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)

Sucralfate, an agent that heals peptic ulcers in humans, has been shown to reduce aspirin-induced gastric mucosal damage in experimental animals. It has been suggested that the protective effect of sucralfate is due to stimulation of local prostaglandin production. The purpose of this study was to establish whether sucralfate was capable of reducing aspirin-induced gastric damage in humans. The effect of 1 g of sucralfate or identical placebo was studied in random order in eight healthy subjects. To determine if the effect of sucralfate was related to local prostaglandin synthesis, a second series of studies was performed in which prostaglandin production was inhibited with indomethacin 50 mg given orally eight hours before sucralfate. In each subject, all studies were performed at least one week apart. Following an overnight fast, upper gastrointestinal endoscopy was performed, with sucralfate or placebo given orally 30 minutes before ingestion of 1,200 mg of soluble aspirin in 50 ml of water. Both endoscopist and subject were unaware of the test agent. Ninety minutes after aspirin ingestion, endoscopy was again performed and gastric mucosal lesions were counted and graded to derive an erosion score. Results are expressed as mean +/- SEM. Aspirin produced endoscopic changes (score of 2.75 +/- 0.49) that were significantly (p less than 0.05) inhibited by sucralfate (score of 1.13 +/- 0.44). The protective effect of sucralfate was abolished by pretreatment with indomethacin (scores of 2.88 +/- 0.55 and 1.88 +/- 0.40, respectively). These results demonstrate that sucralfate significantly protects the human gastric mucosa against the acute damaging effects of aspirin. This effect is abolished by indomethacin, suggesting that the protective action of sucralfate on the gastric mucosa of humans may be related to stimulation of endogenous prostaglandins.
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PMID:Protective effect of sucralfate against aspirin-induced damage to the human gastric mucosa. 366 13

The effect of age on the onset and duration of action of a d-tubocurarine (DTC) neuromuscular blockade with and without pancuronium priming in children was examined. Sixty ASA physical status I or II patients in three age ranges (0-1 yr, 1-3 yr and 3-10 yr) were anaesthetized with thiopentone, halothane and nitrous oxide. Each patient received either a single paralyzing dose of DTC 0.4 mg.kg-1, or DTC 0.36 mg.kg-1 preceded three minutes earlier by pancuronium 0.007 mg.kg-1. Evoked force of contraction of the adductor pollicis was measured using train-of-four stimulation applied every 12 sec. Time to 90 per cent first twitch depression after a single dose of DTC increased with increasing age (r = 0.65, p less than 0.01), and was 1.6 min (SEM +/- 0.3) in the 0-1 yr group, 1.9 +/- 0.3 min (1-3 yr), and 5.2 +/- 1.2 min (3-10 yr). Time to ten per cent spontaneous recovery after single dose DTC was shorter in older individuals (r = 0.40, p less than 0.05), being 36.4 +/- 5.1 min in infants 0-1 yr, 30.6 +/- 4.6 min (1-3 yr), and 24.0 +/- 2.7 min (3-10 yr). Priming with pancuronium accelerated the onset significantly in all age groups with 90 per cent T1 depression occurring at 0.7 +/- 0.1 min (0-1 yr), 0.9 +/- 0.1 min (1-3 yr), and 2.1 +/- 0.6 min (3-10 yr). However, priming delayed recovery, especially in infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Accelerated onset and delayed recovery of d-tubocurarine blockade with pancuronium in infants and children. 367 78

To compare the ability of equipotent doses of neostigmine, pyridostigmine and edrophonium to antagonize intense pancuronium neuromuscular blockade, one hundred and twenty ASA physical status I or II patients scheduled for elective surgery received 0.06 mg.kg-1 pancuronium during a thiopentone nitrous oxide-enflurane anaesthetic. Train-of-four stimulation was applied every 12 s and the force of contraction of the adductor pollicis muscle was recorded. In the first 60 patients, spontaneous recovery was allowed until ten per cent of initial first twitch height. Then neostigmine (0.005, 0.01, 0.02 or 0.05 mg.kg-1), pyridostigmine (0.02, 0.04, 0.1 or 0.2 mg.kg-1), or edrophonium (0.1, 0.2, 0.4 or 1 mg.kg-1) was injected by random allocation. Dose-response relationships were established from the measurement of first twitch height (T1) ten minutes later. From these, neostigmine, 0.04 and 0.08 mg.kg-1 was found to be equipotent to pyridostigmine, 0.2 and 0.38 mg.kg-1, and edrophonium, 0.54 and 1.15 mg.kg-1, respectively. These doses were given by random allocation to the next 60 patients, but at one per cent spontaneous recovery. Neostigmine, 0.04 mg.kg-1, produced a T1 of 73 +/- 4 per cent (mean +/- SEM), and a train-of-four ratio (TOF) of 39 +/- 3 per cent. This was significantly greater than with pyridostigmine, 0.2 mg.kg-1 (T1 = 50 +/- 6 per cent; TOF = 25 +/- 3 per cent), and edrophonium, 0.54 mg.kg-1 (T1 = 54 +/- 3 per cent; TOF = 17 +/- 2 per cent).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neostigmine, pyridostigmine and edrophonium as antagonists of deep pancuronium blockade. 367 83

The measurement of force of contraction of the adductor pollicis muscle following supramaximal stimulation of the ulnar nerve has become a standard method to assess the effect of neuromuscular blocking drugs. However, the diaphragm is regarded as resistant to these drugs, and considerable residual respiratory power might still be present after total block of adductor pollicis function. To quantify this differential effect, train-of-four stimulation was applied to the ulnar and the phrenic nerves in patients under N2O-halothane anesthesia. The force of contraction of the adductor pollicis muscle was measured with a force-displacement transducer and compared with the diaphragmatic electromyogram (EMG). Pancuronium cumulative dose-response curves for both muscles were determined in 10 ASA Class I adults. The mean dose (+/- SEM) required to depress adductor pollicis and diaphragm responses to first twitch stimulation (ED50) was 29.5 +/- 3.5 micrograms/kg and 59.5 +/- 7.0 micrograms/kg, respectively. Corresponding values for ED90 were 45 +/- 5 micrograms/kg and 95 +/- 11 micrograms/kg, respectively, indicating that the diaphragm required approximately twice as much pancuronium as the adductor pollicis block, the diaphragm was only 24 +/- 4% blocked. It is concluded that the adductor pollicis response might underestimate the degree of diaphragmatic relaxation. On the other hand, the administration of pancuronium in a dose sufficient to produce total paralysis might result in the inability to antagonize neuromuscular block in all muscles.
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PMID:Potency of pancuronium at the diaphragm and the adductor pollicis muscle in humans. 372 27

A procedure for preparing highly enriched suspensions of bovine binucleate trophoblastic cells was developed and data showing that these cells produce progesterone, prostacyclin (PGI2), and prostaglandin E2 (PGE2) were obtained. Approximately 200 X 10(6) enzymatically dissociated cells from bovine cotyledons were applied to the surface of a density gradient of 2% to 4% Ficoll-400 using the Wescor CELSEP sedimentation chamber. After 90-120 min of sedimentation at unit gravity, fractions containing binucleate trophoblastic cells were obtained and washed in HEPES-buffered Medium 199. Preparations of 90% to 100% binucleate trophoblastic cells were obtained routinely; viability was 50% to 80%. After incubation at 37 degrees C, concentrations (ng/10(5) cells) of progesterone were greater in those fractions containing binucleate cells than in those containing primarily smaller, mononucleate cells. Total progesterone secreted (mean +/- SEM) after 4 h by 1 X 10(5), 2 X 10(5), 4 X 10(5), 8 X 10(5), and 1.6 X 10(6) binucleate cells was 0.27 +/- 0.03, 1.01 +/- 0.09, 4.02 +/- 0.37, 10.31 +/- 0.92, and 20.96 +/- 2.23 ng, respectively (r = 0.997). Addition of 10% fetal bovine serum (FBS) or normal anestrous cow serum increased (P less than 0.05) production of progesterone by binucleate trophoblastic cells. Luteinizing hormone, follicle-stimulating hormone, prolactin, thyrotropin, and 8-bromo-adenosine 3',5'-cyclic monophosphate had no effect. Binucleate trophoblastic cells also produced PGI2 in relation to number of cells incubated (r = 0.996). Time courses for production of PGI2, PGE2, and progesterone were similar. Aspirin inhibited production of PGI2 and PGE2 by about 50% at a dose of 100 microM; FBS stimulated production of both prostanoids.
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PMID:Progesterone and prostanoid production by bovine binucleate trophoblastic cells. 386 92

Thirty premedicated ASA I or II patients scheduled for minor gynaecological surgery, were randomly allocated to receive either 1.5 mg/kg or 2 mg/kg propofol of the new emulsion formulation, or 4 mg/kg thiopentone, given over 20 seconds. Anaesthesia was successfully induced in all 30 patients. The mean (SEM) induction times were for propofol 1.5 mg/kg 33.3(3.2) seconds, for 2 mg/kg 30.5(2.7) seconds and for thiopentone 34.6(2.7) seconds. The incidence of apnoea greater than 10 seconds, was respectively 60, 80 and 80%, and the mean duration of apnoea 30.8(5.3), 37.1(5.0) and 23.7(5.0) seconds. The mean systolic blood pressure decreased after propofol 1.5 mg/kg by 16.0 mmHg, after 2 mg/kg by 18.6 mmHg, and increased after thiopentone by 1 mmHg, 2 minutes after injection. Heart rate increased significantly 2 minutes after thiopentone by an average of 15.1 beats/minute, but not after propofol. Pain was not reported during or after the injection. No major adverse reactions occurred at induction or during maintenance of anaesthesia with an inhalation agent. One patient who received 2 mg/kg propofol and isoflurane vomited for 24 hours. The recovery of anaesthesia after propofol induction, was quicker than after thiopentone.
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PMID:Comparison of propofol and thiopentone for induction of anaesthesia in premedicated patients. 387 74

The effect of ketamine on the functional residual capacity (FRC) was measured in nine ASA class I children prior to elective surgery. FRC was determined by the closed-circuit helium dilution method on the day prior to surgery in the awake state and also following induction of anesthesia on the day of the operation. Anesthesia consisted of ketamine by continuous intravenous infusion following preanesthetic sedation with atropine and triclofos or flunitrazepam. There were no significant differences in FRC between the measurements in the awake state and anesthetized (392 +/- 43 SEM ml, and 411 +/- 53 SEM ml, respectively), and the authors conclude that ketamine does not affect resting lung volume in young children.
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PMID:The effect of ketamine on the functional residual capacity in young children. 388 93

Monocytes are thought to play a role in host resistance to tumor cell growth in animals and humans. In addition, platelets are known to be involved in tumor metastases. To investigate the interaction of these two cell types and their effect on tumor cells, human monocytes and platelets were examined using an in vitro monocyte-tumor cell cytotoxicity assay. Monocytes alone resulted in 32% +/- 1.5 (mean +/- SEM) tumor cell kill. When platelets were added to monocytes in a 1:1 ratio, an increase in cytotoxicity to 61% +/- 3.2 was observed. The cytotoxicity noted when platelets were added to a fixed number of monocytes and tumor cells was dependent on the number of platelets added. A decrease in cytotoxicity from 32% +/- 1.5 to 12% +/- 2.3 was observed when contaminating platelets were removed from monocyte preparations. Platelets added to tumor cells in the absence of any monocytes were also toxic, resulting in a maximum kill of 95% at a 4:1 platelet/tumor cell ratio. Secreted products of freshly isolated platelets may be responsible for much of the observed cytotoxicity, since supernatants from the platelets were toxic for tumor cells. Platelets pretreated with a cyclooxygenase inhibitor (ASA) or a lipoxygenase inhibitor had decreased cytotoxicity compared with untreated platelets. Our results indicate that products of platelet arachidonate metabolism are toxic for tumor cell lines. They also suggest that the role of the platelet must be considered when studying monocyte-tumor cell cytotoxicity.
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PMID:Human platelets exert cytotoxic effects on tumor cells. 392 50

Postoperative hypoxemia has been well documented in adults but not in infants and children, although they are potentially more susceptible to airway closure and to disturbances in pulmonary gas exchange. In a prospective study, we measured arterial oxygen saturation (SaO2) with a pulse oximeter in 97 ASA class I infants and children breathing room air before and after general anesthesia for superficial surgical procedures. Mean preoperative SaO2 was 97.6 +/- 0.15% (SEM). On arrival in the recovery room after anesthesia mean SaO2 in room air had decreased significantly (P less than 0.01) to 93.0 +/- 0.49% (range 100-71%), corresponding to calculated arterial oxygen tension (PaO2) of about 66 mm Hg. The second reading, 5-15 min later, also showed a statistically significant (P less than 0.01) decrease in SaO2 (94.1 +/- 0.35%). There was no statistical difference in SaO2 between patients who received inhalation anesthesia alone and those who were given narcotics. There was also no correlation between postoperative reduction in SaO2 and duration of anesthesia or patient age. Of 67 patients who were asleep on arrival in the recovery room, 47 who remained asleep at the second SaO2 reading had an average increase in SaO2 of less than 1%. In contrast, in those patients who awoke, average SaO2 increased more than 4% during a similar time period--a difference that was statistically significant (P less than 0.02).
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PMID:Hypoxemia after general anesthesia in children. 395 92

Within 15 minutes of terminating general anaesthesia, progressive recovery of consciousness, spontaneous ventilation and cough, and limb movements were assessed in 60 young children (age range 0-5 years, mean +/- SEM; 2.83 +/- 0.34; weight 13.86 +/- 0.41 kg). All patients were ASA physical status class I-III, received a standard intravenous induction (atropine 0.02 mg X kg-1, thiopental sodium 5 mg X kg-1, diazepam 0.2 mg X kg-1), were intubated with an orotracheal tube following the administration of metocurine, 0.4 mg X kg-1, and were maintained under general anaesthesia with nitrous oxide and oxygen in a 70:30 mixture administered by a T-piece circuit. They were ventilated mechanically to maintain normal blood-oxygen tension and normocarbia. The patients were assessed in three equal groups according to the anaesthetic supplement they received. Group I received intravenous infusions of morphine sulfate (loading dose 60 micrograms X kg-1 administered over 5 minutes followed by a continuous intravenous infusion of 2 micrograms X kg-1 X min-1. Patients in Groups II and III had 0.5 per cent halothane and 1.0 per cent isoflurane respectively added to the nitrous oxide/oxygen fresh gas mixture rather than morphine sulphate infusions. By the end of the study period, there was no significant difference in the degree of recovery between the morphine and the isoflurane groups but the patients in the halothane group had recovered to a lesser degree. Generally, the patients in the morphine group were awake but not crying, while those in the other two groups were less sedated.
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PMID:Assessment of immediate post-anaesthetic recovery in young children following intravenous morphine infusions, halothane, and isoflurane. 669 77


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