Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test the relationship between changes in plasma potassium concentration and pH changes of respiratory origin, we produced hypercapnia (mean PaCO2 71 mmHg = 9.5 kPa) in a group of 17 patients and hypocapnia (mean PaCO2 21 mmHg = 2.8 kPa) in another 20 patients during neurolept analgesia and intraabdominal operations. A control group of 19 patients was studied under normocapnia but otherwise identical conditions. During hypercapnia, serum potassium rose, deltaK/deltapH amounting to -0.82, -1.05 and -1.34 after 30, 60 and 90 min, respectively. During hypocapnia, serum potassium decreased, deltaK/deltapH being a little more negative than during hypercapnia (mean values -1.62, -2.44 and -1.60). Red cell potassium concentration decreased in all three groups to a similar extent. Blood lactate levels during hypercapnia decreased to 75% of control and during hypocapnia rose to a maximum of 186% of control. In order to obtain reasonable values for base excess in primarily respiratory acid-base disorders, it is necessary to use nomograms based on in vivo ECF-CO2-titration curves. With this premise, hypercapnia or hypocapnia in our patients was not associated with significant changes in base excess.
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PMID:Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia. 3 56

The I.V. administration in dogs of high and massive doses of narcotics produced an acute rise in CO2 consumption, a rise of plasma catecholamines and other slight biochemical and metabolic perturbances. A general trend towards metabolic acidosis and hypermetabolism was noticed but important differences appeared according the drugs and doses chosen. The safety margin for metabolic toxicity (ratio between IV doses producing severe metabolic side-effects and doses necessary for deep surgical analgesia) were calculated for each narcotic and found as follows: 1 for pethidine, 3.3 for piritramide, 13 for morphine and phenoperidine, 12.5 for R 39 209, 60 for fentanyl, 800 for sufentanil and 4 000 for R 34 995. Drug associations may decrease or increase the metabolic safety margin of the narcotics. Beneficial associations with morphinomimetics are found with droperidol, etomidate and flunitrazepam.
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PMID:Comparative study of cardiovascular, neurological and metabolic side effects of 8 narcotics in dogs. Pethidine, piritramide, morphine, phenoperidine, fentanyl, R 39 209, sufentanil, R 34 995. III. Comparative study of the acute metabolic toxicity of the narcotics used in high and massive doses in curarised and mechanically ventilated dogs. 3 20

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.
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PMID:Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog. 3 75

A comparison was made between the effects of two different anesthetics, alpha-D-gluco-chloralose and 1-1-phenylcyclohexyl piperidine hydrochloride (Sernylan), on cerebral blood flow (CBF), brain metabolism and cerebrovascular CO2 responsiveness in primates. The experiments were carried out on immobilized and artificially ventilated baboons. Anesthesia was induced either with 100/mg/kg chloralose (i.p.) or with 1 mg/kg Sernylan (i.m.). CBF in 8 different brain regions was measured by the intra-arterial 133Xe clearance technique. The CO2 responsiveness of the cerebrovascular bed was tested by a gas mixture containing 5% CO2. Chloralose depressed total as well as regional CBF compared to the effect of Sernylan. A significant shift occurred toward lower CBF values in the grey matter while white matter flow was identical in the two groups. Brain O2 consumption was significantly higher during Sernylan analgesia (3.35 +/- 0.34 ml/100 g/min) than during chloralose anesthesia (2.42 +/- 0.22 ml/100 g/min). There were no differences in glucose uptake, lactate and pyruvate production, or in arterial and cerebral venous blood gases in the two types of anesthesia. The cerebrovascular CO2 sensitivity of the Sernylan-treated baboons was higher than that of the chloralose-anesthetized animals, in both the grey and white matter.
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PMID:Comparative effects of chloralose anesthesia and Sernylan analgesia on cerebral blood flow, CO2 responsiveness, and brain metabolism in the baboon. 40 48

Different modes of naloxone administration were studied in 100 patients following N2O-O2-relaxant anaesthesia, where fentanyl was administered for analgesia according to a standardized dose schedule (mean 4.3 microgram/kg/h). After reversal of muscular relaxation, the patients were randomly given naloxone--either 1.0 or 2.5 microgram/kg i.v. or 2.5 or 5.0 microgram/kg i.m., or none (control). Each group consisted of 20 patients. Awakening was fastest after 2.5 microgram/kg i.v. of naloxone (1.8 +/- 0.1 min), the time being significantly shorter (P less than 0.025) than in the control group (2.7 +/- 0.4 min). After 15 min, the minute volume and frequency of respiration were significantly higher (P less than 0.05) in all naloxone groups than in the control group. However, the arterialized venous PCO2 did not show significant differences during the recovery. It is therefore suggested that naloxone reversal may cause an increase in CO2 production. The immediate postoperative pain (score 0-3) was mildest in the control group (1.0 mean) and severest after 2.5 microgram/kg i.v. of naloxone (1.8 mean); the difference was statistically significant (P less than 0.05). The groups receiving 1.0 microgram/kg i.v. and 2.5 microgram/kg i.m. did not differ from each other (1.2 mean). Nausea and vomiting were reported more often after 5.0 microgram/kg im. of naloxone than in other groups. After moderate doses of fentanyl during balanced anaesthesia, routine use of naloxone does not seem to be necessary, but if rapid recovery is essential, 1.0 microgram/kg i.v. or 2.5 microgram/kg i.m. of naloxone may be recommended and these doses do not cause a higher incidence of side effects.
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PMID:Naloxone as narcotic antagonist after balanced anaesthesia. 60 62

Study of 34 patients who had undergone thoracotomy revealed that the group given intercostal nerve block analgesia had a significantly smaller decline in vital capacity after operation than did the group given narcotic analgesia only. The postoperative increase in arterial CO2 tension of the nerve block group also was significantly smaller than that of the narcotic group. The study suggests that intercostal nerve block for post-thoracotomy analgesia offers some advantage in preserving effort-dependent pulmonary function when compared with postoperative narcotic analgesia.
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PMID:Post-thoracotomy intercostal block: comparison of its effects on pulmonary function with those of intramuscular meperidine. 94 58

In this comparative study, the abdominal constriction test was used to determine analgesia in mice, and the body plethysmograph was used to study respiratory effects of nalodeine, nalorphine, naloxone, codeine, morphine and various agonist-antagonist combinations in rats. The analgesia dose-response curves for the surrogate pairs, nalodeine-nalorphine and codeine-morphine, were parallel but had significantly different slopes. Naloxone was a more potent antagonist of morphine and codeine than of nalorphine and nalodeine. In antagonizing morphine and codeine analgesia, naloxone was the most potent antagonist, nalorphine had a biphasic effect with decreasing activity at higher doses and nalodeine was not an antagonist. Moderate doses of nalorphrine depressed minute volume largely by their effect on tidal volume, but high doses stimulated respiratory rate and therefore had less effect on minute volume. Nalodeine depressed minute volume by depressing tidal volume, since all doses initially stimulated and then variably affected respiratory rate. Metabolic rate was not increased by either drug short of convulsant doses. Nalodeine depresses the ventilatory response to CO2 and weakly antagonizes the respiratory depressant actions of morphine.
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PMID:A comparative study of the analgesic and respiratory effects of N-allylnorcodeine (nalodeine), nalorphine, codeine and morphine. 94 29

The influence of phenobarbitone anesthesia on blood flow (CBF) and oxygen consumption (GMRO2) was evaluated in the rat brain, using a method that quantitatively measures CBF in mainly cortical areas. The data were compared to those obtained in animals under fentanyl citrate analgesia. Body temperature and arterial CO2 tension were maintained close to normal values in all groups. With 50 mg/kg of phenobarbitone, CBF and CMRO2 were reduced by about 20%. With 150 or 250 mg/kg, further reductions in CBF and CMRO2 were observed. At 250 mg/kg, CBF was reduced to one third, and CMRO2 to about 50% of normal. The results suggest that little further reduction in CBF or CMRO2 can be expected if the dose of phenobarbitone is increased above 250 mg/kg.
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PMID:The effect of phenobarbitone anaesthesia on blood flow and oxygen consumption in the rat brain. 106 78

The intramuscular injection of meperidine (1 mg./kg.) alone causes significant respiratory depression, and doxapram (2 mg./kg.) alone causes significant respiratory stimulation, as evidenced by their ability to shift the carbon dioxide (CO2) response curve to the right and left, respectively. When given together, the mixture of the two drugs does not cause any significant respiratory depression, as indicated by the absence of a significant shift in the CO2 response curve to the right. This mixture has possible clinical usefulness in providing postoperative analgesia without respiratory depression.
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PMID:Doxapram antagonism of meperidine-induced respiratory depression. 116 24

The respiratory effects of analgesia with nalbuphine were studied in 9 patients after thoracotomy. The pain score was measured by a visual analogue scale. Ventilatory pattern and occlusion pressure (P0.1) were studied during spontaneous breathing and during CO2 rebreathing, before and 0.5, 1, 2.5, 3.5 and 6 h after a 0.3-mg.kg-1 dose of intravenous nalbuphine. Compared to baseline values obtained before the injection, nalbuphine produced a decrease in the pain score (p < 0.001) during the 6-hour experiment period. In spontaneous breathing, P.01 was reduced by 15% in 1 h and remained decreased during 3.5 h (p < 0.05), whilst PaCO2 and ventilation (VE) remained unchanged. The P0.1 responsiveness to CO2 was decreased from 0.5 to 2.5 h after the nalbuphine injection (p < 0.05), but the VE responsiveness to CO2 was reduced only after 1 h (p < 0.01). This study shows that, while post-thoracotomy pain was reduced by analgesia, neuromuscular inspiratory drive and chemosensitivity to CO2 were weakened, without any change in spontaneous ventilation. A partial improvement in the thoracopulmonary mechanics induced by the reduction in chest pain could explain the maintenance of ventilatory level in spite of a decreased neuromuscular inspiratory drive.
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PMID:Nalbuphine analgesia preserves ventilation after thoracotomy despite a reduction in inspiratory drive. 143 27


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