Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Suxamethonium increases neuromuscular block produced by non-depolarizing agents administered subsequently. To determine if this effect has a pharmacokinetic or pharmacodynamic origin, 18 ASA physical status I or II adults received atracurium 0.2 mg kg-1, with (n = 10) or without (n = 8) previous injection of suxamethonium 1 mg kg-1, during a thiopentone-nitrous oxide-isoflurane (0.5% end-tidal) anaesthetic. Arterial blood samples were obtained and plasma atracurium concentration measured by HPLC. Train-of-four stimulation was applied to the ulnar nerve and the force of contraction of the adductor pollicis muscle was recorded. Mean (SEM) volume of distribution was slightly greater with previous suxamethonium (143 (13) ml kg-1) than without (109 (5) ml kg-1) (P less than 0.04). Mean elimination half-life was unaffected (20.3 (0.8) min and 20.4 (1.6) min, respectively). Neuromuscular block was more intense and recovery was slower with previous administration of suxamethonium. Atracurium concentration at 50% block (Cpss50) was 305 (30) ng ml-1 with and 454 (25) ng ml-1 without previous suxamethonium (P less than 0.01). It is concluded that suxamethonium may be associated with a slight increase in the volume of distribution of atracurium, but this effect is more than compensated by a decrease in atracurium concentration required for a given effect.
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PMID:Pharmacokinetics and pharmacodynamics of atracurium with and without previous suxamethonium administration. 193 14

Fibreoptic orotracheal intubation was compared with orthodox laryngoscopy and tracheal intubation using a total i.v. technique with propofol in 60 ASA I and II patients. There was no significant difference between the two techniques in haemodynamic profile (before, during and following the intubation procedure) and incidence of postoperative sore throat. Minimal oxygen saturation was 96% during the study; maximal end-tidal PCO2 after intubation was 5.4 kPa. Intubation time was faster (P less than 0.01) in the orthodox group (30.7 (SEM 2.3) s) than in the fibreoptic group (52.7 (4.8) s).
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PMID:Comparison of orthodox with fibreoptic orotracheal intubation under total i.v. anaesthesia. 203 22

Forty-three ASA physical status I and II patients, scheduled for elective urologic surgery, were randomly entered into a randomized double-blind study using 20 ml bupivacaine 0.75% or 20 ml ropivacaine 0.75%, both with 5 micrograms/ml epinephrine. Two patients were excluded from evaluation of efficacy due to technical failure. After a test dose of 3 ml bupivacaine 0.75% with epinephrine or ropivacaine 0.75% with epinephrine, 17 ml of either solution was given in incremental doses over 4 minutes (4, 4, 4, and 5 ml). Analgesia was satisfactory for surgery in all patients except for one in each group. The onset time of analgesia was short: after administration of ropivacaine and bupivacaine, the T12 dermatome was blocked within 6-8 minutes. Mean maximum upper level of analgesia was similar in the groups--T8 +/- 0.6 and T7 +/- 0.6 (mean +/- SEM)--for ropivacaine and bupivacaine, respectively. Duration of analgesia at the T10 level was 190 +/- 12 minutes in the ropivacaine group and 234 +/- 20 minutes in the bupivacaine group and was significantly shorter for ropivacaine at T10, L2, and S5 segments. Frequency of complete motor block was significantly lower in the ropivacaine group (7/21) than in the bupivacaine group (16/20). No differences were found in onset to various degrees of motor block, however, the duration of degree 1 motor block was significantly shorter in the ropivacaine group. Hypotension and bradycardia requiring treatment were experienced by seven and three patients, respectively, in the bupivacaine group, and by two and one patient, respectively, in the ropivacaine group. No postoperative adverse events related to anesthesia were observed. Ropivacaine 0.75% with epinephrine is an effective long-acting local anesthetic. Duration of sensory block is similar to that of bupivacaine 0.75% with epinephrine; however, the motor block is less profound and of shorter duration.
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PMID:Comparison of 0.75% ropivacaine with epinephrine and 0.75% bupivacaine with epinephrine in lumbar epidural anesthesia. 207 86

The purpose of this study is to clarify fetal cardiovascular effects of four popular analgesics administered to a maternal animal model. Clinical doses of aspirin (14 mg/kg), acetaminophen (14 mg/kg), ibuprofen (6 mg/kg), or indomethacin (0.7 mg/kg) were administered orally to near-term rats. At 1, 4, 8, or 24 hours later fetuses were delivered by cesarean section, and were fixed immediately by the whole-body freezing technique. The ductus diameter, pericardial effusion, and volume and mass of the ventricles were studied by photographing multiple planes of the heart. Fetal ductal constriction was most remarkable with ibuprofen, with the diameter decreased 70% +/- 5% (mean +/- SEM) at 1 to 8 hours. Both ventricles were dilated 60% +/- 27%, and pericardial fluid was increased 120% +/- 20%. These changes partly disappeared at 24 hours. Milder but more persistent effects were observed with indomethacin. The fetal ductus was constricted 30% at 4 to 24 hours. Pericardial fluid was increased 140% +/- 30% at 24 hours. Aspirin and acetaminophen constricted the fetal ductus 10%. In conclusion, clinical doses of ibuprofen and indomethacin constricted the fetal rat ductus and caused cardiac failure. The effects of aspirin and acetaminophen were much milder.
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PMID:Transplacental cardiovascular effects of four popular analgesics in rats. 214 Feb 40

The mechanism by which treatment with thrombolytic agents causes bleeding is not known. Recently, frequency of bleeding events has been shown to correlate with bleeding time, particularly in individuals treated with aspirin. We examined the effects of streptokinase (20,000-60,000 IU/kg) on bleeding time in 40 rabbits pretreated with aspirin, a model for fibrinolytic therapy. We then tested the effects of 1-desamino-8-D-arginine vasopressin (DDAVP) (0.3 microgram/kg), an agent known to reduce bleeding time in a variety of bleeding disorders, in 20 rabbits and compared the results with those of a control group of rabbits receiving normal saline placebo. Aspirin increased the bleeding time from a baseline mean +/- SEM value of 119 +/- 15 to 191 +/- 34 seconds in the control group and from 114 +/- 6 to 188 +/- 18 seconds in the experimental group. The addition of streptokinase increased the bleeding time to 592 +/- 119 seconds in the control group and 810 +/- 114 seconds in the experimental group (p = NS). Subsequent infusion of DDAVP decreased the bleeding time in the experimental group to 302 +/- 29 seconds (p less than 0.01 versus streptokinase) compared with 572 +/- 79 seconds (p = NS versus streptokinase) in the control animals given saline placebo. In a subset of rabbits receiving aspirin and streptokinase (40,000-60,000 IU/kg), samples were obtained for platelet aggregation (n = 16), von Willebrand factor antigen concentration (n = 17), and von Willebrand factor multimer distribution (n = 14). Maximal rates of ADP-induced platelet aggregation were not affected by DDAVP infusion, nor was the plasma concentration of von Willebrand factor antigen, quantified by an immunoradiometric assay, significantly affected by DDAVP infusion. Furthermore, the von Willebrand factor multimer ratio decreased with DDAVP administration. These findings indicate that aspirin and streptokinase combined result in a marked increase in bleeding time that can be reduced by DDAVP. This effect of DDAVP is not accompanied by an increase in platelet aggregation response, plasma von Willebrand factor antigen concentration, or von Willebrand factor multimer ratio.
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PMID:Bleeding time prolongation with streptokinase and its reduction with 1-desamino-8-D-arginine vasopressin. 224 38

To compare the disposition of 5-aminosalicylic acid (5-ASA) and its acetylated metabolite during treatment with olsalazine and mesalazine, 14 patients with inactive ulcerative colitis were randomly assigned to olsalazine (1 g twice daily) and the mesalazines, Asacol (800 + 400 + 800 mg daily), Pentasa (750 + 500 + 750 mg daily), and Salofalk (750 + 500 + 750 mg daily) in a crossover design trial so that all received each drug for seven days. Intraluminal colonic concentrations of 5-ASA were estimated after five days by the method of equilibrium in vivo dialysis of faeces. A predose serum sample and a 24 hour urine collection were obtained on day seven. The 5-ASA and acetyl-5-aminosalicylic acid (Ac-5-ASA) values were determined by high performance liquid chromatography. Olsalazine almost doubled the colonic concentrations (mean 23.7 (SEM) (1.9) mmol/l) of its therapeutically active ingredient (5-ASA) compared with equimolar doses of Pentasa (12.6 (2.2) mmol/l; p less than 0.0003) and Salofalk (15.0 (2.0) mmol/l; p less than 0.003). At the same time, olsalazine treatment was associated with lower serum concentrations and urinary excretions (p less than 0.05) of 5-ASA and Ac-5-ASA compared with the mesalazine preparations. The low systemic load of 5-ASA provided by olsalazine reduces the potential risk of nephrotoxicity during long term treatment.
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PMID:Disposition of 5-aminosalicylic acid by olsalazine and three mesalazine preparations in patients with ulcerative colitis: comparison of intraluminal colonic concentrations, serum values, and urinary excretion. 225 12

The effect of pretreatment with fentanyl on the pharmacokinetics of a single bolus of propofol was studied in 17 female patients (mean age 35 yr), ASA grade I. Eight patients received fentanyl 1.5 micrograms kg-1 5 min before induction of anaesthesia. In all patients anaesthesia was induced with propofol 2.5 mg kg-1 and maintained with halothane and nitrous oxide in oxygen. Pretreatment with fentanyl resulted in prolonged apnoea in all eight patients compared with three of nine patients in the control group. The pharmacokinetic values for propofol were described by a three-compartment mammillary model with rapid distribution phases (T1/2 alpha mean (SEM) 3.1 (2.0) min and T1/2 beta 44 (9.1) min) and a slower final phase of T1/2 gamma 520 (96) min. The clearance of propofol was rapid (mean 1.6 (0.24) litre min-1). Propofol was distributed initially into a relatively large central compartment (mean 23.7 (6.6) litre) and was extensively redistributed (mean Vss 593 (157) litre). There was no difference in the pharmacokinetic profile of propofol between the two groups.
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PMID:Pharmacokinetic interaction of propofol and fentanyl: single bolus injection study. 226 45

To determine the influence of enflurane on the ability of edrophonium to antagonize atracurium block, dose-response curves were constructed for edrophonium in the presence of 0%, 1% and 2% enflurane, and for 2% enflurane discontinued at the time of administration of edrophonium. One hundred ASA Physical Status I or II patients (four groups of 25), selected randomly and undergoing elective surgery, received atracurium 0.5 mg kg-1, with thiopentone, nitrous oxide and enflurane. Supplementary doses of fentanyl were given if needed. Train-of-four (TOF) stimulation was applied every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When first twitch height (T1) had recovered spontaneously to 10% of initial value, edrophonium 0.1, 0.2, 0.4 or 1 mg kg-1 was administered by random allocation. Enflurane concentrations remained constant, except that enflurane was discontinued in 50% of the patients who had received 2% enflurane. Monitoring was continued for at least 10 min, at which time T1 and TOF ratio (T4/T1) were measured. The ED80 for T1 recovery depended on the dose of enflurane: 0.08 (SEM 0.03), 0.21 (0.06) and 0.42 (0.18) mg kg-1 for 0%, 1% and 2% enflurane, respectively (P less than 0.005). With enflurane 2% discontinued, the ED80 was 0.095 (0.050) mg kg-1 (P less than 0.02 compared with 2% enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Edrophonium antagonism of atracurium during enflurane anaesthesia. 232 78

The effects of propofol, nitrous oxide, and/or isoflurane on efferent activity of sympathetic muscle nerve fibers (MSA) were studied using percutaneous microneurographic recordings from the peroneal nerve. Eight ASA Physical Status 1 patients (30-70 yr of age) scheduled for otorhinolaryngeal surgery entered the study. The effects of propofol (2-2.5 mg.kg-1.min-1) induction, tracheal intubation, and maintenance of anesthesia with isoflurane (0.3%, 0.6%, and 1.2% end-tidal concentrations) and/or 70% nitrous oxide were studied with respect to MSA, arterial blood pressure, heart rate, and indices of skin blood flow (laser doppler photometry and finger pulse plethysmography). Induction of anesthesia with propofol decreased MSA to 34 +/- 2% (mean +/- SEM) (P less than 0.05), and subsequent tracheal intubation increased MSA rapidly to 151 +/- 23% (P less than 0.05) of the control level. Isoflurane administration both with and without nitrous oxide led to a decrease of MSA (P less than 0.05). However, during nitrous oxide/isoflurane anesthesia (1.0 MAC) MSA was 76 +/- 38% higher than when isoflurane was used alone, although this implied a decrease in anesthetic depth to 0.5 MAC. This indicates that nitrous oxide and isoflurane have opposite effects on sympathetic outflow. During undisturbed propofol, nitrous oxide, and/or isoflurane administration (up to 1.0 MAC), MSA retained its normal pulse synchronous pattern, indicating that modulation of sympathetic outflow from arterial baroreceptors was still present. Skin blood flow increased sevenfold to tenfold in association with propofol induction (P less than 0.05) and was maintained at an 11- to 19-fold increase during nitrous oxide and/or isoflurane anesthesia, without any difference between the two anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous recording of muscle nerve sympathetic activity during propofol, nitrous oxide, and isoflurane anesthesia in humans. 236 Jul 36

Subparalyzing doses of d-tubocurarine (dTC) given before succinylcholine decrease the duration of neuromuscular blockade. In animal preparations, they also abolish succinylcholine-induced twitch augmentation, defined as a greater-than-maximal contraction in response to a single stimulus. To determine quantitatively the effect of dTC on succinylcholine potency and on twitch augmentation in humans, 60 adult patients, ASA physical status I or II, were assigned randomly to receive either 0.05 mg/kg of dTC or saline 2 min before induction of anesthesia with fentanyl and thiopental. Train-of-four stimulation was applied every 12 s to the ulnar nerve and the force of contraction of the adductor pollicis muscle was measured. One minute after induction of anesthesia, 0.15, 0.20, 0.25, 0.35, or 0.50 mg/kg of succinylcholine was given. The height of the first twitch (T1) reached 121% +/- 6% (mean +/- SEM) of control without dTC, and was virtually abolished by dTC pretreatment (105% +/- 1%, P less than 0.01). Twitch augmentation was more noticeable with lower doses of succinylcholine, and was not observed in the response to the fourth stimulus of the train of four (T4). The potency of succinylcholine was decreased by approximately one-half in the dTC-pretreated groups. The ED50 was 0.27 +/- 0.04 mg/kg without dTC and 0.50 +/- 0.06 mg/kg with dTC (P less than 0.002). The corresponding values for ED90 were 0.51 +/- 0.07 and 1.02 +/- 0.12 mg/kg, respectively (P less than 0.02). The ED95 values were 0.63 +/- 0.09 and 1.28 +/- 0.15 mg/kg, respectively (P less than 0.02). The slopes of the regression lines did not deviate significantly from parallelism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of d-tubocurarine pretreatment on succinylcholine twitch augmentation and neuromuscular blockade. 236 29


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