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 (0.02 seconds)

Anesthesia induced by use of a combination of xylazine, ketamine, and halothane, under conditions of spontaneous and mechanically controlled ventilation, was evaluated in 5 llamas positioned in dorsal recumbency. Using chronically implanted catheters, systemic arterial blood pressure, pulmonary arterial pressure, right atrial pressure, heart rate and rhythm, cardiac output, blood pH and gas tensions, body temperature, and respiratory rate were measured before anesthesia induction (baseline), throughout the anesthetic period, and for 1 hour into the recovery period. During anesthesia, llamas undergoing spontaneous ventilation developed hypercapnia and respiratory acidosis. Cardiovascular function was decreased during both types of ventilation. The combination of xylazine, ketamine, and halothane in various doses and 2 ventilation procedures (spontaneous and controlled) provided a reliable method for general anesthesia in llamas, but marked cardiovascular depression developed during anesthesia maintenance with halothane. Spontaneous ventilation resulted in potentially clinically important respiratory acidosis.
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PMID:Evaluation of a combination of xylazine, ketamine, and halothane for anesthesia in llamas. 323 40

High-dose fentanyl anesthesia is widely used in cardiac surgery. Its immediate side-effects are well known. However, its late adverse effect manifested by extreme truncal rigidity, decreased chest wall compliance, hypoventilation, respiratory acidosis and hemodynamic instability is not sufficiently appreciated. Of 380 patients who underwent aortocoronary artery bypass under high-dose (100 micrograms/kg) fentanyl anesthesia, 29 (7.6%) developed the sudden onset of extreme thoracic and abdominal rigidity, leading to respiratory depression 2 to 6 h postoperative, after an apparently normal recovery from the anesthesia. In 15 patients, a high plasma level of fentanyl (5.2 to 7.8 ng/ml) correlated with the clinical events. Administration of naloxone or a muscle relaxant rapidly reversed this late complication of fentanyl, thought to be due to re-entry of fentanyl into plasma from deposits in adipose tissue, muscle and the GI tract, leading to a secondary peak in plasma fentanyl. It is more likely to be encountered when hypothermia, rewarming, and acidosis occur in the postoperative period. Awareness of this life-threatening complication is critical in patients undergoing surgery with fentanyl anesthesia.
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PMID:Delayed respiratory depression following fentanyl anesthesia for cardiac surgery. 325 27

The studies were carried out on 48 sheep, 2-6 years old, weighing 33-67 kg. The animals were divided into two groups, 24 sheep each. From these 24, 16 sheep were tested for the plasma electrolytes contents, and 8 were tested for the acid-base balance and the oxygenation level of the arterial blood. Sheep from the first group were given xylasine in the dose of 0.1-10.3 mg/kg od body weight and etomidate (1 mg/kg of body weight). Sheep from the second group were given diazepam in the dose of 0.5 mg/kg of body weight and ketamine (20 mg/kg of body weight). In the first group the surgically effective anaesthesia lasting 15-20 minutes was obtained. During the anaesthesia a respiratory depression together with the decrease of oxygen saturation of the blood was observed. Also, a respiratory insufficiency leading to a respiratory acidosis, hypokalemia, hypocalcemia, hypomagnesemia and hypochloremia of plasma were observed. In the second group of sheep treated with ketamine and diazepam the increased pulse rate, respiratory insufficiency, hypokalemia, hypocalcemia and hypophosphatemia were observed. It has been said that respiratory and blood oxygenation disorders are the result of the forced long lasting position on one side. After treating with diazepam and ketamine bigger changes were observed. Usually all these changes and disorders recessed at the end of the experiment.
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PMID:[Comparative studies of general anesthesia of sheep with ketamine and etomidate]. 326 7

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-narcotic analgesics. Problems of overdosage. 355 83

A randomized double-blind study compared the effects of equi-analgesic doses of maternally administered meptazinol (1.5 mg/kg) and pethidine (1.5 mg/kg) on neonatal acid-base status. Heel-prick samples were taken for assessment of acid-base status at 10 and 60 min after delivery. Maternal antenatal history, details of labour and neonatal status at delivery were also recorded. Meptazinol produced less neonatal respiratory depression than pethidine: the mean 10 min acid-base data from 16 infants whose mothers received pethidine were indicative of a respiratory acidosis (pH 7.13, SD 0.08, PCO2, 9.11, SD 2.2 kPa; standard bicarbonate 22.3, SD 3.1 mmol/l). This was not evident in the mean acid-base data from 16 infants whose mothers received meptazinol (pH 7.23, SD 0.07; PCO2 6.83, SD 1.6 kPa; standard bicarbonate 20.9, SD 4.2 mmol/l). The mean pH and PCO2 in the two treatment groups were significantly different (P less than 0.002) at 10 min but not at 60 min after delivery.
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PMID:A comparison of the effects of maternally administered meptazinol and pethidine on neonatal acid-base status. 356 24

Gamma-aminobutyric acid (GABA) is a putative central neurotransmitter that depresses respiratory neurons and has a metabolism in the brain that is tied to CO2 fixation and H+ metabolism. Therefore, the effect of 3 concentrations of GABA (10, 30, and 50 mM) in different groups of pentobarbital-anesthetized dogs was investigated by ventriculocisternal perfusion for 15 to 45 min. During multiple perfusion sequences, tidal volume (VT) and respiratory frequency were recorded continuously, whereas heart rate (HR), mean systemic arterial pressure (Psa), cardiac output, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure were monitored periodically. Minute ventilation decreased by a reduction in VT. The mean VT (+/- SEM) decreased after 15 min of GABA perfusion from 365.9 +/- 19.5 to 151.0 +/- 15.0 ml with 50 mM GABA in mock CSF, from 272.8 +/- 25.1 to 110.6 +/- 7.4 with 30 mM GABA, and from 223.6 +/- 22.3 to 155.3 +/- 21.8 with 10 mM GABA. A decrease in mean inspiratory flow was associated with the reduction in VT. The decrease in ventilation was associated with respiratory acidosis. At each GABA concentration, mean Psa decreased, whereas HR fell only with 50 mM. Other cardiovascular parameters did not change. Perfusion with mock CSF alone restored cardiorespiratory depression caused by GABA. Mean Psa fell with GABA whether ventilation was kept constant mechanically or not. These results support the hypothesis of a GABA-sensitive mechanism via a population of receptors that affect respiratory and cardiovascular function and are accessible by ventriculocisternal perfusion.
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PMID:Reversible depression of ventilation and cardiovascular function by ventriculocisternal perfusion with gamma-aminobutyric acid in dogs. 371 57

The effects on the respiratory function of two tranquillising drugs, lorazepam and diazepam, have been compared in 20 patients with chronic obstructive lung disease. Both drugs induce a respiratory depression (decrease in tidal volume and minute ventilation with acceleration of the respiratory frequency) with slight respiratory acidosis, but lorazepam causes no significant hypoxemia and has a shorter duration of action than diazepam. Nevertheless, if tranquillisers are indicated in such patients, they have to be used with care.
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PMID:Double-blind comparison of the respiratory effects of parenteral lorazepam and diazepam in patients with chronic obstructive lung disease. 415 89

1. The respiratory response to inhaled CO(2) was measured in twenty unanaesthetized new-born lambs aged 4 hr-10 days. Measurement of resting arterial pH, P(CO2) and plasma bicarbonate showed a non-respiratory acidosis immediately after birth which was corrected in the first 24-28 hr: thereafter, the acid-base pattern was of a compensated respiratory alkalosis.2. When CO(2) was added to the inspired gases and resting arterial oxygen tension (P(a), (O2)) was controlled, the average increase in minute ventilation (V) was 0.075 l.min(-1).kg(-1).mm Hg, P(a), (CO2) (-1) and duplicate responses in the same lamb differed by 6-22.5%.3. The slope of the V/P(a), (CO2) line (S) varied inversely with P(a), (O2). In one lamb, severe hypoxia (P(a), (O2) = 21 mm Hg) caused a marked depression of the slope.4. Neither the slope S nor the horizontal intercept B of the lines was related to the age of the lamb. B was not related to pH(a) and only slightly affected by acute hypoxia. B was related to arterial [HCO(3) (-)] and values for both were reduced with the acid-base disturbances seen in the first 10 days after birth. Evidence was given which suggested that the response of the new-born lamb to inhaled CO(2) was similar to that of man acclimatized to a P(a), (O2) of 70-75 mm Hg.5. In the lightly anaesthetized lamb, bilateral section of the sinus nerves caused a small reduction in the sensitivity to inhaled 5% CO(2) in air, an increase in the respiratory lag and a reduction in the rate at which V increased.6. It was concluded that, in the new-born lamb, the carotid chemo-receptors are involved in the response to inhaled CO(2) and that hypoxia potentiates this response.
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PMID:The respiratory response of the new-born lamb to inhaled CO-2 with and without accompanying hypoxia. 596 99

The mechanism responsible for the depressive myocardial effects of severe respiratory acidosis is unclear; however, sympathetic stimulation and catecholamines are known to be involved. The influence of beta-adrenergic receptor activity on the myocardial response to severe respiratory acidosis was studied in 18 anesthetized, mechanically ventilated dogs. Arterial CO2 tension (PaCO2) was raised by increasing the inspired CO2 fraction in O2. In control animals, as PaCO2 increased, heart rate (HR) decreased (PaCO2 approximately 110 mmHg), then returned to control (PaCO2 approximately 220 mmHg), whereas arterial blood pressure (Pa) and cardiac output (Q) remained unchanged from prehypercapnia levels. At PaCO2 greater than 350 mmHg, Pa, HR, and Q decreased and left ventricular function (LVF) curves were depressed. Death occurred at a PaCO2 of 404 +/- 25 mmHg (pH 6.48 +/- 0.02). In a second group of animals, administration of isoproterenol during the increase in PaCO2 did not result in depression of myocardial function, and death did not occur even at a significantly higher PaCO2 (PaCO2 496 +/- 12 mmHg; pH 6.39 +/- 0.02) than in the control group. Administration of propranolol to a third group of animals as PaCO2 increased did not change Pa, HR, and Q; however, LVF curves indicated a more rapid and severe depression of myocardial performance than in control, and death occurred at a significantly lower PaCO2 (PaCO2 220 +/- 25 mmHg; pH 6.65 +/- 0.02). We conclude that beta-adrenergic receptor stimulation can prevent hypercapnic heart failure and that beta-adrenergic receptor activity is involved in the mechanism responsible for this failure.
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PMID:beta-Adrenergic activity and cardiovascular response to severe respiratory acidosis. 629 89

In an isolated guinea pig atrial preparation, the bathing solution pH, PO2, and PCO2 were manipulated to mimic normal, acidotic, and hypoxic conditions. The effect of lidocaine and bupivacaine on spontaneous heart rate (HR) and contractile force (CF) was determined for 60 min under conditions of normal pH, PO2, and PCO2. Lidocaine (50 micrograms/ml) reduced HR by a maximum of 34.2 +/- 1.5% and CF by 38.9 +/- 8.1% (mean +/- SEM). Bupivacaine (5 micrograms/ml) reduced HR by a maximum of 30.1 +/- 1.9% and CF by 48.0 +/- 6.5%. Bupivacaine (10 micrograms/ml) caused a maximum HR reduction of 61.7 +/- 9.5% and CF reduction of 66.0 +/- 8.6%. Hypoxia or metabolic or respiratory acidosis did not further enhance the local anesthetic induced atrial depression. However, conditions of combined acidosis/hypoxia, while not significantly altering the HR and CF depression caused by lidocaine, did enhance bupivacaine-induced depression of HR and CF (93.6 +/- 6.3% and 95.2 +/- 4.8%, respectively). The effect of a protein-free bathing solution on the relative toxicities of lidocaine and bupivacaine is discussed.
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PMID:Influence of lidocaine and bupivacaine on isolated guinea pig atria in the presence of acidosis and hypoxia. 669 58


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