Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspirin (ASA) was tested in a group of 8 Oriental and 3 Occidental subjects who were shown in a previous study to respond to small doses of ethanol (0.06-0.25 g/kg) with facial flushing. They were compared to a similar group of 11 non-flushing Occidental subjects following a larger ethanol dose (0.37 g/kg) to determine if similar effects could be produced in less sensitive individuals. Control tests of blood ethanol and acetaldehyde (AcH) levels (calculated from breath), facial and neck skin temperatures, body sway (Romberg test), blood pressure, heart rate and 10 Subjective High Assessment Scales (SHAS-Judd, 1977) were conducted before and at 15, 30, 60 and 90 minutes after drinking ethanol as vodka in orange juice. The tests were repeated one week later one hour after receiving 0.64 gm of ASA orally. ASA produced slight changes in the early absorption of ethanol and small decreases in AcH levels in the flushing and non-flushing groups. Facial flushing was markedly reduced in the flushing group, but was slightly increased in the non-flushing Occidentals. Body sway was reduced by ASA in both groups. An alcohol-induced increase in heart rate in the flushing group was reduced with no change in blood pressure. SHAS subjective parameters were widely variable, but indicated that ASA produced reduced sleepiness and earlier relaxation in the flushing group. It is concluded that ASA can block alcohol-induced facial flushing in sensitive subjects and also reduces body sway in the Romberg test and alters some subjective feelings of alcohol intoxication.
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PMID:Aspirin attenuation of alcohol-induced flushing and intoxication in Oriental and Occidental subjects. 342 38

Acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs (NSAID) cause a variety of symptoms in patients sensitive to these drugs. These include wheezing, rhinorrhea, flushing, pruritus, urticaria, hypotension and loss of consciousness. Conversely, improvement of asthma with the use of these drugs in patients who do not have idiosyncratic reactions to ASA (ASA-nonsensitive) has also been observed both with respect to clinical symptoms and pulmonary function tests.
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PMID:Asthma improved by acetylsalicylic acid and other nonsteroidal anti-inflammatory agents. 347 42

Nicotinic acid flushing after placebo and 975-mg oral doses of aspirin was assessed in 29 normal subjects over a range of nicotinic acid doses. Intensity of flushing was assessed by the change in malar thermal circulation index (delta MTCI). Aspirin pretreatment resulted in smaller delta MTCIs at the higher doses of nicotinic acid. At the lower doses the change in the index after pretreatments with both aspirin and placebo remained low, suggesting that very little flushing was provoked by these doses. These results are compatible with the proposed mediation by prostaglandins of the nicotinic acid-induced flush. According to the delta MCTI method, flushing is quantitatively characterized as a nonquantal, dose-response reaction of variable intensity.
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PMID:Aspirin blocks nicotinic acid-induced flushing. 706 Mar 28

Aspirin therapy for patients with systemic mast cell disease (SMCD) decreases the production of prostaglandin D2, which is thought to be a major mediator of flushing. Paradoxically, in 5 to 10% of patients with SMCD, administration of aspirin causes massive mediator release and an anaphylactoid reaction. We attempted aspirin desensitization in a 34-year-old man with SMCD (confirmed by bone marrow biopsy) who was incapacitated by severe flushing episodes and hypotension. His baseline mediator levels of plasma calcitonin, urinary histamine, and urinary N-methyl-imidazoleacetic acid were abnormal. Pentagastrin stimulation increased the plasma level of calcitonin from 47 pg/mL to 130 pg/mL (normal, less than or equal to 110) at 5 minutes. Oral aspirin desensitization was begun; however, after a cumulative dose of 620 mg, an anaphylactoid reaction ensued in conjunction with hypotension, abdominal cramping, and flushing. Coincidentally, 1 hour after the episode, the plasma calcitonin level increased from 37 pg/mL to 540 pg/mL, and the serum tryptase level increased from 1 ng/mL to 3.9 ng/mL. Six hours after the episode, the urine level of histamine increased from 90 micrograms/g creatinine to 337 micrograms/g creatinine, and the urinary N-methylimidazoleacetic acid increased from 32 mg/24 h to 81 mg/24 h. Hence, the patient had increased basal levels of plasma calcitonin that increased substantially during aspirin desensitization and increased to above the upper limit of normal during pentagastrin stimulation. Human mast cells may be capable of producing calcitonin or causing secretion of calcitonin in response to skeletal changes.
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PMID:Increased plasma calcitonin levels in systemic mast cell disease. 793 97

Duration of neuromuscular block may be prolonged by H1/H2 antagonists. This study was designed to determine the influence of H1/H2 antagonist treatment on onset, duration and recovery after mivacurium chloride (MIV), a new nondepolarizing neuromuscular blocking agent with a relatively short duration of action, which is metabolized by human plasma cholinesterase (PChE). METHODS. After approval from the hospital ethical committee and written informed consent, 48 ASA I-II patients of either sex (ages 18-65 years, weight 45-100 kg) were included in this double blind study and randomly allocated to four groups of 12 each: group A, 0.105 mg/kg MIV (1.5 x ED95) and H1/H2 antagonist; group B, 0.105 mg/kg MIV and placebo; group C, 0.21 mg/kg MIV (3 x ED95) and H1/H2 antagonist; Group D 0.21 mg/kg MIV and placebo. Premedication consisted of 2 mg lormetazepam p.o., 300 mg ranitidine and 0.1 mg/kg dimetindene, or placebo p.o. Anaesthesia was induced with thiopentone (5-7 mg/kg) and maintained with N2O/O2 at a 65/35 ratio, enflurane (0.8-1.5%) and supplements of fentanyl. The ulnar nerve was stimulated with supramaximal 2 Hz train-of-four (TOF) every 10 s. Neuromuscular twitch response was recorded with EMG. Onset time (time from end of injection to maximal or total block), maximal block (%), T125 (time from end of injection to 25% recovery) were recorded after each dose, and recovery index (T1 from 25% to 75% recovery) and TOF70 (time from end of injection to TOF ratio of 70%), after the last dose. RESULTS. The four groups did not differ with respect to age, weight or height. There was no difference in the pharmacodynamics of mivacurium between the groups receiving H1/H2 antagonists and those receiving placebo. Following 1.5 x ED95 the onset was at 3.7 +/- 1.2 (H1/H2) and 3.8 +/- 0.9 min (placebo), respectively. Clinical duration (T125) was 13.1 +/- 3.4 and 12.8 +/- 3.4 min. 3 x ED95 led to a significant faster onset and longer duration (P < or = 0.05). Onset was at 1.9 +/- 0.7 (H1/H2) and 2.1 +/- 0.5 min (placebo), respectively, and clinical duration 19.1 +/- 6.1 and 19.3 +/- 3.8 min. Duration of repetitive doses (10.1 +/- 5.3 min), recovery index (6.8 +/- 2.9 min) and interval from last dose to spontaneous recovery (22.4 +/- 7.0 min) did not differ between groups. Three patients in group D (placebo and 0.21 mg/kg MIV) had haemodynamic changes of over 20% from baseline. Flush and erythema were significantly less pronounced after H1/H2 premedication than after placebo (4 vs 12 pts). CONCLUSIONS. Our results suggest that time of onset and clinical duration of effects of MIV are not altered by dimetindene and ranitidine. The duration depends more heavily on the dose of MIV. The recovery of neuromuscular function, once it has begun, is prolonged neither by MIV nor by H1/H2 antagonists. As MIV is mainly broken down by PChE, it is evident that its duration of action is more prolonged by atypical PChE activity than by interaction with other drugs. Oral H1/H2 premedication may diminish haemodynamic side-effects and clinical signs of histamine release.
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PMID:[Pharmacodynamics and clinical adverse effects of mivacurium. The effect of oral premedication with H1/H2 antagonists]. 810 16

The rapid administration of vancomycin is associated with flushing and hypotension, a consequence of histamine release. The manufacturer discourages administering vancomycin to anesthetized patients, stating that vancomycin aggravates the hypotensive effects of anesthetics. To test this, we randomly assigned 36 adults (ASA classes I through III) to one of two groups: preinduction (Preind, n = 19) and postinduction (Postind, n = 17). Both groups received two different infusions: vancomycin (1 g/250 mL normal saline) and saline (250 mL normal saline) over 30-60 min. The Preind group received vancomycin before anesthesia was induced and saline was administered immediately after anesthesia was induced; for the Postind group, this order was reversed. This was done in a double-blind fashion. The anesthetic induction was standardized by the intravenous administration of thiopental and vecuronium and anesthetic maintenance by inhalation of nitrous oxide and enflurane. End-tidal enflurane, heart rate (HR), and blood pressure (BP) were measured every 3 min. Independent (unpaired) t-test was used in data analysis. The groups did not differ significantly. We conclude that vancomycin infusion may be given under anesthesia without significant adverse hemodynamic consequences if administered over a 30-60 min period of time.
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PMID:Vancomycin does not enhance hypotension under anesthesia. 846 22

This study investigates the effects of mivacurium (3 times ED95) on neuromuscular block, intubation conditions and general safety in comparison with equipotent doses of atracurium and vecuronium. Following Ethical Care Committee approval and informed consent, 90 ASA I+II patients aged 18 to 65 were studied undergoing elective ENT surgery. Anaesthesia was induced with 1.5 mg/kg propofol and 0.2 mg/kg alfentanil and maintained through continuous infusion of propofol (8 to 10 mg . kg-1 . h-1) and nitrous oxide in oxygen. After achieving stable anaesthesia, the patients received bolus injections of mivacurium (0.20 mg/kg, n = 30), atracurium (0.69 mg/kg, n = 30) or vecuronium (0.14 mg/kg, n = 30) for endotracheal intubation. Intubation was attempted 120 s after drug application and the intubation conditions were assessed. Relaxation was recorded using peripheral nerve stimulation (Train of four). During the observation period, signs of histamine release, respiratory difficulty, cardiovascular events or other adverse signs were monitored. Onset of relaxation was longer for mivacurium (2.3 +/- 1.3 min) compared with atracurium (1.4 +/- 0.7 min) or vecuronium (1.3 +/- 0.3 min). Intubation conditions 120 s after drug application were good or very good in only 67% of cases given mivacurium compared with 90% given atracurium and 100% given vecuronium. The recovery time (DUR 25) was shorter in the mivacurium group (19.5 +/- 7.9 min) compared with atracurium (54.7 +/- 6.6 min) and vecuronium (44.3 +/- 8.6 min). Heart rate and blood pressure were similar in all groups. Facial flushing and mild bronchospasms as signs of histamine release resulted more often in the mivacurium (20%) and atracurium groups (23%) than in the vecuronium group (3%). In contrast to atracurium and vecuronium, recovery from mivacurium-induced neuromuscular blockade is rapid. However, the onset time after 3 times ED95 was significantly longer for mivacurium than for atracurium or vecuronium.
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PMID:[Mivacurium--a new muscle relaxant compared with atracurium and vecuronium]. 937 44

Crystalline nicotinic acid (immediate-release niacin) is effective therapy for lipoprotein regulation and cardiovascular risk reduction. However, inconvenient regimens and unpleasant side effects decrease compliance. Sustained-release formulations designed to circumvent these difficulties increase hepatotoxicity. Niaspan, a new US Food and Drug Administration (FDA)-approved, once-daily, extended-release form, has been found effective and safe in short-term trials. The long-term efficacy and safety of Niaspan lipid monotherapy was studied in 517 patients (aged 21-75 years) for < or =96 weeks in dosages < or =3,000 mg/day. Primary efficacy endpoints were low-density lipoprotein (LDL) cholesterol and apolipoprotein B (apo B) changes from baseline; secondary efficacy endpoints were changes in total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, lipoprotein(a), and total cholesterol/HDL-cholesterol ratio; safety data included adverse events and laboratory values over the 2-year study period. LDL-cholesterol levels decreased significantly: 18% at week 48 and 20% at week 96; apo B reduction was similar (16% decrease at week 48 and 19% at week 96). Large elevations in HDL cholesterol (26%, week 48; 28%, week 96) allowed only modest decreases in total cholesterol (12% and 13%, respectively), whereas total cholesterol/HDL-cholesterol ratio decreased by almost one third. Triglyceride and lipoprotein(a) levels were decreased by 27% and 30%, respectively (week 48), and by 28% and 40%, respectively (week 96). All changes from baseline were significant (p <0.001). Niaspan was generally well tolerated, although flushing was common (75%); however, there was a progressive decrease in flushing with time from 3.3 episodes in the first month to < or = 1 episode by week 48. Aspirin was used by one third of patients before Niaspan dosing to minimize flushing episodes. Although serious adverse events occurred in about 10% of patients, none were considered probably or definitely related to Niaspan. Adverse events in general varied widely, but their true relation to the study drug is difficult to ascertain without a placebo (control) group. No deaths occurred. There were statistically significant changes in hepatic transaminases, alkaline phosphatase, direct bilirubin, phosphorus, glucose, amylase, and uric acid. However, these changes were mostly small and are not likely to be biologically or clinically significant (the decrease in phosphorus is a new finding in niacin therapy). No myopathy was observed. Thus, this long-term study confirms the earlier short-term findings that Niaspan is safe and effective as monotherapy in plasma lipoprotein regulation.
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PMID:Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. 991 66

Nitrogen (N2) may accumulate to unacceptable levels during closed-circuit anesthesia (CCA) when the sampled gases are redirected to the anesthesia circuit, because many gas analyzers entrain air as a reference gas to calibrate for oxygen analysis. Using oxygen instead of air as the reference gas for paramagnetic oxygen analysis could attenuate N2 accumulation. Forty-three adult ASA physical status I-III patients undergoing a variety of peripheral and abdominal procedures were assigned to one of two groups, depending on the reference gas used by a paramagnetic oxygen analyzer, either air (group I, n = 23) or oxygen (group II, n = 20). Gases sampled by the multigas analyzer were redirected to the anesthesia circuit. End-expired N2 (N2Et) was calculated as "balance gas": (100 - %O2 - %anesthetic vapor - %CO2). N2Et after 55 min (N2Et55min) was correlated with the end-expired N2 concentration when the circuit was closed (N2Et0min) and 5 min (N2Et5min) thereafter. In group I, N2Et accumulated almost linearly over time (t, min): N2Et (%) = 2.47 + 0.61 * t (r2 = 0.999). N2Et0min, N2Et5min, and N2Et55min were 1.3+/-0.8, 5.3+/-1.7, and 35.3+/-5.3%, respectively (mean +/- SD). The correlation (r2) between N2Et55min and N2Et0min was 0.19, and between N2Et55min and N2Et5min it was 0.56. In group II, N2Et increased exponentially: N2Et (%) = 1.01 + 11.9 * (1 - e(-t/43.5)) (r2 = 0.99). N2Et0min, N2Et5min, and N2Et55min were 0.87+/-0.93, 2.6+/-1.5, and 10.1+/-2.9%, respectively. The correlation (r2) between N2Et55min and N2Et0min was 0.04, and between N2Et55min and N2Et5min it was 0.40. We conclude that paramagnetic oxygen analyzers that use oxygen as the reference gas significantly attenuate N2 accumulation during CCA, which may reduce the need for frequent flushing of the anesthesia system, may provide more constant oxygen and nitrous oxide concentrations, and may simplify pharmacokinetic studies of potent inhaled anesthetics.
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PMID:Influence of the reference gas of paramagnetic oxygen analyzers on nitrogen concentrations during closed-circuit anesthesia. 1002 34

This study was designed to measure ischaemic pain during and after infusion of adenosine. In a double-blind, placebo-controlled, crossover study, eight ASA 1 male volunteers received infusion of adenosine 100 micrograms kg-1 min-1 or placebo for 10 min. This was repeated 1 week later with the alternate infusion. Pain measurements were made during tourniquet-induced ischaemia in an exercising arm before infusion, during infusion and for 24 h afterwards. Pain was reduced significantly in the adenosine group compared with the saline group during infusion (median difference 20.8; 95% confidence interval 2.0-40). There was no significant difference in pain after infusion and there were no significant changes in cardiovascular variables. During infusion of adenosine, transient mild chest discomfort, shortness of breath and facial flushing occurred. We conclude that adenosine had measurable effects on ischaemic pain which were not sustained after discontinuation of infusion.
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PMID:Analgesic effect of adenosine on ischaemic pain in human volunteers. 1043 28


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