1.67 MAC enflurane in oxygen (three patients). Twitch depression following dTc, 1.5 mg/m2, was related directly to alveolar enflurane concentration. Ability to sustain tetanus decreased progressively with increasing tetanic frequencies and decreased with increasing alveolar enflurane concentrations. The authors concluded that smaller doses of dTc and pancuronium are needed for adequate relaxation during enflurane anesthesia than during equi-MAC halothane anesthesia, and that higher alveolar enflurane concentrations reduce the dose of dTc necessary to produce a given amount of paralysis. Also, neuromuscular effects of enflurane in combination with dTc or pancuronium are not significantly different from those seen suring equi-MAC isoflurane anesthesia.
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PMID:Neuromuscular effects of enflurane, alone and combined with d-Tubocurarine, pancuronium, and succinylcholine, in man. 111 66

The effects of halothane on the effective refractory period (ERP) and the ventricular activation were examined in a canine myocardial infarction model, and compared with those of propranolol. Halothane reduced the heart rate and prolonged the ERP in both normal and infarcted zones. A prolongation of ERP with halothane was also observed during atrial pacing at the same rate as in control, but the effect was less than during sinus rhythm. Halothane (1 MAC) further delayed or blocked the delayed activation in the infarcted zones with only slight effects on the activation of the normal zones. Propranolol (0.2 mg/kg) prolonged ERP during sinus rhythm, but it did not affect either the ERP or ventricular activation during atrial pacing. In conclusion, halothane produced a selective depression of the delayed activation and the prolongation of ERP, which may be caused by both direct effects on the myocardium and secondary effects such as a reduction of the heart rate. These effects of halothane may contribute to its antiarrhythmic effects in the myocardial infarction model which have been previously reported.
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PMID:Comparison of the effects of halothane and propranolol on the effective refractory period and the ventricular activation in a canine myocardial infarction model. 128 97

We have examined the sensitivity of the geniohyoid, an upper airway dilating muscle, to vecuronium in 12 anaesthetized dogs undergoing mechanical ventilation of the lungs and compared it with that of the diaphragm. Dogs were allocated randomly to two groups: pentobarbitone alone (group 1, n = 7); pentobarbitone combined with 0.2 MAC (0.44%) of enflurane anaesthesia (group 2, n = 5). Supramaximal single twitch stimulations (0.1 Hz) were applied to the phrenic nerves in the upper thorax and the geniohyoid branches of the hypoglossal nerves at the neck. The evoked responses were assessed by the transdiaphragmatic pressure (Pdi) and the isometric force of the geniohyoid muscles (Tgh) until complete recovery of these variables after i.v. administration of vecuronium 0.02 mg kg-1. In both groups, the magnitude of the depression of twitch response was greater and time required to reach control amplitude was longer in the geniohyoid than the diaphragm. The depression of Tgh was significantly greater in group 2 than in group 1, whereas no change was observed in Pdi between the two groups. We conclude that the geniohyoid is more sensitive to vecuronium than the diaphragm and the differential effects of vecuronium are facilitated by a low concentration of enflurane.
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PMID:Differential effects of vecuronium on diaphragm and geniohyoid muscle in anaesthetized dogs. 154 42

Dexmedetomidine (DMED) is a novel alpha 2 adrenergic agonist that has been shown to have potent analgesic and anesthetic sparing effects. This study was designed to investigate the effects of DMED, both alone and combined with isoflurane, on resting ventilation, the hypercapnic response, and the hypoxic response in dogs. When given alone, 1 microgram/kg decreased resting ventilation by 22% but at larger doses (10, 20, and 100 micrograms/kg) resting ventilation increased, doubling at 100 micrograms/kg. Doses of 10 micrograms/kg and greater caused a maximum depression of 60% in the slope of the hypercapnic response, but no dose had a significant effect on the hypoxic ventilatory response. A dose of 3 micrograms/kg of DMED reduced isoflurane MAC from 1.3% to 0.37%, and the ventilatory effects of this 1 MAC combination were intermediate between the awake values and those of isoflurane-anesthetized (1.3%) dogs. Atipamezole is a specific centrally acting alpha 2 receptor antagonist and when given with DMED in isoflurane-anesthetized dogs prevented the ventilatory depression. However, atipamezole alone also ventilatory stimulating effects, which may indicate tonic alpha 2 adrenergic activity. The ventilatory depression caused by DMED, either alone or combined with isoflurane, at doses that significantly reduce anesthetic requirements are relatively mild.
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PMID:Ventilatory effects of dexmedetomidine, atipamezole, and isoflurane in dogs. 134 80

This study was designed to determine the effect of prolonged infusion on the ease of reversal of atracurium and vecuronium, and whether factors which potentiate the block delayed reversal. In phase one, 40 patients were randomized (double blind) to determine the steady state conditions for atracurium and vecuronium. Fourteen atracurium patients and 17 vecuronium patients were evaluable. The unblinded second phase involved the steady state conditions using halothane or isoflurane and atracurium infusions. The infusion required for 95% twitch depression (TD95) for atracurium was 7.6 +/- 1.1 micrograms.kg-1 x min-1. The requirement for vecuronium changes with time: TD95 at 30 min was 1.01 +/- 0.16, at 60 min 0.89 +/- 0.12 and after 90 min 0.85 +/- 0.17 micrograms.kg-1 x min-1 (P < 0.05). The mean TD95 was 0.94 +/- 0.23 micrograms.kg-1 x min-1. Multivariate regression analysis of the infusion data revealed a vecuronium model predicting TD95 by the duration of infusion (P < 0.05) and weight (P = 0.05). Atracurium TD95 was predicted by age (P = 0.05). The addition of an inhalation agent to atracurium reduced the infusion rate by 2.01 +/- 0.28 micrograms.kg-1 x min-1 (P = 0.0001) for each increase in MAC. The mean reversal times for atracurium with three different anaesthetics and for vecuronium were not different. Reversal of pancuronium blockade, from less profound twitch depression (86.4 vs 95%) took twice as long as for atracurium and vecuronium for which the following predictors were identified: age, weight, duration of infusion, level of blockade, and type of anaesthetic, using a stepwise regression model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Continuous infusions of atracurium and vecuronium, compared with intermittent boluses of pancuronium: dose requirements and reversal. 136 Mar 37

General anaesthesia is the reversible depression of central nervous system function. There is still no agreement over what constitutes depth of anaesthesia, and the clinical anaesthetist must thus titrate drug input according to clinical signs (heart rate, blood pressure, somatic movement, autonomic responses). The potency of inhalational agents may be expressed in terms of the MAC (minimum alveolar concentration); comparable end-points (including blood concentrations) have been proposed for the intravenous agents. Kinetic infusion regimens can be constructed for the intravenous agents to achieve the ED95 concentrations required to provide clinically adequate anaesthesia. However, because of individual differences in drug kinetics and dynamics, as well as the influences of disease states and intercurrent therapy, the clinician will titrate the dose according to response. Administration of volatile or intravenous anaesthetics by fixed regimens may result in either overdosage or the risk of patient awareness. The choice of anaesthetic drug is usually based on the nonhypnotic side effects of the different agents--including their central and regional cardiovascular effects, the speed and completeness of recovery, and the need to provide intraoperative analgesia. In addition, special techniques and drugs are often needed for neurosurgical, cardiothoracic and obstetric anaesthesia. All anaesthetic agents (inhalation and intravenous) have other side effects (such as cardiorespiratory depression and organ toxicity related to the liver or kidney). Both halothane and enflurane may be responsible for postoperative hepatic dysfunction, while the metabolism of enflurane can also result in nephrotoxicity in patients with pre-existing renal dysfunction. Isoflurane has been reported to cause 'coronary steal' in patients with ischaemic heart disease through its coronary vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Practical treatment recommendations for the safe use of anaesthetics. 137 60

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