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At least 145 records · Page 8Linked to original sources
PubMed1986

Compliance of patients with asthma with an experimental aerosolized medication: implications for controlled clinical trials.

A Nebulizer Chronolog, a portable device that houses a standard nebulizer canister, was used in a unique method to measure compliance with aerosolized medication. Each actuation is tabulated to within 4 minutes of the actual time of usage and can subsequently be displayed in a day-hour-minute format. Of the 19 patients studied for 12 weeks with a cromolyn-like agent, appropriate usage four times a day ranged from 4.3% to 94.8%. Underusage exceeded overusage and ranged from 5.2% to 95% of the study days. Younger subjects and male subjects were less likely to use the aerosol appropriately. Patients failed to write the truth in their diaries with overreporting of appropriate usage more than 50% of the times. Lack of compliance with aerosolized medication represents an important medical issue for the physicians caring for patients with asthma. The Nebulizer Chronolog elicits new insight into the disparity between reported and observed compliance.

Adolescent↗
PubMed1984

Urothelial lesions in mice given 4-ethylsulfonylnaphthalene-1-sulfonamide, acetazolamide, and oxamide.

4-Ethylsulfonylnaphthalene-1-sulfonamide, acetazolamide and oxamide were administered in the diet to female BALB/c mice for varying periods of time from three to eighty weeks. All three compounds induced lesions in the urothelium. In the bladder, these included simple hyperplasia, nodular hyperplasia, inflammation and calculi. Similar lesions were observed in the ureter and urethra, along with a novel lesion, diverticulum, in the ureter. The diverticular lesions existed as down-growths of the transitional epithelium which often extended from the mucosa through the muscle layers to the adventitial surface. The etiology of the lesions appeared to be related to urinary physiological alterations (crystalluria, calculi, hypoosmolality) caused by administration of the compounds.

Acetazolamide↗
PubMedDate not supplied

Effects of lodoxamide on ischemic reperfused myocardium.

The beneficial effects of lodoxamide tromethamine (U42585E) have been examined in a canine model of myocardial ischemic injury. Lodoxamide was infused 20 mg/kg/h i.v. starting 30 min before occlusion of the proximal left circumflex coronary artery (LCX) and continuing through 90 min of ischemia. Lodoxamide produced a significant reduction in ultimate infarct size measured at 24 h by postmortem tetrazolium perfusion staining. Infarct size expressed as a percent of the anatomical area at risk was 21.7 +/- 2.7 in the treated group vs. 47.0 +/- 3.1 in the control group (mean +/- SEM). No significant difference in area at risk was observed between treated and control groups. Salvage occurred primarily in subepicardial and midmyocardial tissue without apparent lateral protection. Histological examination confirmed gross results of postmortem staining. The protection appeared to be unrelated to myocardial oxygen demand since no hemodynamic differences between groups were observed at the time of occlusion of throughout the 24-h experimental course. Concurrent studies of ex vivo platelet aggregation showed no effect of lodoxamide on adenosine diphosphate (ADP), collagen, and arachidonic acid-induced aggregation. In vivo antithrombotic effects were evaluated in four conscious dogs by inducing LCX thrombosis with low-amperage stimulation (50 microA for 24 h) of the intimal surface. Occlusive thrombi occurred in all four dogs and were similar to controls. These results suggest that lodoxamide reduces myocardial ischemic injury by a mechanism unrelated to oxygen demand or antiplatelet effects.

Amino Acids↗
PubMed1983

Oxalurate induction of multiple URA3 transcripts in Saccharomyces cerevisiae.

The URA3 gene from Saccharomyces cerevisiae is localized on a 1.1-kilobase (kb) DNA fragment. By using this fragment as a hybridization probe, we found that oxalurate, a gratuitous inducer of the allantoin degradative system, also serves to induce URA3 specific RNA. This response is restricted to oxalurate; other conditions which bring about high-level synthesis of the allantoin degradative enzymes did not produce the effect. Two classes of RNA (1.0 and 1.5 kb) were found to be oxalurate induced. Both classes are encoded by the URA3 gene, overlap, and probably do not significantly differ at their 5' termini. Northern blot mapping of the transcripts indicated that the 1.5-kb transcript was likely encoded by sequences extending up to 0.5 kb downstream from the 3' terminus of the 1.0-kb transcript. Analysis of the endpoints of the major 1.0-kb URA3 transcript by S1 nuclease mapping revealed the existence of two 5' termini, separated by 5 to 10 nucleotides, and seven 3' termini, separated by 5 to 20 nucleotides each, over a range of about 70 bases.

Amino Acids↗
PubMed1982

Inhibition of the adverse reaction to diethylcarbamazine in Dirofilaria immitis-infected dogs by lodoxamide ethyl.

Lodoxamide ethyl, a new oral anti-allergy drug, was tested for its ability to inhibit the post-treatment adverse reaction to diethylcarbamazine (DEC) in Dirofilaria immitis-infected dogs. Lodoxamide was highly effective, as judged by the absence of both overt signs and characteristic post-DEC changes in platelet numbers, serum fibrinogen level, and serum transaminase (SGOT, SGPT) levels, in blocking the reaction in dogs with a microfilaremia level that would make them moderately reactive. Lodoxamide was less effective in blocking the reaction in dogs with microfilaremias greater than approximately 10,000 mf/ml, a level which is regularly associated with a severe post-DEC adverse reaction. Some dogs with this level of microfilaremia were fully protected, others partially protected, and others were afforded no protection. Two other agents tested, indomethacin and homochlorocyclizine, were found to have comparatively little or no blocking activity.

Amino Acids↗
PubMed1988

Allopurinol and lodoxamide in complement-induced hepatic ischemia.

Intravascular complement activation with either zymosan or cobra venom factor (CVF) impairs hepatic blood flow. Oxygen radical scavengers given at the time of complement activation attenuate the resulting hepatic ischemia. It is not clear whether complement-stimulated phagocytes or transiently ischemic then reperfused endothelial and parenchymal cells generated the toxic oxygen radicals. In this study, a group of rats were given allopurinol (50 mg/kg/day postoperatively X 3 days plus 100 mg/kg iv at t = 0), a specific inhibitor of xanthine oxidase, prior to complement activation with CVF (20 units/kg iv at t = 30 and 60 min) to determine whether xanthine oxidase-derived oxygen radicals contributed significantly to the hepatic perfusion abnormalities. Additional rats received lodoxamide tromethamine (10 mg/kg iv bolus at t = 0 followed by 20 mg/kg/hr iv infusion), a novel and potent inhibitor of mast cell release and inhibitor of xanthine oxidase, prior to the same CVF challenge to determine whether mast cell mediators were involved in the flow disturbance. Thermodilution cardiac output, mean arterial pressure, heart rate, hematocrit, and effective hepatic blood flow (EHBF) by galactose clearance were determined at t = 2 hr. The percentage change in total hemolytic complement activity (% delta CH50) was determined between serum obtained prior to sacrifice and at t = 0. Systemic hemodynamics and HCT were for the most part unaffected regardless of pretreatment group or challenge with CVF or saline. CVF challenge produced a 25% reduction (P less than 0.05) in EHBF in vehicle-pretreated rats compared to saline challenge. Neither allopurinol nor lodoxamide tromethamine significantly improved EHBF when given prior to CVF challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1980

Protective effect opf lodoxamide tromethamine on allergen inhalation challenge.

Lodoxamide tromethamine (U-42,585E) is a new drug intended for prophylaxis of mast cell-mediated allergic disease. It is a water-soluble, cromolyn-like agent with demonstrated activity in rat peritoneal mast cell assay, rat percutaneous anaphylaxis (rat PCA) and sensitized rhesus monkey airway system. Ten allergen-sensitive asthmatics were pretreated with lodoxamide (0.01, 0.1, or 1.0 mg) or placebo, then challenged with serial dilutions of allergen extract. Analysis of allergen dose-response curve parameters shows that pretreatment with lodoxamide offers significant protection against experimental allergen-induced bronchoconstriction. At 0.01 mg, lodoxamide was effective in over half the subjects tested. Administration of lodoxamide by inhalation at doses of 0.1 and 1.0 mg uniformly allowed subjects to tolerate significantly larger doses of inhaled allergen. Side effects observed at these doses were minimal.

Adolescent↗
PubMed1985

Inhaled lodoxamide tromethamine in the treatment of perennial asthma: a double-blind placebo-controlled study.

The efficacy of lodoxamide tromethamine in the treatment of asthma was studied in a 16-week double-blind, placebo-controlled study of 68 perennial allergic subjects with asthma. Patients received either lodoxamide tromethamine, 0.25 mg four times daily, or placebo, administered by metered-dose inhaler. Response to treatment was assessed by analyzing changes in asthma symptoms, inhaled bronchodilator requirements, and pulmonary function when compared to a 2-week baseline period. Patients treated with lodoxamide tromethamine demonstrated an improvement in daytime breathing difficulty, cough, sputum production, and sleep (p less than 0.01 to 0.05), but improvement was not significantly different from that demonstrated by placebo-treated patients. Patients from both treatment groups were able to reduce their inhaled bronchodilators (p less than 0.01), but again no significant difference was apparent between lodoxamide tromethamine and placebo treatment, nor were there any differences in peak expiratory flow rate or FEV1 between the two groups. Seven patients who received lodoxamide tromethamine withdrew because of a sensation of heat and gastrointestinal symptoms. Thus, although lodoxamide tromethamine possesses potent mast cell-stabilizing activity in vitro, we have failed to demonstrate any useful long-term effect in the treatment of mild allergic asthma.

Adolescent↗
PubMed1989

Lodoxamide tromethamine prevents neutrophil accumulation in reexpansion pulmonary edema.

Reexpansion pulmonary edema (RPE) is an acute, unilateral lung injury initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils (PMNs); these toxic oxygen products appear to result from reoxygenation of chronically collapsed lung. Lodoxamide tromethamine (U-42585E) reduces infarct size after reperfusion of ischemic myocardium. The possible protective effects of lodoxamide in RPE were examined. Right lungs of rabbits were collapsed for 7 days by injection of air into the pleural space. Reexpansion was accomplished by chest tube with negative pressure in spontaneously ventilating rabbits. Twelve pairs of animals received either lodoxamide (20 mg/kg/h intravenously (i.v.) from 30 min before reexpansion until they were killed) or an equivalent volume of sterile saline. After 2 h, animals were killed by i.v. pentobarbital. Right and left lungs of six pairs of animals were lavaged with 25 ml saline each; the remaining six pairs of animals were studied by measurement of lung wet/dry weight ratio. Albumin concentrations in lavage fluid (BAL) of lodoxamide-treated animals were 243 +/- 165 micrograms/ml in right lung and 29 +/- 15 micrograms/ml in left lung (p less than 0.03); albumin concentration in right lung BAL of untreated animals was 1,180 +/- 319 micrograms/ml (p less than 0.02 vs. lodoxamide-treated animals). PMN percentages in right BAL (3.8 +/- 3.1) and left BAL (2.9 +/- 2.2) did not differ in lodoxamide-treated animals (p greater than 0.65); PMN percentage in right BAL of untreated animals was 18.7 +/- 2.9 (p less than 0.001 vs. lodoxamide-treated animals).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1983

A neuraminidase from Streptococcus sanguis that can release O-acetylated sialic acids.

The naturally occurring sialic acids can have different types of N- and O-substitutions, resulting in more than 20 known isomers and compounds. Most methods for the detailed study of these various sialic acids require that the molecules be first released from their alpha-glycosidic linkage. When mild acid hydrolysis is used for this purpose, significant destruction of O-substituent groups occur. On the other hand, the presence of O-substituent groups renders the sialic acid molecule partially or completely resistant to the action of the currently known neuraminidase. To circumvent this problem, we searched for a neuraminidase whose activity is not affected by O-substitution. We reasoned that because Streptococcus sanguis from the human oral cavity is continually exposed to O-substituted sialic acids, its extracellular neuraminidase might not be blocked by O-substitution. We therefore purified this enzyme 3100-fold (56% yield) using ammonium sulfate precipitation, N-(p-aminophenyl)oxamic acid-agarose affinity chromatography, and chromatography on quaternary aminoethyl (QAE)-Sephadex, sulfopropyl (SP)-Sephadex, and Sephacryl S-200. The purified preparation is free of other significant glycosidase activities and proteolytic activities. It is capable of quantitatively releasing all the O-acetylated sialic acids that we studied with the single exception of the 4-O-acetylated sialic acid of equine submaxillary mucin. The activity of the enzyme is also not restricted by the type pf sialic acid linkage or the nature of the underlying oligosaccharide. However, it has maximal activity on gangliosides only in the presence of detergents. The general properties of this enzyme are described and its substrate specificities are contrasted with those of the commonly used neuraminidase from Vibrio cholerae.

Animals↗
PubMed1974

Oxaluric acid: a non-metabolizable inducer of the allantoin degradative enzymes in Saccharomyces cerevisiae.

Saccharomyces cerevisiae degrades allantoin in five steps to ammonia, CO(2), and glyoxylate. Previously we demonstrated that allophanic acid, the last intermediate of the pathway, was required for induction of all five degradative enzymes. The data presented here indicate that oxaluric acid, an allophanate analogue, is capable of serving as a non-metabolizable inducer. Oxaluric acid brings about a high level of induction even in strains lacking urea carboxylase. Induction observed with parabanic acid was found to result from its spontaneous breakdown to oxaluric acid.

Allantoin↗
PubMed1985

Hepatic microvascular regulatory mechanisms. VI. Effects of lodoxamide tromethamine or phentolamine-HCl on early hemodynamic and glucoregulatory alterations evoked by endotoxin.

Initial changes in hepatic microvasculature and systemic arterial blood pressure were measured in non-fasted and anesthetized Sprague-Dawley rats receiving an i.v. infusion, or a topical application to the surface of the liver, of endotoxin (S. typhimurium) and/or phentolamine or lodoxamide. Circulating blood glucose and hepatic glycogen content were determined in infused rats. Injection of 10 mg per kg b.w. endotoxin, or topical administration of 10 micrograms endotoxin and/or antagonists, elicited no change in carotid (arterial) blood pressure. Infusion was accompanied by an elevation in blood glucose within 15 min and a decrease in hepatic glycogen content by 35 min. Injection of 1.0 mg per kg b.w. phentolamine blocked the endotoxin-induced hyperglycemia without affecting hepatic glycogenolysis. However, the alpha-adrenergic antagonist by itself provoked systemic hypotension, mild hypoglycemia, and hepatic glycogen depletion within 35 min. In vivo microscopy revealed that 10 micrograms endotoxin evoked immediate constriction of portal venules and periportal sinusoids. Vasoconstriction was accompanied by an increase in the percentage of microvascular segments containing decreased cellular blood flow velocity. These responses were blocked by 0.1 microgram lodoxamide but not by 100 micrograms phentolamine. The lodoxamide-induced inhibition was reversed by reapplication of 10 micrograms endotoxin 15 min following blockade. Given these results, it is suggested that (a) microvascular responses elicited by endotoxin were mediated by released constituents from intrahepatic mast cells and not by activation of alpha-adrenergic receptors, and (b) phentolamine blocked endotoxin-induced initial hyperglycemia by virtue of its hypoglycemic, glycogenolytic and/or hypotensive effects.

Amino Acids↗