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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.
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PMID:Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration. 1 56

Volatile anesthetics are known to decrease the requirements for neuromuscular blocking agents. To obtain a quantitative measure of the extent of this drug interaction, studies were performed on isolated guinea pig nerve--lumbrical muscle preparations exposed to methoxyflurane, halothane, isoflurane, diethyl ether, fluroxene, and enflurane in concentrations equal to MAC. From the relationship between indirect twitch height and d-tubocurarine concentration, the concentration depressing the twitch height by 50 per cent was determined. In the presence of MAC levels of anesthetic, the ED50 was decreased by the following fractional amounts: methoxyflurane, 0.311; halothane, 0.334; isoflurane, 0.335; diethyl ether, 0.462; fluroxene, 0.580; enflurane, 0.697. Comparison of the fractional decrease of d-tubocurarine dose requirement by an anesthetic at MAC and previously obtained values for the fractional depression of end-plate depolarization by an anesthetic at MAC showed that the more the anesthetic depresses depolarization, the smaller the d-tubocurarine dose requirement. Thus, clinically observed decreases in dose requirements may be explained by the effects of the anesthetics on chemosensitivity of the end-plate region.
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PMID:Decrease in dose requirement of d-tubocurarine by volatile anesthetics. 3 76

The direct myocardial effects of fluroxene were examined in isometrically and isotonically contracting isolated rat heart muscle. MAC, the minimum anesthetic concentration needed to prevent movement in response to tail clamping, was found to be 5.0 vol per cent fluroxene in the rat. At 4.6 vol per cent fluroxene, peak developed isometric tension and maximum rate of tension development were decreased 29 and 24 per cent, respectively. At 11 vol per cent, the depressions were 39 and 33 per cent. At 26.4 vol per cent, the depressions were around 60 per cent. Vmax (the maximum shortening velocity of unloaded muscle) of the force-velocity relation was unaltered by fluroxene concentrations of 0.8, 4.6, and 11 vol per cent. Even at 26.4 vol per cent, the depression in Vmax was only 25 per cent. Po (the maximum force at zero velocity), work, and power were lowered much more, with reductions ranging from 15 to 27 per cent at 4.6 vol per cent, from 40 to 42 per cent at 11.0 vol per cent, and from 65 to 69 per cent at the 26.4 vol per cent. Series elastic extension was unchanged at 0.8 and 4.6 vol per cent fluroxene, but was decreased 16 per cent at 11.0 vol per cent and 46 per cent at 26.4 vol per cent fluroxene. The data indicate the fluroxene has a direct negative inotropic effect that is associated with increased series elastic stiffness, but does not involve Vmax of the force-velocity relation until quite high anesthestic concentrations are reached. Comparative studies were also carried out with halothane. MAC for halothane in the rat was 1.0 vol per cent. The relative potency of halothane compared with fluroxene in depression of Vmax was 13.2, and its relative potency in depression of Po, 4.0.
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PMID:Fluroxene and isolated heart muscle. 23 6

Maternal and foetal cardiovascular, blood gas and acid-base changes were studied during 90 minutes of methoxyflurane anaesthesia. At 1.0 and 1.5 MAC anaesthesia, despite slight to moderate falls in maternal blood pressure, cardiac output and uterine blood flow, no serious foetal deterioration was seen. 2.0 MAC methoxyflurane was associated with marked falls in maternal blood pressure, cardiac output and uterine blood flow. Foetal hypoxaemia and a mixed respiratory and metabolic acidosis developed. Little foetal cardiovascular depression was seen with any level of anaesthesia. There was no direct effect of methoxyflurane on the uterine vasculature.
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PMID:Maternal and foetal effects of methoxyflurane anaesthesia in the pregnant ewe. 23 12

The effects of enflurane anaesthesia on central circulation, total oxygen uptake, splanchnic circulation and splanchnic oxygen uptake were studied in 10 artifically ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. The end-tidal enflurane concentration was kept at about 1 MAC (= 2.2%). Arterial blood pressure diminished 54% of control value due to decreases of cardiac output to 65% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows decreased to 65-70% of control levels and the corresponding vascular resistances all declined to about 80-85% of control values. Total oxygen uptake decreased, but less than cardiac output, leading to an increased arterio-venous oxygen content difference. Oxygen uptake of the preportal tissues was unchanged and hepatic oxygen uptake was not significantly altered, although there were decreases in hepatic oxygen uptake in some of the individual experiments. It is suggested that the cardiovascular depression following enflurane anaesthesia in the dog was due, to a great extent, to a primary myocardial depression. It is further concluded that the splanchnic blood flows were relatively well preserved, due to decreases in splanchnic vascular resistances, and that hepatic and preportal tissue oxygen consumptions were maintained by increased oxygen extraction.
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PMID:Effects of enflurane on haemodynamics and oxygen consumption in the dog with special reference to the liver and preportal tissues. 42 10

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.
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PMID:Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. 61 5

The effects of equipotent concentrations of enflurane, isoflurane, and halothane on isolated human uterine muscle have been evaluated. Three anesthetic concentrations (0.5, 1.9, and 1.5 MAC) were studied. Specimens included myometrial strips from 45 non-gravid and seven gravid uteri. Both groups of muscle strips showed significant (P less than 0.05) and progressive depression of contractility with all anesthetics. However, the extents of depression at each anesthetic level studied were similar with all drugs. Enflurane, isoflurane, and halothane are equally depressing to isolated human uterine muscle.
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PMID:Enflurane, isoflurane, and halothane and isolated human uterine muscle. 83 87

The relationship between cerebral oxygen consumption (CMRO2) and anesthetic concentration has been assumed (based upon isolated measurements) to be approximately linear at concentrations less than 1 MAC. The shapes of the anesthetic dose-response curves for both CMRO2 and cerebral blood flow (CBF) were examined by multiple measurements made at small, progressive concentration increments from 0 to 2 MAC halothane (six dogs), enflurane (six dogs), and isoflurane (six dogs), and during a constant 23 mg/kg/hr infusion of thiopental (six dogs). The EEG was continuously recorded and changes in EEG patterns from "awake" to "anesthetic" were correlated with changes in anesthetic concentration, CBF, and CMRO2. The significance of changes in the slopes of regression lines for CMRO2 before, during and after changes in EEG patterns from "awake" to "anesthetic" were then determined. Contrary to previous inferences, CMRO2 dose-response curves were found to be nonlinear at anesthetic concentrations less than 1 MAC for all anesthetics studied. CMRO2 decreased precipitously until a stable "anesthetic" pattern was observed on the EEG; thereafter, CMRO2 decreased at a markedly reduced rate. The onset of this change occurred at concentrations well below MAC for the inhalational anesthetics. With the thiopental infusion, CMRO2 decreased most rapidly during the first 25 minutes. With halothane and enflurane, CBF was maximal during the period of transition in the EEG from an "awake" to an "anesthetic" pattern. CBF was elevated at all concentrations of isoflurane studied. CBF decreased rapidly during thiopental infusion until the EEG pattern changed from "awake" to "anesthetic" and then more slowly. The results demonstrate that the change in the EEG to an "anesthetic" pattern, which occurs at concentrations well below MAC, is accompanied by an abrupt metabolic depression. It is speculated that these events coincide with the onset of functional depression.
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PMID:The nonlinear responses of cerebral metabolism to low concentrations of halothane, enflurane, isoflurane, and thiopental. 83 91

Tracheal mucociliary flow rates in dogs were measured with a radioactive droplet technique during thiopental anesthesia, and subsequently during enflurane, either, and nitrous oxide-morphine anesthesia on different occasions. Enflurane, at 0.6, 1.2, 1.8 MAC, produced a dose-dependent, reversible depression of mucociliary flow equal to that previously reported for halothane. Nitrous oxide-halothane and nitrous oxide-morphine depressed mucociliary flow to the same extent as halothane at equivalent MAC levels. Ether did not depress mucociliary flow significantly from the thiopental control at any MAC level.
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PMID:Mucociliary flow in the trachea during anesthesia with enflurane, ether, nitrous oxide, and morphine. 85 Dec 41

Trans-1,2-dichloroethylene (t-DCE), an industrial solvent, proved to be moderately toxic when studied in small laboratory animals. In adult female rats brief (8 h) and prolonged (8 h daily, on 5 consecutive days a week, for more than 16 weeks) inhalation of 200 ppm--the current TLV/MAC in various countries--produced histological evidence of slight to severe fatty degeneration of the liver lobules and Kupffer cells. In addition marked pulmonary hyperaemia and alveolar septal distention were noted. Fibrous swelling of the cardiac muscle (with striation) just barely maintained) and hyperaemia remained detectable for as long as 14 h post-exposure, but only occurred at 3000 ppm/8 h. A concentration of 1000 ppm/8 h was required to produce a fall in blood albumin, urea nitrogen, alkaline phosphatase activities and erythrocyte count. The cited concentrations failed to produce prenarcotic symptoms of narcosis (central nervous system (CNS) depression). The LD50 was found to be 6.0 ml/kg i.p. and 1.0 ml/kg p.o. for female rats, and 3.2 ml/kg i;p. for female mice. In some of the rats killed in these experiments the organ changes were found to be identical to those observed after inhalation.
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PMID:Toxicity studies on trans-1,2-dichloroethylene. 85 30


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