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)

Analgesic poisoning is a common medical emergency, and these drugs account for about 30% of self-poisoning in adults. Aspirin and paracetamol are taken most often, and can cause significant morbidity and mortality. However, problems with the hepatotoxicity of paracetamol have been greatly reduced by the introduction of effective treatment with agents such as N-acetylcysteine. The non-steroidal anti-inflammatory analgesics are not commonly taken in overdosage but the incidence of self-poisoning with mefenamic acid is increasing at an alarming rate. With the exception of phenylbutazone and mefenamic acid these drugs rarely seem to cause serious toxicity. The narcotic analgesics can cause profound respiratory depression and are the most dangerous drugs in overdosage.
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PMID:Clinical features and management of analgesic poisoning. 614 6

The neuromuscular effects of atracurium were studied in 25 A.S.A. class I or II patients anesthetized by a N2O-O2 narcotic technique. In five patients incremental doses of 0.05 to 0.1 mg/kg of atracurium were given intravenously every 3 minutes until approximately 95% depression of the evoked electromyographic (EMG) response of the adductor policus muscle was produced. This required 0.25 to 0.35 mg/kg of atracurium. The duration of block (return to 95% of control) was 25 to 50 minutes. In addition, four groups of five patients each received 0.15, 0.25, 0.375, or 0.6mg/kg of atracurium. The block produced by 0.15 mg/kg was 10% to 92% and lasted 8 to 55 minutes. The block produced by 0.25, 0.375, and 0.6 mg/kg was 95% or greater with a duration of action of 30 to 68 minutes, 52 to 70 minutes, and 65 to 95 minutes, respectively. Tracheal intubation was easily carried out in all patients in whom there was a block of 90% or greater. The block could be antagonized by the common clinical combination of atropine and neostigmine. Changes in heart rate and blood pressure following atracurium were less than 5%.
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PMID:Neuromuscular effects of atracurium in man. 628 67

Currently available anesthetic induction agents provide adequate hypnosis but are not ideal, particularly in the high risk patient (ASA class III-V), because most cause myocardial and/or respiratory depression and some have other important side effects. Etomidate was recently marketed as an intravenous anesthetic induction agent. It is a non-barbiturate hypnotic without analgesic properties that has less cardiovascular and respiratory depressant actions than sodium thiopental, even in patients with minimal cardiovascular reserve. Laboratory studies indicate that etomidate is approximately 25 times more potent and has a therapeutic index six times greater than sodium thiopental. In contrast to most other induction agents, etomidate does not cause histamine release. Furthermore, tolerance does not occur with repeated administration. Etomidate's rapid distribution half life (t 1/2 alpha = 2.81 +/- 1.64 min), short elimination half life 1/2 beta = 3.88 +/- 1.11 hr) and rapid clearance (954 +/- 178 ml/min) explain its rapid onset and short duration of action. The compound produces electroencephalographic changes and effects on cerebral blood flow, metabolism and intracranial pressure that are similar to sodium thiopental, suggesting that it may have a place in neurosurgery and as a "brain protective" agent in patients at risk of a brain hypoxic insult. Etomidate did not affect hepatorenal and hematologic function after repeated injections in animal toxicology studies, but few investigations addressing its effects on hepatic, renal, and neuromuscular function in man have been accomplished. The most noticeable side effects of etomidate include myoclonia, pain on injection and postoperative nausea and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etomidate: a new intravenous anesthetic induction agent. 635 80

Sodium arachidonate (AA, 1.5 mg/kg) was injected into the coronary arteries in 16 rabbits. Arrhythmia, marked ST-T depression and apnea appeared in all cases, and 7 cases died within 10 min after the AA. Before the injection, the thromboxane B2 (TXB2) value was 1.2 +/- 0.2 ng/ml (mean +/- SE) and the 6-keto-PGF1 alpha value was 2.1 +/- 0.4 ng/ml. Three minutes after the AA, TXB2 values were 5.0 +/- 1.1 in the surviving cases and 17.9 +/- 6.5 ng/ml in the cases which died. 6-keto-PGF1 alpha values were 47.7 +/- 4.6 in the surviving cases and 248.5 +/- 69.3 ng/ml in the cases which died. There occurred no deaths in 7 cases pretreated with aspirin (ASA) and in 11 cases pretreated with OKY-046 and 1581, which are specific inhibitors of TXA2 synthetase. TXB2 values did not change in the ASA and OKY groups after the AA injection. 6-keto-PGF1 alpha values did not change in the ASA group and increased in the OKY group after the AA injection. Histological findings of the heart showed more remarkable ischemic changes in the non-pretreated group than in the ASA and OKY groups. These results suggest a role for TXA2 in sudden death. PGI2 production was extremely enhanced, suggesting the presence of a protective mechanism against thrombogenesis in vivo.
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PMID:Sudden death induced by intracoronary platelet aggregation. 640 15

This study determined the cardiovascular effects of percutaneous radiofrequency coagulation of the Gasserian ganglion, performed under neuroleptanalgesia and intermittent ultrashort-acting barbiturate anaesthesia. Twelve ASA physical status class II patients were studied. Highly significant increases in mean heart rate and arterial blood pressure followed the insertion of the cannula electrode into the Gasserian ganglion (p less than 0.001). In six randomly assigned patients severe tachycardia and hypertension also accompanied the progress of the thermal lesion (p less than 0.0001). Three patients developed premature ventricular contractions, and two developed significant ST segment depression. Intravenous nitroglycerin, used during current generation, successfully controlled the hypertensive response in the other six patients. In percutaneous thermocoagulation of the Gasserian ganglion the patient's co-operation is essential. In addition to providing suitable operating conditions for both surgeons and patient, we should also be able to maintain normal and stable cardiovascular haemodynamics. Intravenous nitroglycerin used as an adjunct to light general anaesthesia safely maintained intraoperative normotension. It is also suggested that patients with coronary artery disease be adequately monitored and protected during the procedure.
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PMID:Anaesthetic considerations in percutaneous radiofrequency coagulation of the Gasserian ganglion. 642 54

The role of natural killer (NK) cells in vivo remains uncertain, but they have been implicated in a number of protective and aggressive host responses. We have found the NK activity of most patients with rheumatoid arthritis (RA) to be significantly depressed below the values for a control healthy population. This depression is not related to the use of myochrysine, methotrexate or penicillamine. Auranofin, which has a stimulatory effect in vitro, seemed in vivo to cause a further depression. ASA and indomethacin, when given to normal subjects, stimulated NK activity. The reduced NK activities seen in patients with RA taking these and other non-steroidal anti-inflammatory agents remains unexplained.
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PMID:The activity of natural killer cells in patients with rheumatoid arthritis: I. The effect of drugs used in vivo. 644 25

In 60 ASA class I or II patients given intravenous fentanyl for elective operations in doses large enough to produce postoperative respiratory depression, the intravenous administration of 20 mg nalbuphine resulted in prompt reversal of respiratory depression without loss of analgesia.
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PMID:Reversal by nalbuphine of respiratory depression caused by fentanyl. 646 75

Thromboxane A2 (TxA2) may aggravate myocardial ischemia by inducing vasoconstriction and platelet aggregation in small coronary vessels, whereas prostacyclin (PGI2) counteracts these effects. Acetylsalicylic acid (ASA) inhibits the formation of TxA2 as well as PGI2, whereas dazoxiben, a thromboxane synthetase inhibitor, reduces TxA2 formation selectively. In 25 patients with coronary artery disease, 2 identical atrial pacing stress tests were performed: before and after the administration of dazoxiben (200 mg) in 15 patients and before and after ASA (250 mg) in 10. The ischemic response, quantified by coronary sinus and aortic lactate levels and by ST depression, was significantly reduced after administration of dazoxiben (p less than 0.02) but not after ASA. Heart rate at rest, myocardial extraction of free fatty acids and the arteriovenous oxygen difference was unaffected by medication. Both drugs reduced TxB2 levels to the same extent, whereas collagen-induced aggregation was more reduced after ASA than after dazoxiben. The effect of dazoxiben on ischemia was probably a result of inhibited TxA2 and preserved PGI2 production, which increased blood flow to ischemic regions.
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PMID:Effects of a selective thromboxane synthetase inhibitor, dazoxiben, and of acetylsalicylic acid on myocardial ischemia in patients with coronary artery disease. 653 40

Spontaneous contractions and those elicited by two different methods of electrical stimulation were studied in isolated segments of bovine mesenteric lymphatic vessels. The effect of aspirin (a cyclo-oxygenase inhibitor) on spontaneous and evoked contractions of isolated lymphatic vessels was investigated. Aspirin at doses of 10(-6) M or greater depressed both spontaneous and action potential-dependent evoked contractions, but failed to inhibit contractions evoked by high current field stimulation. These latter contractions were rapidly depressed by the application of D600. When aspirin was applied for five minute periods, inhibition never occurred within the period of drug administration but was delayed, with maximum inhibition occurring approximately 10 min after washout of the drug. It is concluded that the inhibitory action of aspirin is unlikely to be a non-specific depression of the contractile mechanism, but rather a reduction in excitability probably as a result of cyclo-oxygenase inhibition.
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PMID:The inhibitory effect of aspirin on lymphatic contractility. 673 66

Several recent studies with different anesthetic agents have reported increases in plasma norepinephrine concentration during induction. To determine if induction with intravenous injection of thiopental also is associated with initial sympathetic activation, 24 ASA class I patients were assigned randomly to receive one of the following anesthetics: Group I, thiopental 3 mg/kg, iv, followed by inhalation of 100% oxygen and a continuous intravenous infusion of thiopental 0.2-0.3 mg X kg-1 X min-1; Group II, thiopental 3 mg/kg followed by inhalation of halothane (1.5% end-tidal concentration) in oxygen; and Group III, thiopental 3 mg/kg followed by inhalation of 70% nitrous oxide in oxygen. After thiopental injection, ventilation was controlled to maintain PCO2 near control levels. In Group I, plasma norepinephrine concentration decreased with continued administration of thiopental. This decrease became statistically significant (P less than 0.05) 10 min after injection. Plasma epinephrine concentration did not change. For Groups II and III, both plasma norepinephrine and epinephrine concentration did not change. For Groups II and III, the stability of the catecholamine concentrations during induction may have been caused by the circumvention of the second stage of anesthesia, equal depression of both inhibitory and excitatory synapses, or the combined effects of the agents. Regardless of the cause, the use of a modest induction dose of thiopental appears to allow the induction of anesthesia without sympathetic activation. When it is important to prevent sympathetic activation, administering a modest dose of thiopental before the inhalation of halothane or nitrous oxide may be preferable to inducing anesthesia with inhalation agents or narcotics alone.
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PMID:Effect of thiopental induction on sympathetic activity. 685 7


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