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)

In one multicenter, double-blind study, 659 hypertensive patients were treated for 16 weeks with either nilvadipine (n = 326) or nifedipine (n = 333). The major objective of the study was to compare the compatibility of the two calcium antagonists with regard to hepatic compatibility and side-effect profiles. The dosages were chosen so that the effective blood pressure reduction in both groups was equally good (mean decreases in systolic pressure of 27 +/- 12 mm Hg with nilvadipine and 26 +/- 15 mm Hg with nifedipine, and in diastolic pressure of 18 +/- 6 mm Hg with nilvadipine and 19 +/- 7 mm Hg with nifedipine). The mean heart rate was slightly lowered by about 2 beats/min by both substances. Although there was no effect on lipid or glucose levels, the serum glutamate-pyruvate transaminase (SPGT) levels were more often found to be raised in the nifedipine group than in the nilvadipine group (p < 0.05). The vasodilator effect of both calcium antagonists was responsible for side effects, of which the most common were flushing, edema, headache, and palpitations. The number of complaints was less in the group treated with nilvadipine than with nifedipine, especially flushing and edema. Significantly more patients in the nifedipine group withdrew from treatment due to undesirable side effects (p < 0.05).
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PMID:The tolerability of nilvadipine compared to nifedipine in patients with essential hypertension. 128 91

Antisera raised against glutamate or aspartate bound to bovine serum albumin were purified by affinity chromatography, and their specificities were verified by immunoblotting and by enzyme-linked immunosorbent assay. Immunohistochemical investigation using materials perfusion-fixed after long flushing demonstrated distinct laminar terminals with glutamate- or aspartate-like immunoreactivity throughout the limbic structures. This technique may offer a valuable tool for revealing the distribution of glutamatergic or aspartatergic nerve terminals.
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PMID:Immunohistochemical visualization of glutamate- and aspartate-containing nerve terminal pools in the rat limbic structures. 288 19

The Restaurant syndromes can be caused by five major factors: food allergens, sulfites, monosodium glutamate (MSG), tartrazine, and scombroidosis (and other seafood poisoning). A history of atopy and ingestion of known food allergens such as peanuts, egg, fish, and walnuts, together with positive results of skin tests or RAST to these foods, will favor a diagnosis of food allergy. Allergic reactions to peanuts have produced fatalities in minutes through an IgE mediated reaction. An extremely rapid onset (minutes) of symptoms consisting of flushing, bronchospasm and hypotension is consistent with a sulfite reaction. Burning, pressure, and tightness or numbness in the face, neck, and upper chest following ingestion of Chinese food favors a diagnosis of adverse reaction to MSG. Also, development of late onset bronchospasm (up to 14 hours) may be related to MSG reactions. Bronchospasm and urticaria in a patient with a history of aspirin intolerance suggests tartrazine sensitivity. If everyone ingesting a fish meal develops flushing, urticaria, pruritus, gastrointestinal complaints, or bronchospasm, this implies scombroidosis, ciguatera, or other seafood poisoning. Finally, severe headache or hypertension can result from ingestion of naturally occurring amines, such as tyramine (cheese, red wine) and phenylethylamine (chocolate). A double-blind oral challenge test may be the only way of confirming the diagnosis for most of the etiological factors of the Restaurant syndromes. The treatment of choice for acute reaction is epinephrine followed by antihistamine. Proper labeling and avoidance of these ingredients in sensitive individuals are the best preventive measures.
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PMID:The restaurant syndromes. 330 66

Monosodium glutamate is widely regarded as the provocative agent in the "Chinese restaurant syndrome," of which flushing is regarded as part of the reaction. Six subjects were monitored by laser Doppler velocimetry for changes in facial cutaneous blood flow during challenge with monosodium glutamate and its cyclization product, pyroglutamate. Additionally, records of patients challenged with monosodium glutamate in the laboratory were reviewed. No flushing was provoked among the twenty-four people tested, eighteen of whom gave a positive history of Chinese restaurant syndrome flushing. These results indicate that monosodium glutamate-provoked flushing, if it exists at all, must be rare. Monosodium glutamate and its cyclization product, pyroglutamate, may provoke edema and associated symptoms.
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PMID:Does monosodium glutamate cause flushing (or merely "glutamania")? 374 27

The mechanisms of flushing reactions are pharmacologically and physiologically heterogeneous. Flushing may result from agents acting directly on the vascular smooth muscle or may be mediated by vasomotor nerves. Vasomotor nerves may lead to flushing as a result of events at both peripheral and central sites. In susceptible persons, frequent, intense flushing leads to a cluster of physical signs (rosacea). Flushing provoked by alcohol has been associated with ethnic sensitivity, a possible predisposition to alcoholism, various disulfiramlike agents, one type of diabetes mellitus, and the carcinoid syndrome and other types of neoplasia. Flushing reactions also occur during the menopause, after glutamate ingestion, and in response to oral thermal challenges.
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PMID:Flushing reactions: consequences and mechanisms. 616

The aldehyde dehydrogenase I (ALDH I) gene codes for a mitochondrial enzyme which plays a major role in hepatic alcohol detoxication. It has been related to alcohol flushing in Orientals bearing the atypical ALDH I2 gene. The variant protein results from a lysine for glutamate substitution at position 487 (G-->A change in exon 12). A procedure for ALDH I2 detection consisting in a differentiation between the 'atypical' allele and the 'wild' allele has been improved through PCR and subsequent MboII digestion. Blood samples collected on anticoagulant or directly absorbed on blotting paper were used for DNA amplification in the presence of two specific oligonucleotidic primers, each one able to incorporate a restriction site in the amplimer. After MboII digestion, PCR products were separated by polyacrylamide gel electrophoresis and then visualized with ethidium bromide. This technique permits a rapid and non-radioactive detection of atypical ALDH I2 on a PCR product without the use of allele specific oligonucleotides. It was applied to the study of ALDH I2 allele frequency in random population samples of three ethnic groups: Caucasians, Orientals and African blacks.
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PMID:The frequency of the mitochondrial aldehyde dehydrogenase I2 (atypical) allele in Caucasian, Oriental and African black populations determined by the restriction profile of PCR-amplified DNA. 747 12

Reperfusion is a critical phase of organ preservation. The purpose of this study was to develop a solution specifically for postischemic kidney reperfusion. Unilateral left normothermic kidney ischemia was induced for 60 minutes in two groups of micropigs. In group 1 (control pigs, n = 6) the kidney was reperfused immediately with pure blood at systemic pressure by unclamping the renal artery. In group 2 (test animals, n = 6) the kidney was initially reperfused with an intracellular flush solution enriched with solution BT01 composed of cytoprotectors (natriuretic factor, PGI2), free radical chelating agents (allopurinol, mannitol), and substrates for the mitochondrial respiratory chain (aspartate, glutamate). This solution was mixed immediately before use with blood in a ration of 1:4 parts and injected into the left renal artery with a perfuser at a constant pressure of 60 mm Hg. After 20 minutes, the kidney was reperfused with systemic blood for 100 minutes. Glomerular filtration rate (GFR) was determined by measuring inulin clearance. Kidney blood flow was measured throughout the experiment. After 120 minutes of reperfusion, the kidneys were removed for histologic examination. In the control pigs (group 1) 50% of the animals were anuric. The ratio between GFR measured in the left kidney at the end of perfusion and at equilibrium in the remaining animals was 0.16 +/- 0.01. In test animals (group 2) all animals recovered diuresis. The ratio between GFR measured in the left kidney at the end of perfusion and equilibrium was 0.51 +/- 0.12 (p < 0.001, group 2 vs. group 1). In group 2 postperfusion kidney blood flow was higher than in group 1 (63.0 ml/min vs. 27.4 ml/min; p < 0.05) because of a decrease in renal vascular resistance. Light microscopic examination of kidneys form animals in group 1 revealed tubular necrosis that extended to the parenchyma, with exposure of tubular interstitium. In group 2 only degenerative lesions with edema of tubular cells and disappearance of brush borders were observed. Our findings indicate that flushing the kidneys with BT01 solution mixed with blood improves postischemic kidney function by reducing reperfusion damage.
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PMID:Improvement of postischemic kidney function by reperfusion with a specifically developed solution (BT01). 868 15

Monosodium glutamate (MSG) has been allocated an "ADI not specified" by the JECFA, which indicates that no toxicological concerns arise associated with its use as a food additive in accordance with good manufacturing practice (GMP) and for that reason it is not necessary to allocate a numerical ADI. The question in this case, then, is not whether excursions above a numerical ADI might occur but whether high peak intakes might arise which could invalidate the assumption of absence of hazard. Two major issues have arisen in relation to high intakes of MSG: (1) What is the significance of neural damage (focal necrosis in the hypothalamus) seen following high parenteral or intragastric doses of MSG to neonatal animals and is this a particular risk for children? (2) What is the role of MSG in "Chinese Restaurant Syndrome" (flushing, tightness of the chest, difficulty in breathing, etc.) following consumption of Chinese foods? In relation to the first issue, human studies have been crucial in resolving the question. The threshold blood levels associated with neuronal damage in the mouse (most sensitive species) are 100-130 mumol/dl in neonates rising to > 630 mumol/dl in adult animals. In humans, plasma levels of this magnitude have not been recorded even after bolus doses of 150 mg/kg body wt (ca. 10 g for an adult). Additionally, studies in infants have confirmed that the human baby can metabolize glutamate as effectively as adults. It is concluded that blood levels of glutamate + aspartate do not rise significantly even after abuse doses and babies are no more at risk than adults. Intake levels associated with the use of MSG as a food additive and natural levels of glutamic acid in foods therefore do not raise toxicological concerns even at high peak levels of intake. It is not envisaged that use of MSG according to GMP requires the allocation of a numerical ADI. With regard to the second issue, controlled double-blind crossover studies have failed to establish a relationship between Chinese Restaurant Syndrome and ingestion of MSG, even in individuals reportedly sensitive to Chinese meals, and MSG did not provoke bronchoconstriction in asthmatics. Thus, high usage of MSG in ethnic cuisines does not represent a situation in which intakes might achieve unsafe levels, even among individuals claiming idiosyncratic intolerance of such foods. In the light of the toxicological studies, the human metabolic studies in neonates and adults, and the physiological and nutritional role of glutamic acid and the fact that food additive use does not markedly increase the total dietary burden, no foreseeable circumstances arise in which intakes would be such as to invalidate the appropriateness of allocating an ADI not specified to MSG.
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PMID:The significance of excursions above the ADI. Case study: monosodium glutamate. 1059 25

The transport of transmitter, ions and water through a positively-charged nanopore was investigated through computer simulations. The physics of the problem is described by a coupled set of Poisson-Nernst-Planck and Navier-Stokes equations in a computational domain consisting a cylindrical pore, whose radius ranged from 1 to 8 nm and which was flanked by two compartments representing the vesicular interior and extra-cellular space. The concentration of co-ions is suppressed and of counter-ions enhanced, especially near the pore wall owing to electrostatic interactions. Glutamate (i.e. the transmitter considered) is negatively charged and is simulated as a counter-ion. The electro-kinetically induced pressure due to the movement of ions is negative and very pronounced near the pore wall where the concentration and flux of counter-ions is very high. The water velocity peaks in the pore center, diminishes to zero at the pore wall, but is constant along the pore axis. The mean velocity of the water/fluid is proportional to the vesicular pressure and pore cross-sectional area. Interestingly it is inversely related to the vesicular glutamate concentration. The factors determining the glutamate flux are complex. The diffusive flux generally predominates for narrow pore, and convective flux may dominate for wide pore if the vesicular pressure is high. Surprisingly at low vesicular pressure the mean total glutamate flux per unit cross-sectional pore area is higher for narrow pores. Higher flux is probably due to the rise of glutamate concentration in the nanopore, which is much more pronounced for narrow nanopores, due to the maintenance of approximate neutrality of charges in the pore and on the pore wall. In conclusion intra-vesicular pressure helps 'flushing-out' the transmitter, but the induced pressure 'drags-out' the water into the extra-cellular space.
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PMID:Glutamate, water and ion transport through a charged nanosize pore. 1701 22

Administration of N-carbamylglutamate (NCG), an analogue of endogenous N-acetyl-glutamate (an activator of arginine synthesis) has been shown to enhance neonatal growth by increasing circulating arginine levels. However, the effect of NCG on pregnancy remains unknown. This study examined the effects of NCG on pregnancy outcome and evaluated potential mechanisms involved. Reproductive performance, embryo implantation, and concentration of amino acids in serum and uterine flushing, were determined in rats fed control or NCG supplemented diets. Ishikawa cells and JAR cells were used to examine the mechanism by which NCG affects embryo implantation. Dietary NCG supplementation increased serum levels of arginine, onithine, and proline, as well as uterine levels of arginine, glutamine, glutamate, and proline. Additionally, it stimulated LIF expression, and enhanced the activation of signal transduction and activator of transcription 3 (Stat3), protein kinase B (PKB), and 70-kDa ribosomal protein S6 kinase (S6K1) during the periimplantation period, resulting in an increase in litter size but not birth weight. In uterine Ishikawa cells, LIF expression was also enhanced by treatment with arginine and its metabolites. In trophoblast JAR cells, treatment with arginine and its metabolites enhanced Stat3, PKB, and S6K1 activation and facilitated cellular adhesion activity. These effects were abolished by pretreatment with inhibitors of phosphatidylinositol 3-kinase (wortmannin) and mammalian target of rapamycin (rapamycin). The results demonstrate that NCG supplementation enhances pregnancy outcome and have important implications for the pregnancy outcome of mammalian species.
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PMID:N-carbamylglutamate enhances pregnancy outcome in rats through activation of the PI3K/PKB/mTOR signaling pathway. 2284 42


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