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)

A shortened histamine challenge test was used in a study of occupational airway disease. We evaluated the safety, defined as the absence of a decrease in forced expiratory volume in one second (FEV1) of greater than 40%. The occurrence of complaints, the repeatability of test results, and the average amount of time saved were measured. A standard protocol was used comprising 30 s tidal breathing with sequential doubling concentrations from 1 to 32 mg.ml-1 histamine. Subjects with no indication of hyperresponsive airways started at 4 mg.ml-1. If the decrease in FEV1 was < 6%, a concentration step was skipped (fourfold increase in concentration). The test was terminated when the decrease in FEV1 was at least 18%. A total of 697 subjects performed a test. All subjects with a provocative concentration of histamine producing a 20% decrease in FEV1 (PC20) value of < or = 4 mg.ml-1 (n = 16) started at the lowest concentration. Six subjects reached a > or = 20% decrease in FEV1 (range 21-24%) after a fourfold increase in concentration. Five subjects had a decrease in FEV1 of greater than 40%, and this decrease occurred after a doubling concentration. Cough, flushing, and chest tightness were noted in 18% of the subjects. In 56% of the tested subjects, the shortest provocation scheme (phosphate solution followed by 4, 16 and 32 mg.ml-1 histamine) was applied, resulting in a time reduction of nearly 50% per test, and reducing the time needed to complete the study from 5 to 3 months. The shortened test was repeatable within one concentration difference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use and safety of a shortened histamine challenge test in an occupational study. 765 44

The effects of initial lung flushing with intracellular and extracellular fluid type solutions were studied in lungs stored with the University of Wisconsin solution. Excised Sprague-Dawley rat lungs (n = 39) were flushed first with one of the following solutions: (1) the University of Wisconsin solution (K+ = 140 mmol/L), (2) modified (low potassium) University of Wisconsin solution (K+ = 20 mmol/L), (3) phosphate buffered saline solution (K+ = 3.9 mmol/L), (4) modified low-potassium phosphate-buffered saline solution (K+ = 20 mmol/L), (5) modified high-potassium phosphate-buffered saline solution (K+ = 40 mmol/L), and (6) Euro-Collins solution (K+ = 115 mmol/L) followed by secondary flush with storage solution and cold (4 degrees C) storage in University of Wisconsin solution for 24 hours. The lungs were then reperfused in the isolated, pulsatile, blood-perfused working lung system for 2 hours or until lung failure. Blood gas analysis and shunt fraction, aerodynamic parameters (airway resistance, lung compliance, elastic work, and flow resistive work), and total pulmonary vascular resistance were measured throughout the perfusion period. The mean oxygen tensions (in millimeters of mercury) at 30 minutes after the onset of reperfusion for University of Wisconsin solution, modified University of Wisconsin solution, phosphate-buffered saline solution, modified phosphate-buffered saline solutions (20 and 40 mmol/L), and Euro-Collins solution were 56.1 +/- 4.2, 72.7 +/- 9.1, 87.7 +/- 6.9 (p < 0.01 versus University of Wisconsin solution; p < 0.01 versus Euro-Collins solution), 86.0 +/- 9.6 (p < 0.01 versus University of Wisconsin solution; p < 0.01 versus Euro-Collins solution), 87.9 +/- 7.7 (p < 0.01 versus University of Wisconsin solution; p < 0.01 versus Euro-Collins solution), and 53.5 +/- 6.0, respectively. All aerodynamic parameters in the lungs flushed with extracellular fluid type solutions were superior to those flushed with intracellular fluid type solutions. We conclude that the efficacy of initial flushing was essential for successful lung preservation and that extracellular fluid type solutions were superior to intracellular fluid type solutions, at least for flushing the lung before storage with University of Wisconsin solution. Potassium concentration in flushing solution should be 20 mmol/L or less to obtain appropriate flushing and subsequent adequate distribution of the storage solution.
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PMID:Impact of initial flush potassium concentration on the adequacy of lung preservation. 777 73

Mn++ complexed to DPDP (N,N'-dipyridoxylethylenediamine-N,N'-diacetate-5,5'-bis(phosphate) generic name: mangafodipir), abbreviated MnDPDP, acts as an effective contrast enhancing agent for liver MRI. In clinical trials, a commonly reported side effect after i.v. administration of MnDPDP was facial flushing, most probably due to peripheral vasodilation. The present study was conducted to address possible mechanisms to explain the flushing effect. Nitric oxide is known to be stabilized in the presence of both uncomplexed and complexed Mn++ and this stabilization is probably due to the superoxide-scavenging properties of Mn++. The present study has demonstrated that both MnDPDP and MnCl2 relax phenylephrine precontracted bovine mesenteric artery strips in concentration-dependent manner. It was also found that a concentration of 10 microM MnDPDP, MnEDTA or MnCl2 gave approximately the same relaxation response as 0.1 microM acetylcholine. DPDP and EDTA had no appreciable intrinsic relaxation potential Mn(++)-induced relaxation was abolished when the endothelial layer was removed from the arteries. In addition, the Mn(++)-induced relaxation was attenuated by the nitric oxide synthase inhibitor N-nitro-arginine and the putative superoxide anion generator 6-anilino-5,8-quinolinedione, but not by the cyclooxygenase inhibitor indomethacin. Both N-nitro-arginine and 6-anilino-5,8-quinolinedione were found to induce an endothelium-dependent constriction of the bovine mesenteric artery strips. An approximately 2-fold increase in the intracellular concentration of cyclic GMP was detected after the addition of 10 microM MnDPDP or 0.1 microM acetylcholine. The increase in cyclic GMP coincided with the onset of relaxation and was effectively abolished by pretreatment with N-nitro-arginine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mangafodipir (MnDPDP)-and MnCl2-induced endothelium-dependent relaxation in bovine mesenteric arteries. 796 75

We studied the effect of Coenzyme Q10 (CoQ10) on lung preservation using an isolated rat lung reperfusion model. After the lung of a Wistar male rat was flushed with a solution consisting of 40 mM phosphate buffered saline, the heart-lung block was excised and immersed in the same solution at 10 degrees C for 6 hours. In experiment 1, CoQ10 was added to the flushing solution. In experiment 2, CoQ10 was injected i.v. 1 hour before the organ was harvested. After the preservation, both lungs were reperfused and ventilated for 30 minutes. No benefit was noted when CoQ10 was added to the flushing solution. However, when CoQ10 was pretreated one hour before harvesting, the lungs showed significantly better preservation in pulmonary artery pressure, airway pressure, gas exchange function and the wet/dry weight ratio than those of the control group. Thus, appropriate pretreatment of CoQ10 may have a beneficial effect on lung preservation.
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PMID:Effects of coenzyme Q10 on lung preservation: a study with an isolated rat lung reperfusion model. 814 2

Using 31P nuclear magnetic resonance spectroscopy, we compared the state of the high-energy phosphates in rabbit kidneys stored at 4 degrees C for 24 hr with 3 different solutions: Ringer (Rg), University of Wisconsin (UW), and Euro-Collins (EC) solutions. We found the highest phosphomonoester/inorganic phosphate (MP:Pi) ratio in the group of kidneys stored in the Rg solution (Rg, 0.93 +/- 0.04; UW, 0.36 +/- 0.02; EC, 0.28 +/- 0.02). This medium has been demonstrated in previous physiological studies to give poor results in terms of organ preservation compared to the solutions that mimic the "intracellular" fluid, such as the EC and UW solutions. Because the commonly used cold storage solutions contain phosphates, which superimpose on the intracellular Pi and, thus, can distort the results, we attempted to eliminate the contaminating solution around the kidney and in the vasculature by flushing the kidney with a phosphate-free solution (Rg). The MP:Pi ratio increased in the UW and EC groups (UW, 0.82 +/- 0.04; EC, 0.64 +/- 0.04) in identical proportion in the 2 groups. It remained highest in the Rg group (1.02 +/- 0.03). Comparisons of data before and after flush showed that external phosphate contamination was not predominant. There was no equilibrium in phosphate distribution between intra- and extracellular spaces at 24 hr of storage. We conclude that the validity of the MP:Pi ratio, as a viability index of renal transplant, might have to be restricted to comparisons of kidneys preserved in the same storage conditions. Therefore, it would be necessary to establish normal and pathological values of this ratio for each cold storage solution.
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PMID:The effect of technical conditions and storage medium composition on the phosphomonoesters to inorganic phosphate ratio determined by 31P nuclear magnetic resonance spectroscopy in rabbit kidney. 821 69

For lung transplantation the technique of flushing the donor pulmonary vascular bed may provide advantages in lung preservation such as rapid cooling and washout of blood. However, rapid cooling of the ischemic lung may also produce adverse effects. The aim of this study was to compare methods of cold flushing and topical cooling, and to evaluate the effect of temperature of the flushing solution on lung preservation. A total of 25 rabbit lungs were studied. Using an ex vivo rabbit lung model, postischemic function was assessed by the ability of the lung to oxygenate perfused blood and by measurement of pulmonary artery and airway pressures. The lungs in group I were preserved with simple immersion at 10 degrees C for 30 hours. The lungs in groups II through V were flushed with solution containing phosphate-buffered dextran (LPD) at different temperatures (groups II and IV, 10 degrees C; groups III and V, 23 degrees C) and stored at 10 degrees C for various ischemic periods (groups II and III, 30 hours; groups IV and V, 36 hours). Pulmonary vascular resistance during flushing at 10 degrees C was significantly higher than that at 23 degrees C (p < 0.001). Flushing resulted in better preservation than topical hypothermia. Flushing at 23 degrees C resulted in superior postischemic function compared with flushing at 10 degrees C. We conclude that in lung preservation, uniform flushing with LPD solution improves the ischemic tolerance as compared with topical hypothermia, and that flushing with solutions at too low temperatures may have adverse effects on lung preservation.
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PMID:Influence of temperature of flushing solution on lung preservation. 845 35

The analysis of hemodialysis (HD)-related bioincompatibility is focused mainly on phenomena observed in peripheral blood. However, since biocompatibility originates inside the dialyzer, white blood cells (WBC) adhering to the dialyzer are probably most subject to the influence of both dialyzer membrane and dialysate. In order to collect membrane-adherent cells, a reliable and reproducible elution technique was developed. After 3 h of HD, blood was returned to the patient with 0.9% NaCl. Then, dialyzers were eluted by recirculation of phosphate-buffered saline (PBS) or PBS/3 mM EDTA for 20 min, with or without prior flushing with 200 ml PBS. Finally, remaining adherent cells were collected by an afterwash with 10% trypsin. These solutions, as well as blood samples, were analyzed for WBC count, viability and differentiation. Random eluate samples were analyzed by flow cytometry, and the influence of elution on PMN activation was tested in a separate control experiment. WBC numbers decreased by flushing before elution, whereas cell numbers were maximal after elution with PBS/3 mM EDTA (30 x 10(6)). Trypsin afterwash resulted in a further yield of 12 x 10(6) cells. The eluates contained 81% PMN (blood 68%, p < 0.01), with a degranulated appearance, and only 12% lymphocytes (blood 21%, p < 0.05); cell viability in the eluates was > 95%. The eluted cells could be analyzed by flow cytometry, and the procedure itself induced only minimal PMN activation. In conclusion, a maximal number of adherent cells, consisting mainly of PMN, was obtained by direct elution with PBS/3 mM EDTA. The method itself did not induce marked PMN activation, and the cells obtained were suitable for further investigations, including flow cytometry.
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PMID:Ex vivo elution of hemodialyzers. An additional criterion for the assessment of bioincompatibility. 891 71

A sensitive and highly automated high-performance liquid chromatography (HPLC) column-switching method has been developed for the simultaneous determination of the active metabolite III and its prodrug II, both derivatives of the oral platelet inhibitor Ro 48-3657 (I), in plasma and urine of man and dog. Plasma samples were deproteinated with perchloric acid (0.5 M), while urine samples could be processed directly after dilution with phosphate buffer. The prepared samples were injected onto a pre-column of a HPLC column switching system. Polar plasma or urine components were removed by flushing the precolumn with phosphate buffer (0.1 M, pH 3.5). Retained compounds (including II and III) were backflushed onto the analytical column, separated by gradient elution and detected by means of UV detection at 240 nm. The limit of quantification for both compounds was 1 ng/ml (500 microl of plasma) and 25 ng/ml (50 microl of urine) for plasma and urine, respectively. The practicability of the new method was demonstrated by the analysis of about 6000 plasma and 1300 urine samples from various toxicokinetic studies in dogs and phase 1 studies in man.
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PMID:Oral platelet aggregation inhibitor Ro 48-3657: determination of the active metabolite and its prodrug in plasma and urine by high-performance liquid chromatography using automated column switching. 917 77

We gave miproxifene phosphate to six patients with recurrent breast cancer and to one patient with advanced breast cancer. This drug was orally administered at a daily dose of 20 mg in the morning, and serial blood samples were obtained just before the drug administration. Treatment was discontinued in 16 days in the patient with advanced breast cancer. Tumor response was 2 PR and 4 NC (3MR) with an efficacy rate of 29%. Adverse effects of grade 2, such as anorexia, nausea or vomiting and fatigue with grade 3 flushing and chilling were observed in the one patient with advanced breast cancer. This climacteric syndrome disappeared after cessation of administration. In one of the patients with recurrent breast cancer, a calf muscle cramp was observed. Steady plasma levels were observed in one week or two for miproxifene and in 2 to 8 weeks for desmethyl miproxifene, which were active metabolites of miproxifene phosphate. The half lives of these metabolites for disappearance were calculated in three patients. That of miproxifene was 27 to 36 hours and that of desmethyl miproxifene was 156 to 202 hours. Miproxifene phosphate is a promising drug for breast cancer, and the results of pharmacokinetics of active metabolites will suggest the time to obtain maximum efficacy and for it to disappear.
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PMID:[Steady state and disappearance of the metabolites of miproxifene phosphate in the treatment of breast cancer]. 972 50

Hypersensitivity reactions to etoposide are reported infrequently and consist of hypotension, hypertension, flushing, diaphoresis, dyspnea, bronchospasm, and loss of consciousness. A 23-year-old woman experienced acute bronchospasm, tachycardia, hypoxia, and moderate hypertension minutes after an infusion of etoposide was begun. Symptoms resolved within an hour after administration of intravenous fluids, methylprednisolone, diphenhydramine, and oxygen. Subsequently, the patient was given etoposide phosphate without incident. To our knowledge, this is the first report of successful rechallenge with etoposide phosphate after an acute hypersensitivity reaction to etoposide.
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PMID:Successful rechallenge with etoposide phosphate after an acute hypersensitivity reaction to etoposide. 1045 71


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