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)

Thirty-six ASA I patients received either propofol 2.25 (0.07) mg kg-1 (mean (SEM] or thiopentone 4.8 (0.18) mg kg-1, for induction of general anaesthesia together with fentanyl and a neuromuscular blocking drug. This technique was repeated in 12 ASA III patients, using propofol 1.8 (0.18) mg kg-1 or thiopentone 4.7 (0.37) mg kg-1. There was a significant decrease in systolic arterial pressure following induction of anaesthesia with both drugs; this was more pronounced after propofol, and in ASA III patients. Plasma noradrenaline concentrations increased after tracheal intubation only in the thiopentone group, but the pressor response to tracheal intubation was not attenuated by the use of propofol.
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PMID:Haemodynamic changes after induction of anaesthesia and tracheal intubation following propofol or thiopentone in patients of ASA grade I and III. 281 19

To evaluate possible interactions between residual succinylcholine and vecuronium, the amount of vecuronium required to maintain the twitch height (TH) at 10% of its initial value was measured over a 90-min period by the on-demand infusion method in two series of 15 adult patients (ASA class I-II). One group, the vecuronium treatment (V) group, received 70 micrograms X kg-1 of vecuronium and the on-demand infusion. The second group, the succinylcholine-vecuronium treatment group (SV), was given 30 micrograms X kg-1 of vecuronium and on-demand infusion 5 min after the complete recovery of TH after administration of 1 mg X kg-1 of succinylcholine. During the first 10 min, the amount of vecuronium required to maintain TH at 10% of its control was significantly greater in the group given V than in the group given SV, 15122 +/- 856 (mean +/- SEM) vs 9851 +/- 486 micrograms X m-2 X hr-1 (P less than 0.001). Thereafter, the amount of vecuronium required to maintain TH at 10% of control was similar: 2808 +/- 275 and 3068 +/- 206 micrograms X m-2 X hr-1. When the infusion of vecuronium was stopped after 90 min, the time required for spontaneous recovery from 25 to 75% of control TH levels was similar: 20.1 +/- 3.3 min in the group given V and 18.9 +/- 2.5 min in the group given SV (not significant). We conclude that after a vecuronium on-demand infusion of long duration (lasting more than 90 min), previous succinylcholine administration does not interfere with late vecuronium requirements and the spontaneous rate of recovery of TH.
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PMID:Evolution of vecuronium requirements for stable mechanical effect: comparison with or without previous succinylcholine administration. 285 68

To measure the ability of neostigmine and edrophonium to reverse moderate and profound atracurium blockade, dose-response relationships were established for these reversal agents given at 1% and 10% twitch height recovery. Eighty-five ASA I and II adult patients received atracurium, 0.4 mg/kg, during a thiopental-nitrous oxide-enflurane anesthetic. Train-of-four stimulation was applied every 12 seconds, and the force of contraction of the adductor pollicis muscle was recorded. Edrophonium, 0.1, 0.2, 0.4, or 1 mg/kg; neostigmine, 0.005, 0.01, 0.02 or 0.05 mg/kg; or no reversal agent was given when there was either 1% or 10% recovery of the first twitch response. With profound blockade, the slope of the edrophonium dose-response relationship was significantly flatter (P less than 0.05) than that of neostigmine. The dose of neostigmine required to achieve 80% first twitch recovery (ED80) after 10 minutes was 0.013 +/- 0.003 mg/kg (mean +/- SEM) if given at 10% recovery, and 0.032 +/- 0.004 mg/kg if given at 1% recovery. The ED80 for edrophonium was 0.22 +/- 0.04 mg/kg and 1.14 +/- 0.33 mg/kg, respectively. These values corresponded to neostigmine:edrophonium potency ratios of 16.6 +/- 3.5 and 35.3 +/- 8.9 at 90% and 99% blockade respectively (P less than 0.006). We conclude that the relative potency of neostigmine is greater than that of edrophonium for antagonism of profound atracurium blockade.
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PMID:Dose-response relationships for edrophonium and neostigmine as antagonists of moderate and profound atracurium blockade. 291 Jan 33

Aspirin plus dipyridamole reduces platelet accumulation on short-term Dacron vascular grafts in man. To determine whether drug inhibition of platelet deposition is sustained on older grafts, we studied 18 men aged 41 to 87 years who had Dacron aortic bifurcation grafts in place a mean of 43.4 months (range 9.8 to 121.0) before and during short-term therapy with aspirin (325 mg tid) plus dipyridamole (75 mg tid). During both the baseline and drug studies, indium-111 (111In) platelet deposition was quantitated by two techniques, standard planar imaging performed at 24, 48, and 72 hr after injection of platelets and single photon emission computed tomographic imaging performed at 24 and 72 hr after injection. All analyses were performed in a blinded fashion. On both the planar and tomographic images, platelet accumulation on the graft was quantitated by a graft/blood ratio that compared activity in the graft to simultaneously collected whole blood 111In platelet activity. Aspirin plus dipyridamole reduced the tomographic graft/blood ratio at 24 hr (20.6 +/- 3.5 vs 17.3 +/- 2.5) (+/-SEM) and at 72 hr (29.0 +/- 4.8 vs 25.0 +/- 4.1) after injection of platelets (p = .02). Dacron vascular grafts. Similarly, the planar graft/blood ratio was reduced at 24 hr (2.7 +/- 0.5 vs 2.4 +/- 0.5), 48 hr (3.7 +/- 0.9 vs 3.1 +/- 0.7), and 72 hr (4.0 +/- 0.9 vs 3.6 +/- 0.8) (p = .04). We conclude that aspirin (325 mg tid) plus dipyridamole (75 mg tid) reduces platelet accumulation on long-term Dacron vascular grafts.
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PMID:Reduction of indium-111 platelet deposition on Dacron vascular grafts in humans by aspirin plus dipyridamole. 293 27

The synergistic effect of pancuronium bromide (PCB) and d-tubocurarine (DTC) on the onset time of neuromuscular blockade was tested in 108 ASA physical status I and II adults anaesthetized with thiopentone, nitrous oxide and halothane. Either saline or a small (priming) dose (DTC, 0.04 mg X kg-1, or PCB, 0.007 mg X kg-1) was administered 3 min before a paralyzing dose of either DTC or PCB. The total dose of relaxant was equivalent to DTC, 0.4 mg X kg-1, or PCB, 0.07 mg X kg-1. Neuromuscular activity was measured using train-of-four stimulation applied every 12 s. Time to 50 per cent first twitch blockade was 63 +/- 4.6 s (mean +/- SEM) with DTC and 88 +/- 5.2 s with PCB (p less than 0.002). Times to 90 per cent blockade were not different between the two drugs (161 +/- 20 s and 141 +/- 21 s respectively). Priming a DTC blockade with either DTC or PCB or priming a PCB blockade with PCB produced an acceleration of less than 10 s at all levels of blockade. Compared with PCB alone, priming PCB blockade with DTC reduced the time to 50 per cent blockade to 71 +/- 4.5 s (p less than 0.02) and to 90 per cent blockade to 111 +/- 8 s (p less than 0.05). Priming did not affect the duration of action significantly, except in the case of PCB priming of DTC, where duration was increased from 39 +/- 4.4 to 57 +/- 4 min (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Onset of pancuronium and d-tubocurarine blockade with priming. 302

Using probit analysis, dose-response curves for induction of anesthesia with midazolam or ketamine were constructed in ASA class III and IV patients premedicated with morphine, 0.1 mg/kg, and glycopyrrolate, 4 micrograms/kg. For ketamine, ED50 values for abolition of the response to verbal commands, eyelash stimulation, and painful stimulation were 0.9, 1.3, and 1.3 mg/kg, respectively; corresponding ED95 values were 1.6, 2.3, and 4.3 mg/kg, which are within the range of clinically recommended doses. For midazolam, ED50 values for verbal commands, eyelash stimulation, and painful stimulation were 0.19, 0.24, and 0.36 mg/kg, significantly greater than those previously reported for unpremedicated ASA class I and II patients. The corresponding ED95 values, 0.35, 0.43, and 1.04 mg/kg exceed previously reported values and are appreciably greater than the doses used in most previous studies of midazolam induction. Midazolam decreased systolic blood pressure slightly but significantly (from 138 +/- 4 to 128 +/- 4 mm Hg, mean +/- SEM, P less than 0.005), while diastolic blood pressure and heart rate remained unchanged. In contrast, ketamine increased systolic blood pressure (from 141 +/- 4 to 164 +/- 5 mm Hg, P less than 0.005), diastolic blood pressure (from 71 +/- 3 to 88 +/- 4 mm Hg, P less than 0.005), and heart rate (from 84 +/- 2 to 102 +/- 4 beats/min, P less than 0.005). On the basis of these data, we conclude that in ASA class III and IV patients, midazolam induction allows for hemodynamic stability and avoids the significant tachycardia and hypertension associated with equipotent doses of ketamine.
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PMID:Induction dose-response curves for midazolam and ketamine in premedicated ASA class III and IV patients. 316 Feb 64

Dissemination of neoplastic cells within the body involves invasion of blood vessels by tumor cells. Since platelets have been shown to contribute to this process, we studied the interaction in vitro of platelets and malignant cells with the vascular endothelium and its underlying basement membrane-like ECM. A metastatic subline (ESb) of the methylcholanthrene-induced DBA/2 T-lymphoma invaded the vascular endothelium at a higher rate than its parental nonmetastatic (Eb) subline. ESb cells also exhibited a much higher ability to degrade the proteoglycan scaffold of the ECM by means of a specific HS degrading endoglycosidase (heparanase). The interaction of platelets with this ECM was associated with platelet activation, aggregation, and degradation of HS by means of the platelet heparanase. Degradation of ECM-HS was facilitated by proteolytic activity that produced a more accessible substrate for further cleavage by heparanase. A similar enhancement was exerted by plasminogen via the activity of the tumor cells or ECM associated PAs. Heparin and chemically modified heparins that lack anticoagulant activity inhibited degradation of the ECM-HS by heparanase. Interaction of platelets and lymphoma cells with ECM covered with vascular endothelial cells was investigated by SEM and by determination of ECM-HS degradation products. SEM studies demonstrated that platelets may adhere to minor gaps between adjacent endothelial cells and degrade the ECM-HS. Platelets were also shown to recruit lymphoma cells into these interendothelial gaps, suggesting that by binding to ECM and release of heparanase, platelets may play an active role in tumor cell invasion and metastasis. Our observation that nonanticoagulant heparins may interfere with heparanase-mediated degradation of ECM-HS suggests a potential therapeutic use for such heparins in neoplastic disorders.
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PMID:Role of heparanase in platelet and tumor cell interactions with the subendothelial extracellular matrix. 332 38

Blood samples were drawn from 10 ASA physical status 1 and 2 patients before (baseline) and after the administration of cimetidine to determine the in vivo effect of cimetidine on plasma cholinesterase (PCHE) activity. The in vitro effects of cimetidine at different plasma concentrations were also studied using the same blood samples. PCHE activity in the baseline samples was 432 +/- 4.6 (mean +/- SEM) U/ml, the dibucaine number 82. Administration of oral cimetidine (300 mg) the night before and 2 hours before surgery, failed to have any effect on PCHE activity (no in vivo effect). Plasma cholinesterase activity in the presence of cimetidine in vitro at plasma concentrations of 1.5, 15, 150, and 1500 micrograms/ml was 428, 420, 397, and 177 U/ml, respectively. Thus, in vitro data showed that cimetidine at plasma concentrations (1.5 to 15 micrograms/ml) achieved with clinical doses also has no effect on PCHE activity.
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PMID:Cimetidine does not affect plasma cholinesterase activity. 333 48

The anesthetic effect of 2 ml of 5% lidocaine in 7.5% glucose (LG) or 5% meperidine in water were evaluated and compared in 40 ASA class 1 or 2 patients. Patients were randomly assigned to one of the two groups (20 patients in each) according to the anesthetic agent, which was injected into the lumbar subarachnoid space in the sitting position. The patients remained sitting for 5 min before being placed in the supine position. Times of onset of sensory and complete motor blockade were significantly more rapid with LG. The extent of maximum cephalad spread of analgesia and the time to maximum height of analgesia in the two groups were not different. Duration of analgesia at the T-7 (48.96 +/- 6.64 min with LG, 44.74 +/- 6.14 min with meperidine; means +/- SEM) and L-1 (94.37 +/- 7.42 min with LG, 76.19 +/- 5.64 min with meperidine) dermatomes was not different in the two groups but was statistically longer at the T-10 dermatome with LG (66.83 +/- 6.72 min) than with meperidine (46.66 +/- 6.26 min). The duration of complete motor blockade was also significantly longer with LG (66.44 +/- 7.05 min) than with meperidine (42.67 +/- 4.47 min). Complications in both groups included decrease in blood pressure and nausea and vomiting intraoperatively, and urinary retention, nausea and vomiting, and mild headache postoperatively. Complications that occurred only in the meperidine group were intraoperative drowsiness, respiratory depression, bronchospasm, and itching. The frequency of complications was greater wit meperidine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Meperidine as a spinal anesthetic agent: a comparison with lidocaine-glucose. 354 85

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children. 360 47


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