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

Immune depression occurs after general anaesthesia. It is related to depression of serum factors after anesthesia with ether or chloroform, or secondary to depression of antibody-producing cells after anaesthesia with halothane, nitrous oxyde or Pentothal. This immune depression augments proneness to bacterial and viral infection and to malignant disease.
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PMID:[Does anesthesia have an immunosuppressive effect?]. 1 Jul 75

The chronotropic effects of all currently available volatile anesthetics were investigated in isolated rat atrial preparations. Anesthetic ethers, diethyl ether, methoxyflurane, and enflurane elicited a dose-dependent positive chronotropic effect. Fluroxene produced a slight depression at low concentrations. The halogenated hydrocarbon anesthetics, halothane, chloroform, and trichloroethylene, did not show a uniform pattern. Halothane's effect was small and biphasic. Chloroform caused a dose-dependent decrease in heart rate, and trichloroethylene caused a marked positive chronotropic effect. The dose-response curves in all anesthetics remained unaltered in the presence of either 3 x 10(-7) M dl-propranolol or 1 x 10(-6) M atropine. It is concluded that volatile anesthetics elicit significant direct chronotropic actions on rat atrial preparations. The mechanism of their actions does not involve stimulation of beta-adrenergic or cholinergic receptors.
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PMID:Mechanisms of chronotropic effects of volatile inhalation anesthetics. 1 71

Having studied anaesthetic drug interactions in rats, we report the effects of halogenated anaesthetics on the liver glutathione levels and histology, as well as the results of the enhancement of these effects by microsomal enzyme induction. The anaesthetic agents studied included methoxyflurane, halothane, ethrane, chloroform and fluroxene. While exposure of rats to methoxyflurane, helothane and ethrane produced no significant changes in hepatic glutathione levels, or in liver histology, exposure to chloroform and fluroxene produced marked depression of liver glutathione, especially after microsomal enzyme induction. Furthermore, rats exposed to thses agents after enzyme induction developed gross centrilobular necrosis and died. It is suggested that the study of the effects of any new anaesthetic agent on liver glutathione levels could be a valuable screening test of its hepatotoxic potential, before its clinical trial.
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PMID:The effect of exposure to halogenated anaesthetics on liver glutathione levels in rats. An index of hepatotoxicity. 3 73

McN-2840-46, 2.5 mg/kg, i.v., protected against atrial tachyarrhythmias induced by three different methods in dogs and monkeys. The compound was inactive against ventricular arrhythmias produced by ouabain and by chloroform-epinephrine interaction at a four-fold higher dose. Significant reversal of ventricular arrhythmias produced by occlusion of the left anterior descending coronary artery in dogs was achieved by infusion of 8.8 +/- 2.4 mg/kg, i.v. of McN-2840-46. Myocardial electrogram studies confirm that the atrium is preferentially affected. McN-2840-46 does not possess beta 1- or beta 2-adrenergic blocking activity when evaluated on isolated rabbit atrial and guinea-pit tracheal chain preparations. McN-2840-46 is vagolytic but not anticholinergic. The vagolytic activity is attributed to its local anesthetic effect. Depression of myocardial function was observed in anesthetized dogs and in the heart-lung preparation. However, the isolated cat papillary muscle was stimulated by McN-2840-46 and doses considerably above the effective anti-arrhythmic dose did not significantly decrease cardiac output in the non-anesthetized dog. The results of these experiments suggest that McN-2840-46 is a potent "preferential" atrial anti-arrhythmic agent.
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PMID:Cardiovascular profile of 2-(3,4-diethyoxy-beta-methoxyphenethyl) imino-1-methylpyrrolidine fumarate (McN-2840-46), a preferential atrial anti-arrhythmic agent. 3 28

The effects of ether, chloroform, and halothane on calcium accumulation and ATPase activity of rat heart microsomes and mitochondria as well as on myofibrillar ATPase activity were investigated. Chloroform and halothane depressed microsomal and mitochondrial calcium uptake and binding in a parallel fashion. Ether decreased microsomal calcium binding and mitochondrial calcium uptake to varying degrees, while mitochondrial calcium binding was slightly enhanced. Whereas ether had no effect, chloroform depressed microsomal and mitochondrial total APTase activities and halothane decreased microsomsl ATPase and slightly stimulated mitochondrial total ATPase activities. Halothane was found to depress myofibrillar Mg2+-ATPase and ether was capable of decreasing myofibrillar Ca2+-ATPase. Chloroform was seen to inhibit both myofibrillar enzymes. These results suggest that the cardiodepressant actions of volatile anesthetic agents may be due to alterations in the calcium accumulating abilities of microsomal and mitochondrial membranes while direct myofibrillar effects may contribute to the depression seen with relatively higher concentrations of anesthetics.
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PMID:Subcellular effects of some anesthetic agents on rat myocardium. 15 65

Three analogs of lidocaine (benzyl carbamyl, benzyl nitrile and methyl nitrile) were synthesized and examined for cardiovascular and central activity. The benzyl carbamyl analog was more potent than lidocaine in lowering blood pressure but possessed only slight local anesthetic, antiarrhythmic and CNS-depressant activity. At 40 mg/kg the benzyl nitrile derivative was superior to lidocaine in protecting against chloroform-induced arrhythmias. The methyl nitrile analog was less active than the benzyl nitrile analog in most parameters examined. The benzyl nitrile derivative and lidocaine had similar potencies on blood pressure depression, local anesthetic activity and ability to protect against calcium chloride-induced arrhythmias. Unlike the benzyl carbamyl derivative both lidocaine and the benzyl nitrile compounds appear to depress the cardiovascular system via a common mechanism.
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PMID:Selected cardiovascular and central properties of three lidocaine analogs. 51 67

The melting and energy characteristics of several drug-wax combinations were investigated using differential scanning calorimetry. The phase diagrams of binary mixtures of tripelennamine hydrochloride and tolazoline hydrochloride with carnauba wax and castor wax showed no eutectic formation and gave no indication that a significant interaction was involved. However, in tripelennamine mixtures, a slight depression in the drug melting point was observed at around 50% concentration. For ternary systems, i.e., drug, carnauba wax, and stearyl alcohol, thermograms of samples prepared by a fusion method differed slightly from those obtained with mixtures formulated by dissolving all ingredients in chloroform and evaporating the solvent. However, the location of the peak of each component remained essentially the same. A plot of melting point versus concentration of each compound showed insignificant changes in melting point and indicated that no interaction was occurring. The phase diagrams suggested that the combinations are strictly physical and that it is the physical characteristics, such as the hardness and composition of the core and drug particle size, that influence the release or dissolution of drug from the waxy matrix.
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PMID:Sustained release from inert wax matrixes I: drug-wax combinations. 64 21

Pre- and postjunctional effects of three ethers (enflurane, diethyle ether, and methoxyflurane) and three non-ethers (chloroform, halothane, and trichloroethylene) were studied in the rat phrenic nerve diaphragm preparation using standard microelectrode recording techniques. Depression of postjunctional function included depression of the amplitude of miniature endplate potentials, inhibition of suxamethonium induced depolarization of the muscle endplate, prolongation of duration of the endplate potential, and increase in threshold for generation of the muscle action potential. The last two effects were more marked for the ethers than for the non-ethers. Effects on pre-junctional function included a slight increase in fluctuation of the endplate potential (EPP) amplitude associated with the thers and chloroform, a faster rate of decline of EPP amplitude during a tetanus in presence of the ethers, and prolongation of the normal facilitatory period during paired stimulation in the presence of chloroform. Chloroform had no effect on the rate of decline of EPP amplitude during tetanic stimulation and the ethers had no effect on the facilitatory period during paired stimulation. These results indicate that volatile anaesthetic agents depress synaptic transmission by acting on multiple sites, and that the pattern of this depression is different for each drug or group of similar drugs.
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PMID:Comparative site of action of various anaestetic agents at the mammalian myoneural junction. 113 70

The question as to whether or not the hypotension observed as part of the effect of tricholorofluoromethane (FC11), dichlorofluoromethane (FC 12), dichlorotetrafluoroethane (FC 114) and methyl chloroform was due to a vasodepressor component of action, in addition to the previously documented depression in myocardial contractile force, was answered by testing these agents in an anesthetized dog preparation in which one hind limb was perfused at constant flow through the femoral artery. 5% FC 11, 20% FC 12 and 20% FC 114 decreased vascular resistance of the perfused limb, as reflected by decrease in mean femoral arterial perfusion pressure, in vagotomized but not in intact preparations. Methyl chloroform decreased vascular resistance even in intact preparations. Spontaneous blood flow in the intact femoral artery decreased following FC 11 and methyl chloroform administration in vagotomized preparations and was associated with marked decrease in mean aortic pressure. Blockade of alpha and beta adrenergic receptors with phentolamine and propranolol in the vagotomized preparation had no modifying influence of the effect of FC 11 and methyl chloroform. It may be concluded from this study that FC 11, FC 12 and FC 114 exhibit a vasodepressor activity on skeletal muscle vascular bed which is readily overcome by the hypotension-induced activation of the sympathetic system but which becomes evident when reflex activity is prevented by vagotomy. Methly choloroform exhibits a vasodepressor effect even in intact preparations probably because of concomitant depression of reflex activity through its general anesthetic action. A decrease in spontaneous femoral blood flow following FC 11 and methyl chloroform administration is referable to the accompanying severe hypotension notwithstanding concomitant vascular relaxation. Neither FC 11 nor methly chloroform directly liberate catecholamines from their sites of storage.
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PMID:Hemodynamic effects of aerosol propellants. III. Vascular resistance in the canine hind limb. 126 70

Hydrostatic pressure and anesthetic agents exert mutually antagonistic effects, including pressure reversal of anesthesia and anesthetic amelioration of the high-pressure nervous syndrome. To clarify the cellular basis for these phenomena, twitch tension and electromyogram (EMG) were monitored in the indirectly stimulated isolated rat diaphragm. Compression to 137 atm increased twitch tension without changing EMG amplitude. Partial phrenic nerve block accompanied EMG depression induced by methoxyflurane and chloroform; pressure antagonized these effects. To examine subthreshold pressure effects, calcium concentration was decreased from 2.5 to 0.5 mM. Compression to 137 atm then reversibly decreased EMG amplitude, while enhancing twitch tension. In 0.5 mM calcium, methoxyflurane and chloroform depressed EMG amplitude before blocking phrenic nerve conduction; pressure to 137 atm produced additional depression. These results suggest that pressure enhances twitch tension by acting on excitation-contraction coupling or on the contractile mechanism. They also indicate that pressure may inhibit transmission at the neuromuscular junction, and they do not support synaptic transmission as a site of pressure-anesthetic antagonism.
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PMID:Neuromuscular function at hyperbaric pressures: pressure-anesthetic interactions. 127 64


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