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Query: UMLS:C0278134 (anesthesia)
110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients scheduled for aortic valve replacement during extracorporal circulation were randomly allocated to either morphine anaesthesia or fluroxene anaesthesia. Morphine in a total dose of 4 mg/kg was administered before skin incision. At the start of extracorporal circulation all patients received 25 g glucose intravascularly. The endocrine-metabolic response to surgery, as expressed by changes in plasma ACTH, cortisol, insulin, growth hormone, cyclic adenosine-3',-5'-monophosphate (cyclic AMP), glucose, free fatty acids, blood b-hydroxybutyrate and cumulative nitrogen balance was measured before and during anaesthesia and surgery, and on the first five post-operative days. It was found that morphine anaesthesia blocked the increase in ACTH, cortisol, growth hormone, cyclic AMP, and glucose during surgery. However, after initiation of extracorporal circulation only ACTH, cortisol, and, to a lesser degree, the glucose and insulin response to glucose were lowered by morphine anaesthesia. From the first to the fifth days after operation no differences between the two groups could be demonstrated in any parameter. Cumulative nitrogen balance was similar in the two groups. It is concluded that morphine in large doses administered before skin incision inhibits the initial endocrine-metabolic response to open-heart surgery, but that the effect is short-lasting and without effect on overall postoperative protein catabolism.
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PMID:Influence of morphine anaesthesia on the endocrine-metabolic response to open-heart surgery. 3 57

Cortical reflectance, mean arterial blood pressuees, electroencephalograms, and cortical blood flow were continuously recorded together with fluorescence of reduced pyridine nucleotides (PN) at various carbon dioxide tensions before, during, and following middle cerebral artery occlusion in 10 squirrel monkeys receiving halothane or babiturate anesthesia. Measurements were continued through a nitrogen breathing cycle and to death produced by anoxia. The anesthetic agent produced no detectable differences in PN fluorescence in cerebral tissue during ischemia and anoxia. The known cerebral protective action of barbiturates is apparently unrelated to the intracellular redox state.
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PMID:Intracellular redox states under halothane and barbiturate anesthesia in normal, ischemic, and anoxic monkey brain. 3 37

1 The effects of high pressures of helium and of nitrogen on acetylcholine release were tested using the guinea-pig ileum as a model preparation. A superfusion system was designed in which this tissue could be maintained under physiological conditions in a high pressure chamber.2 Helium, at a pressure of 136 atm slightly increased the spontaneous output of acetylcholine but produced no significant changes at 68 atm (136 atm is close to the lethal pressure for small mammals).3 The acetylcholine release evoked by electrical stimulation or by 55 mM potassium was not altered by 136 atm of helium. Effects on tetrodotoxin-treated tissues were not consistent.4 Nitrogen, which in contrast to helium possesses general anaesthetic properties, caused considerable increases in spontaneous and in electrically evoked acetylcholine output at pressures which produce anaesthesia. These increases were not changed when helium was used to increase the total pressure to 136 atm, although this reverses the general anaesthetic actions of nitrogen in vivo.5 The increases in rate of acetylcholine release produced by nitrogen were observed in tetrodotoxintreated tissues and in tissues from reserpine-treated animals. In a calcium-free medium the increases were considerably smaller.6 The conclusions from these results are that while high pressures of helium caused little or no change in acetylcholine release rates, nitrogen produced large changes, which were not due to effects on axonal conduction. The effect of nitrogen is not apparently related to its general anaesthetic actions. Differences such as these in transmitter release would be likely to contribute to the differing physiological effects of these two gases.
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PMID:The effects of high pressure helium and nitrogen on the release of acetylcholine from the guinea-pig ileum. 4 Jun 48

25 patients--19 to 73 years old--who underwent maxillofacial operations, received Spontavix for 10 to 12 days via a nasogastric tube. In 20% of the patients nausea, vomiting, diarrhea and/or abdominal pain occurred and disappeared after finishing nutrition with Spontavix. Mean frequency of defecation was 0.5/patient/24 hours. Body weight, serum electrolytes, blood gases, pH and base excess in the arterial blood, urea-nitrogen, hemoglobin and albumin content of the blood did not change significantly. Lipids in the serum increased insignificantly without leaving normal limits. During nutrition with Spontavix serum transaminases (SGOT, SGPT) showed a statistically significant increase which is believed to be caused by general anesthesia.
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PMID:[Postoperative feeding of patients after maxillofacial surgery with the tube feeding preparation Spontavix]. 4 69

During surgical procedures in which nitrous oxide (N2O) anaesthesia was administered there was an increased concentration of both nitric oxide (NO) and nitrogen dioxide (NO2) in operating-room air. Preliminary studies suggest that the use of certain devices (e.g., electric cauteries, X-ray machines) capable of releasing energy in the operating-room produce the oxidation of nitrous oxide. Further evaluation of gas phase reactions of anaesthetic agents within the operating-room appear warranted, particularly in relation to the occupational risks of operating-room personnel.
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PMID:Atmospheric derivatives of anaesthetic gases as a possible hazard to operating-room personnel. 5 46

Documentation in the literature indicates that death is as painless following the induction of hypoxia by rapid decompression as by other methods that lead to hypoxia, such as exposure to high altitude, carbon monoxide, and inert gases (nitrogen, xenon, and krypton). Many of the signs and symptoms of hypoxia are the same as those for alcoholic intoxication and inert gas narcosis. Moreover, there is good evidence that analogous relationships or mechanisms may exist for hypoxia, inert gas narcosis, and anesthesia.
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PMID:Effect of rapid decompression and associated hypoxic phenomena in euthanasia of animals: a review. 9 10

Cerebral blood flow (CBF) was determined in the rat under 70% nitrous oxide anesthesia and pentobarbital anesthesia. The application of the Fick principle technique of Kety et al. was modified utilizing 133Xe infused intravenously steadily for 30 seconds, at which time the animal was decapitated and the head frozen in liquid nitrogen. A prior femoral artery to femoral vein shunt was led through a polyethylene catheter of 0.13 ml volume. This catheter passed as a coil in a NaI crystal well-counter with the arterial 133Xe concentration curve recorded by a ratemeter-recorder system. The results of the hemispheric blood flow (HBF) were: under 70% nitrous oxide anesthesia in normocapnia (Paco2 38 mm Hg), 86 +/- 15 ml/100 gm per minute; with hypocapnia (Paco2 20 mm Hg), 40 +/- 5 ml/100 gm per minute; with hypercapnia (Paco2 63 mm Hg), 187 +/- 10 ml/100 gm per minute; and with pentobarbital anesthesia (Paco2 38 mm Hg), 41 +/- 8 ml/100 gm per minute.
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PMID:The measurement of cerebral blood flow in the rat. 12 60

The accuracy of the IL404 oxygen alarm monitor has been tested against oxygen/nitrogen mixtures of known composition. The effects of inhalational anaesthetic agents and of changes in flow rate, PCO2 and humidity have also been investigated. The instrument was found to be sufficiently stable and accurate for clinical use and was unaffected by the presence of volatile anaesthetics, change in gas flow rate and the presence of nitrous oxide, carbon dioxide or water vapour. The instrument incorporates an efficient alarm system which gives both audible and visible warning should the oxygen concentration fall or exceed pre-set limits.
Anaesthesia 1976 May
PMID:An evaluation of IL-404 oxygen alarm monitor. 13 76

The physiological effects on mammals of elevated pressures (approximately 100 atmospheres) must be considered in the context of the inert gases breathed. The most striking effect of pressure per se is a central hyperexcitability manifest at first by trembling of the entremities and finally by convulsions. Paralysis and death occur at higher pressures. The primary effects of the inert gases breathed are inert gas narcosis and general anesthesia. The exciting effects of pressure per se and the depressive effects of the inert gases tend to oppose each other. Thus consciousness may be restored to anesthetized mice by raising the pressure, and conversely the threshold pressure that causes convulsions is elevated in the presence of anesthetics. These mutually antagonistic effects can be rationalized in terms of model which proposes that both anesthetics and pressure non-specifically perturb thelipid bilayer regions of neutral membranes. This model is termed the critical volume hypothesis. Anthesthetics dissolve in and expand these lipid bilayer regions, while pressure causes mechanical compression. Expansion leads to anesthesia and compression to convulsions if a critical degree of change is achieved. At elevated partial pressures of inert gas the gas-induced expansion is opposed by the compression of pressure per se. With very insoluble gases, such as helium, this expansion is so small that net compression results and the effects of helium differ little from those of pressure per se. With more soluble gases, such as nitrogen, net expansion results in inert gas narcosis and anesthesia. The critical volume hypothesis enables "safe" mixtures of "expanding" and "compressing" gases to be defined. These enable higher pressures to be better tolerated by mammals.
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PMID:The opposing physiological effects of high pressures and inert gases. 19 Dec 96

In vitro phosphorylation of rat cerebral cortex synaptosomes was measured in animals that had been acutely treated with sodium pentobarbital. [32P]Labelled phosphoproteins were separated by SDS-slab gel electrophoresis, and the autoradiographs were analyzed by densitometry. We report here that Band F of our previous reports can be separated into two components, F1 and F2, using an improved gel system. This separation is particularly relevant in this report since these components appear to be differentially sensitive to the manipulations used. Specifically, we found that while F1 phosphorylation was markedly diminished by deep barbiturate anesthesia, F2 was relatively stable. While phosphorylation of F2 was also stable 24 h post-mortem, Band F1 phosphorylation was no longer detectable. Finally, while osmotic shock treatment of synaptosomes reduced phosphorylation of F2 somewhat, it eliminated the in vitro phosphorylation of Band F1. We found that under light barbiturate anesthesia, just at the time when the animals lost the righting reflex, the in vitro phosphorylation of Bands D (MR 78,000--80,000 daltons), F1 (MR 47,000--49,000) and F2 (MR 40,000--45,000) increased relative to unanesthetized controls. The in vitro labelling of Bands D and F1 was depressed in tissue prepared from animals that were deeply comatose. These effects of pentobarbital were more pronounced when animals were sacrificed by liquid nitrogen immersion, rather than by decapitation. Cyclic AMP-dependent phosphorylation of Band D exhibited remarkable stability 24 h post-morten (7 days in one case), even when brain tissue was left at room temperature (21--23 degrees C). Phosphorylation of Band F1, however, was not detectable in post-mortem tissue. The results of these studies indicate that phosphorylation of Band F1 is: (1) sensitive to pentobarbital, and (2) unstable post-mortem. Previous findings from our laboratory suggest that Band F1 is: (3) increased in phosphorylation in liquid nitrogen P2 preparations, and may be (4) cAMP-independent, (5) rapidly turning over its phosphate in vivo, and (6) altered by a training experience. Other evidence suggests that: (7) Band F1 phosphorylation may be Ca2+-dependent and that: (8) its phosphorylation is sensitive to osmotic lysis of synaptosomes. The results suggest an important and perhaps unique role for Band F1 in neuronal function.
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PMID:Endogenous phosphorylation in vitro: differential effects of brain state (anesthesia, post-mortem) on electrophoretically separated brain proteins. 22 23


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