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)

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

Concentrations of meperidine and its active metabolite, normeperidine, were measured in plasma of patients receiving the drug for analgesia. Meperidine levels in cancer patients were 0.10 to 0.55 microng/ml 1 h after a dose and were 0.05 to 0.14 in patients in the oliguric period after renal transplantation. Normeperidine levels were 0.05 to 0.28 microng/ml in the cancer patients and 0.13 to 0.36 in the renal failure patients. The ratio of normeperidine to meperidine levels was always higher in the renal failure patients than in the cancer patients. Additionally, two patients receiving multiple doses of meperidine had high normeperidine levels and very high normeperidine/meperidine ratios when they showed signs of central nervous system excitation. These data indicate that normeperidine can contribute to the excitatory effects seen after multiple doses of meperidine and suggest that patients with renal failure are particularly susceptible to this problem.
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PMID:Accumulation of normeperidine, an active metabolite of meperidine, in patients with renal failure of cancer. 86 53

Acute tubulo-interstitial nephritis was diagnosed post mortem when a dog died four days after surgery for a femoral head resection. Possible causative factors associated with halothane anaesthesia, flunixin meglumine analgesia and prophylactic antibiotic therapy with trimethoprim-sulphadiazine are discussed. It is concluded that death was due to renal failure associated with tubulo-interstitial nephritis as a result of a combination of ischaemic and toxic events.
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PMID:Acute tubulo-interstitial nephritis in a dog after halothane anaesthesia and administration of flunixin meglumine and trimethoprim-sulphadiazine. 146 25

Seventeen cynomolgus monkeys under N2O analgesia and sedation were subjected to severe volume-controlled hemorrhagic shock (shed blood volume of 21 or 27 ml/kg). In 12 monkeys, resuscitation was started after increasing periods of hemorrhagic shock from 30 min to 5 h. In five additional monkeys, volume-controlled hemorrhage was modified at hemorrhagic shock 30 min to control MAP at 30 mmHg: resuscitation was started at hemorrhagic shock of 2 h. A clinically relevant resuscitation protocol consisted of a field phase from 0 to 6 h (lactated Ringer's solution, spontaneous breathing), and a hospital intensive care phase from 6 h to 48 h (blood, lactated Ringer's solution to mean arterial pressure (MAP) greater than or equal to 70 mmHg, controlled ventilation, advanced life support). Fifteen of the 17 monkeys survived. After outcome evaluation at 4 or 7 days, the eight monkeys with "moderate insult" had only transient functional impairment. Of the nine with "severe insult," three showed signs of moderate transient non-oliguric renal failure. Eight of the 12 monkeys studied morphologically showed scattered liver cell damage. None of the monkeys developed pulmonary dysfunction or functional or morphologic evidence of cerebral damage. This study establishes a new hemorrhagic shock-resuscitation model simulating field-to-hospital life support. Severe hemorrhagic shock with MAP 30-40 mmHg for 90-120 min (without trauma or sepsis) can lead to complete functional recovery after transient malfunction of liver and kidneys.
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PMID:Monkey model of severe volume-controlled hemorrhagic shock with resuscitation to outcome. 165 92

The effectiveness of intravenous administration (i.v.) of L-tryptophan, which is the precursor of cerebral serotonin, was verified in the treatment of postoperative pain. The study was carried out on 45 female patients, aged between 34 and 61 years, undergoing cholecystectomy who were randomly divided into three groups. Group 1 (age: 50.33 +/- 8.64 years) received 100 ml of 5% mannitol solution i.v.; group 2 (age: 49.80 +/- 11.11 years) 100 ml of a mannitol solution containing 7.5 mg/kg L-tryptophan; and group 3 (age: 53.46 +/- 9.60 years) 100 ml of a mannitol solution containing 15 mg/kg L-tryptophan. Vital capacity (preoperative VC) was measured before surgery. Anesthesia used was isoflurane. Narcotics or neuroleptics were not used. Pain was assessed before treatment (T-0 min), at the end of administration (T-30) and at T-60, 120, 180, 240, 300 and 360 min by the following variables: respiratory rate (RR), heart rate (HR), mean arterial pressure (MAP), Scott-Huskisson test (VAS), pain vital capacity (PVC), analgesic vital capacity (AVC), and respiratory restoration factor (RRF) calculated from Bromage's formula (RRF = (AVC - PVC/preoperative VC - PVC) X 100). As regards variables RR, HR, MAP and VAS, differences between the values from T-30 to T-360 and the value at T-0 were calculated. Means and S.E.M. were calculated on the obtained values and on RRF values for each group. The significance of the differences between groups was calculated using Student's t test and Bonferroni's test. Results show a significant decrease of pain in groups 2 and 3 treated with L-tryptophan, in comparison with group 1 (controls). No significant difference was observed between the treated groups, although more lasting pain relief was observed in group 3 in comparison with group 2. Intravenous L-tryptophan showed its effectiveness in the treatment of postoperative pain even when used alone. Its use may be considered for patients with renal failure, in order to strengthen pharmacological analgesia or to prevent postoperative pain by its intraoperative administration.
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PMID:Postoperative pain treated by intravenous L-tryptophan: a double-blind study versus placebo in cholecystectomized patients. 176 11

The brain uptake of a number of benzodiazepines with different lipophilic and protein binding characteristics was investigated in male Sprague-Dawley rats using the rapid intracarotid artery injection technique. When the compounds were administered as a solution in Ringer's buffer, pH 7.4, the uptake was in the order of [14C]diazepam greater than [14C]L-663,581 (anxiolytic agent) greater than [3H]L-364,718 (morphine analgesia potentiator) greater than [14C]L-365,260 (anxiolytic agent) and their extraction ratio values were 71.0 +/- 6.8, 65.0 +/- 12.0, 42.0 +/- 5.0 and 6.0 +/- 2.0%, respectively. The respective permeability-surface product values were 0.755 +/- 0.152, 0.647 +/- 0.180, 0.329 +/- 0.05 and 0.035 +/- 0.011 ml/min/g. The rank order of brain extraction did not correlate well with the drugs' lipophilicity determined by octanol-buffer partition coefficient. For example, L-365,260 had the highest octanol/buffer partition coefficient, but the lowest brain extraction. Plasma protein binding significantly decreased the uptake by the brain but to a lesser extent than that predicted from the unbound drug fraction in vitro, suggesting that drug binding to plasma protein did not limit the transport of drug through the blood-brain barrier. For one compound, L-364,718, the extraction ratio and permeability-surface product values were increased markedly in CC1(4)-induced hepatic injury. Other disease states, uranyl nitrate-induced renal failure and streptozotocin-induced diabetes, had no apparent effect on the uptake of the compounds tested. The effect of disease state on the brain uptake of drug appeared to be dependent on the type of disease and the type of drug studied.
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PMID:Effects of protein binding and experimental disease states on brain uptake of benzodiazepines in rats. 197 Mar 63

The disposition of buprenorphine has been studied in two patient groups to assess the influence of impaired renal function on the metabolism of buprenorphine and two of its metabolites, buprenorphine-3-glucuronide (B3G) and norbuprenorphine (NorB). A single i.v. dose of 0.3 mg was given to 15 patients (nine with dialysis-dependent renal failure) undergoing lower abdominal or peripheral body surface surgery. Blood was sampled up to 24 h. Concentrations of buprenorphine, B3G and NorB were assayed by a differential radioimmunoassay technique. There were no differences in buprenorphine kinetics between anaesthetized healthy patients and those with renal impairment: mean elimination half-lives 398 and 239 min; clearance 651 and 988 ml min-1; apparent volume of distribution at steady state 313 and 201 litre, respectively. Both metabolites were undetectable following the single i.v. dose. In a second group of 20 patients (eight with renal impairment), buprenorphine was administered by continuous infusion for provision of analgesia and control of ventilation in the ITU (median infusion rate 161 micrograms h-1 (range 36-230 micrograms h-1) for a median duration of 30 h (2-565 h). Buprenorphine clearance in patients with normal and impaired renal function was similar (934 and 1102 ml min-1, respectively), as were dose-corrected plasma concentrations of buprenorphine. In patients with renal failure, plasma concentrations of NorB were increased by a median of four times, and B3G concentrations by a median of 15 times.
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PMID:Buprenorphine disposition in patients with renal impairment: single and continuous dosing, with special reference to metabolites. 232 75

Two patients given methoxyflurane for analgesia over 14 and 16 days developed renal failure and died. The inhaler was withdrawn from the New Zealand market in 1984.
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PMID:Renal failure following methoxyflurane analgesia. 345 63

Patients with renal disease are at risk of further deterioration of renal function and acute tubular necrosis when subjected to anaesthesia and surgery. Optimal fluid loading and careful selection of anaesthetic techniques and agents, appropriate monitoring and the use of mannitol and dopamine assist in the maintenance of renal blood flow and help preserve renal function in these patients. In association with renal failure, physiological changes in other systems result in reduced oxygen supply to the tissues, metabolic disturbances, impairment of the coagulation and immune defence mechanisms and an increased risk of cardiac and cerebrovascular catastrophe. Although many anaesthetic techniques including regional analgesia may be used successfully in these patients caution with most drugs, especially pethidine, phenoperidine, suxamethonium and all non-depolarising neuromuscular relaxants is recommended. Of the volatile anaesthetics currently available, halothane is the agent of choice. Oxygen therapy and close monitoring of cardiorespiratory function are necessary postoperatively.
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PMID:Anaesthesia for the patient with impaired renal function. 635 49

We describe a patient with membranoproliferative glomerulonephritis, renal failure, hypoalbuminemia and massive proteinuria. Attempts to reduce the protein loss with corticosteroids, indomethacin and mercurial diuretics were unsuccessful. Renal artery occlusion via Gianturco stainless steel coils was accomplished with the sole major complication of an ileus, probably caused by narcotics given for analgesia. The coils provide a convenient means of terminating renal function without resort to nephrectomy.
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PMID:Renal ablation with the Gianturco stainless steel coil for control of massive proteinuria. 732 Nov 31


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