Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

d-Tubocurarine (dTc) was infused intravenously into 35 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch height of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean infusion rates that produced 90 per cent depression were not significantly altered by respiratory acid-base changes. Metabolic alkalosis decreased (32.5 per cent) and metabolic acidosis increased (27.7 per cent) the required infusion rate of dTc. When pH and Paco2 were maintained at 7.37 and 38 torr, respectively, the addition of a bolus of neostigmine, 10.5 mug/kg, intravenously, to the continuing infusion of dTc produced 50 per cent antagonism of the dTc-depressed twitch. Respiratory alkalosis and metabolic acidosis did not alter the dose of neostigmine needed to produce 50 per cent antagonism. However, during respiratory acidosis (pH 7.13, Paco2 66 torr) and metabolic alkalosis (pH 7.59, Paco2 36 torr) 20.0 and 18.0 mug/kg neostigmine, respectively, were needed to produce 50 per cent antagonism. Still larger doses of neostigmine (75 mug/kg) could not completely antagonize the block unless pH and Paco2 were returned to 7.30-7.50 and 35-45 torr, respectively. It is concluded that respiratory acidosis and metabolic alkalosis limit and oppose antagonism of dTc by neostigmine.
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PMID:The effect of acid-base balance on neostigmine antagonism of d-tubocurarine-induced neuromuscular blockade. 23 27

A case of cardiac arrest is presented which was caused by improper connection of a modified Mapleson D circuit (Bain breathing circuit). Excessive enternal deadspace was created by interchanging the gas inflow line and the attachment for an airway pressure manometer. This resulted in a marked respiratory acidosis, clinically undetected until the concomitant hypoxia produced a severe cardiac depression and arrest. The sequence of events was reproduced in a dog under comparable anaesthetic conditions. In order to avoid this error it is recommended to permanently fuse the connecting piece placed in the circuit with the tubing leading to the airway pressure manometer of the respirator.
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PMID:A hazard associated with improper connection of the Bain breathing circuit. 23 10

Respiratory function and acid-base variables were studied in Welsh Mountain ponies before and at predetermined times after the intravenous injection of Immobilon and Revivon.A marked depression of respiratory rate was accompanied by large reductions in arterial blood oxygen tension and saturation and the development of a mild respiratory acidosis following the injection of Immobilon. It was concluded that at least three factors contributed to the hypoxic hypoxia produced by Immobilon; the posture of lateral recumbency, the decrease in respiratory rate and the laboured character of the respiration. Arterial oxygen and carbon dioxide tensions returned towards control levels soon after administering Revivon. Mixed venous oxygen tensions were little affected by either Immobilon or Revivon, and mixed venous carbon dioxide tensions were increased to smaller degrees that those of arterial blood. Haemoglobin was increased initially by Immobilon, had returned to the control level by 30 min and fell below the control following the administration of Revivon.
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PMID:Influence of the neuroleptanalgesic combination of etorphine and acepromazine on the horse: blood gases and acid-base balance. 23 46

In 40 cases anesthetized with chloralose and urethane, pancuronium was infused i.v. at a constant rate to produce and maintain 90% depression twitch tension of the anterior tibialis muscle following supramaximal stimulation of the peroneal nerve. Neither respiratory alkalosis nor metabolic acidosis influenced the infusion rate required to produce 90% depression of twitch tension or antagonism of this depression yb neotigmine. Respiratory acidosis (pH 7.15; PaCO2 10 kPa) did not alter the required infusion rate but did prevent complete antagonism by neostigmine. Metabolic alkalosis (pH 7.65; PaCO2 4.8 kPa) reduced both the required infusion rate and prevented complete restoration of twitch tension by neostigmine. The duration of neostigmine antagonism was shortened by metabolic alkalosis. We conclude that respiratory acidosis and metabolic alkalosis prevent antagonism of pancuronium by neostigmine.
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PMID:Acid-base balance and neostigmine antagonism of pancuronium neuromuscular blockade. 65 47

The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.
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PMID:Respiratory influence on the total and regional cerebral blood flow responses to intracranial hypertension. 84 90

Six pregnant sheep were chronically prepared with indwelling catheters in maternal and foetal vessels and a flow probe around a maternal uterine artery. They were anaesthetized the following day with thiopentone and nitrous oxide (70 per cent)--oxygen (30 per cent) maintenance with tracheal intubation. Maternal uterine blood flow fell about 20 per cent following induction of anaesthesia. This resulted from uterine vasoconstriction which, in turn, probably resulted from maternal catecholamine release during light anaesthesia. The foetus in utero developed a mixed metabolic and respiratory acidosis and a fall in oxygen saturation. The possibility that light maternal anaesthesia increases rather than decreases neonatal depression is discussed.
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PMID:Foetal deterioration following thiopentone-nitrous oxide anaesthesia in the pregnant ewe. 87 39

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.
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PMID:An analysis of changes in blood pH following exhausting activity in the starry flounder, Platichthys stellatus. 90 8

Fifty healthy mothers, with normal placental function, were anaesthetised with ketamine (2 mg/kg body mass) for Caesarean section. Surgery was conducted with the patient in the lateral tilt position and anaesthesia was maintained with nitrous oxide, oxygen, muscle relaxants and controlled ventilation. Eight of the 50 infants delivered were clinically depressed, judged on the basis of the modified Apgar score at 2 minutes after delivery. The average time to sustained respiration was 58, 1 minutes. Studies of maternal blood gases before induction and at delivery revealed mild respiratory alkalosis, associated with an appropriate degree of compensatory metabolic acidosis. Umbilical cord blood gas analysis showed the presence of a fetal respiratory acidosis. The average derived fetal base excess levels were similar to those obtained in a previous study with thiopentone anaesthesia, but calculated mean maternal-to-fetal pH and base excess gradients were slightly greater in the present study. Prolonged induction-to-delivery intervals were associated with an increase in maternal metabolic and fetal respiratory acidosis. Slow delivery of the infant after invasion of the uterus magnified the degree of fetal metabolic acidosis, and widened the maternal-to-fetal acid-base gradients. Convincing evidence of maternal awareness during surgery was not obtained in this study. Five patients had hallucinations in the immediate postanaesthetic period. Unpleasant dreams were reported by 10% of patients. Delirium on emergence from anesthesia was not encountered. In this study, ketamine appeared to maintain fetoplacental exchange adequately, but may have been responsible for some degree of drug-induced neonatal depression. It is suggested that ketamine should be re-evaluated, using a lower dosage schedule, for Caesarean section.
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PMID:Ketamine for anaesthetic induction at Caesarean section. 93 71

Intracranial hypertension and brain hydration were scrutinized during acute ethanolism for consideration in the combined head injury setting. Intraventricular pressures and whole brain water levels rose with moderate or high ethanol dosages. The most prominent alterations were associated with respiratory acidosis and hypoxia; less marked changes were found in their absence and point to a second mechanism. Elevated central venous pressures appeared as well in some instances to constitute a third action. It is accordingly suggested that ethanol may add significantly to the combined pathology with associated acute head injury in several ways. These include: contributions to edema formation, to respiratory depression, and to alterations in local hemodyamics.
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PMID:Changes in intracranial pressure and brain hydration during acute ethanolism. 123 77

Sixty-five patients with myocardial infarction were observed for comparison of the values of nalorphine and Micoren in prevention of respiratory depression caused by fentanyl. The patients were divided into 4 groups receiving NLA II with or without nalorphine, morphine or Micoren. In all cases paO2, paCO2 and acid-base equilibrium were determined before and after administration of drugs. In the group receiving only NLA II paO2 fell in 50% of cases, in other groups receiving nalorphine or Micoren it increased in most cases. The paCO2 increased in most cases in groups receiving only NLA II or NLA II with nalorphine with or without morphine and respiratory acidosis developed in 4 cases. In the group receiving NLA II with Micoren paCO2 fell. The results indicate the necessity of administration of respiratory stimulants with NLA II and Micoren appears to be preferable to nalorphine in this respect.
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PMID:The effects of nalorphine and Micoren on blood oxygenation and acid-base equilibrium in patients with myocardial infarction treated with neuroleptanalgesia II. 124 37


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