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At least 127 records · Page 7Linked to original sources
PubMed1989

Improved survival from compound 48/80-induced lethal stress and inhibition of myocardial histamine and carnosine mobilization by lodoxamide.

The precise roles of carnosine and histamine in the physiologic response of the cardiovascular system to stress are unknown. We have previously shown in skeletal and cardiac muscle that carnosine serves as a histidine reservoir available for subsequent histamine synthesis following trauma and sepsis. This study was designed to quantify the effect of histamine-releasing and blocking agents on the myocardial carnosine-histamine pathway as well as on survival during severe stress. Four groups of mature (9-month-old) Sprague-Dawley rats were treated with either (1) saline, (2) lodoxamide (L, mast cell degranulation inhibitor), (3) compound 48/80 (a mast cell degranulator which causes stress), or (4) L followed by 48/80, and observed until agonal or the end of 30 min. When either endpoint was reached the animals were sacrificed and their hearts were removed for tissue analyses of histidine, histamine, 3-methylhistamine, and carnosine via high-pressure liquid chromatography. All five L-pretreated animals survived challenge with 48/80 while all five animals given 48/80 alone died (P less than .005). This mortality correlated well with the increase in the myocardial levels of histidine (P less than or equal to .0005), histamine (P less than or equal to .0077), and 3-methylhistamine (P less than or equal to .0004) and the decrease in carnosine (P less than or equal to .009) experienced by the animals treated with 48/80 alone in comparison to the control, L-only- and L + 48/80-treated groups. A protective effect of L was shown against the deleterious effects of 48/80 which is associated with prevention of myocardial carnosine mobilization to histidine and histamine. These data support the role of carnosine as a nontoxic myocardial histidine reservoir which is mobilized in response to stress-induced increases in histamine requirements.

Amino Acids↗
PubMed1978

Structure-activity correlations for a series of antiallergy agents. Oxanilic, quinaldic, and benzopyran-2-carboxylic acids.

Ab initio Hartree-Fock SCF calculations with the molecular fragment technique have been performed on several drugs which exhibit activity in the rat passive cutaneous anaphylaxis (PCA) assay. Representative molecules of the following types were included in the series: oxanilic acids, 1,4-dihydro-4-oxoquinaldic acids, and 4-oxo-4H-1-benzopyran-2-carboxylic acids. A quantitative relationship has been established between the observed biological activity and an electronic index obtained from the calculations. The correlation is rationalized in terms of charge-transfer stabilization of the drug-receptor complex.

Amino Acids↗
PubMed1981

Light and scanning electron microscopic studies of oxamide urolithiasis in rats.

The formation of urinary oxamide stones was induced in rats by feeding them oxamide mixed with powdered rat chow. The structure of these stones and the changes in the rat renal papillary structure following oxamide administration were studied using bright field and polarizing light microscopy as well as scanning electron microscopy. Oxamide appeared in the papillary collecting ducts, pelvis, ureters and urinary bladder of the rats in the form of yellow spherulitic units composed of dendritic crystals. Oxamide stones in turn were aggregates of these spherulites. Our results indicate the renal stone formation started with the crystallization of oxamide in the tubular lumina of the collecting ducts of the papillae. Crystal formation in the tubules was associated with epithelial necrosis. Some of the crystals became attached to injured epithelium, thus impeding urinary flow. The attachment of the crystals resulted in their retention in the renal tubules. These oxamide deposits then grew or aggregated to form stones. The formation of oxamide deposits in the ducts of Bellini resulted in dilatation, compression of the epithelium and destruction of the papillary urothelium. These factors resulted in the deformation of the papillary tip of the kidney.

Amino Acids↗
PubMed1985

Analysis of the variance components in a pharmaceutical aerosol product: lodoxamide tromethamine.

The contributions of several components to the variance in lodoxamide delivery from lodoxamide tromethamine metered-dose aerosol containers have been estimated. Two aerosol lots, manufactured with mean diameters of 2.3 and 7.2 micron, exhibited approximately equal variances. The variance was apportioned to the following components: container-to-container, 27%; mouthpiece-to-mouthpiece 18%; valve-to-valve, 11%; assay, 6%. The largest single contribution to the variance (38%) is attributed to unassignable variations which include within-container variations in the dose; quality improvement efforts should concentrate on this area. Little effort should be expended to minimize the assay, valve delivery, or mouthpiece variation as their contribution to lodoxamide dose variation is small. Likewise, the bulk drug particle size did not contribute appreciably to within-lot dose variation.

Aerosols↗
PubMed1980

Effect of iodoxamide ethyl on allergy skin tests.

Lodoxamide ethyl is a new cromolyn-like drug which prevents antigen-induced mediator release from mast cells and antigen-induced bronchoconstriction in sensitive animals and man. The purpose of this study was to determine the effect of a single administration of lodoxamide ethyl on allergy skin tests. The effect of this drug on allergy skin testing was studied in a double-blind design on ten adult subjects allergic to ragweed. Serial end-point titrations with short ragweed extract and with histamine were performed after a placebo and 1- and 3-mg capsules of lodoxamide ethyl. The immediate wheal-and-flare responses as well as the late allergic reaction were recorded. No statistically significant difference was found between lodoxamide ethyl and placebo in the suppression of the allergen-induced immediate wheal-and-flare response or the late allergic reaction. Furthermore, 1 and 3 mg of oral lodoxamide ethyl did not inhibit the histamine-induced cutaneous reactions.

Amino Acids↗
PubMed1975

Biosynthesis of the polyoxins, nucleoside peptide antibiotics: glutamate as an origin of 2-amino-2-deoxy-L-xylonic acid (polyoxamic acid).

The biosynthetic origin of the carbon skeleton of 2-amino-2-deoxy-L-xylonic acid (polyoxamic acid) is described. This aminoaldonic acid is the N terminus of the nucleoside peptide antibiotics, the polyoxins, produced by Streptomyces cacaoi var. asoensis. In vivo experiments concerning incorporation and distribution of radioactivity from a number of 14C-labeled compounds have clearly shown that the carbon skeleton of glutamate is a precursor for this aminoaldonic acid and sugars are incorporated only after their conversion into gluamate through the glycolytic and the tricarboxylic acid cycle pathways. Experiments utilizing [14C]-acetate and succinate have also indicated multiple passages through the Krebs cycle are operating before their incorporation into polyoxamic acid via glutamate. The distribution of 14C between C-1 and C-5 of polyoxamic acid from [5-14C]glutamate experiment has indicated that 40% of glutamate incorporated only after the reversible conversion into alpha-ketoglutarate followed by the passage through the Krebs cycle. Lack of incorporation of 3H in the [1-14C;2-3H]- and [5-14C;2-3H]glutamate experiments is discussed in terms of a reaction(s) between glutamate and polyoxamic acid.

Acetates↗
PubMed1987

Effects of lodoxamide tromethamine on paraplegia that occurs after infrarenal aortic occlusion in the rabbit.

The antioxidant lodoxamide tromethamine was assessed for effects on experimental spinal cord ischemia in the rabbit. Lodoxamide (20 mg/kg/hr) or 0.9% sodium chloride was infused beginning 15 minutes before infrarenal aortic occlusion and continuing for 105 minutes. With an occlusion time of 20 minutes, eight of eight lodoxamide-treated animals and five of eight saline-treated animals regained function after reperfusion. However, by 48 hours after occlusion, seven of eight saline-treated animals were completely paralyzed, whereas only two of eight lodoxamide-treated animals were paralyzed. An ischemia time of 30 minutes exceeded the protective capacity of this treatment. These results suggest lodoxamide may be useful in alleviating ischemic damage to the spinal cord.

Amino Acids↗
PubMed1975

The influence of polyglycolic acid (Dexon) on the formation of urinary calculi in rats fed with oxamide.

Rats fed with 2% oxamide diet were considered as a model for the patient with a tendency to stone formation. Polyglycolic acid (Dexon) sary stream caused formation of oxamide deposits in a percentage as high as that observed with silk sutures. A high degree of toxicity was observed with the chosen concentration of oxamide diet (weight loss, mortality). The importance of oxamide concentration is underlined for further experiments on the influence of suture material on urinary infection and stone formation.

Amino Acids↗
PubMed1984

Hepatic microvascular regulatory mechanisms. V. Effects of lodoxamide tromethamine or phentolamine-HCl on vascular responses elicited by serotonin.

Initial changes in hepatic microvasculature and carotid (arterial) blood pressure were measured in anesthetized Sprague-Dawley rats receiving an endoportal injection or topical application of serotonin alone, or in combination with selected doses of lodoxamide tromethamine or phentolamine-HCl. Although infusion of 1.0 microgram per 100 g b.w. serotonin and/or 10 micrograms per 100 g b.w. lodoxamide produced no change in arterial blood pressure, 10 or 20 micrograms per 100 g b.w. serotonin evoked hypotension within 40 sec. During this period, in vivo microscopy of transilluminated livers revealed that 1.0 or 10 micrograms per 100 b.w. serotonin elicited constriction of portal venules and sinusoids, and a significant increase in the percentage of these microvessels containing decreased cellular flow. None of these responses was antagonized by 10 micrograms per 100 g b.w. lodoxamide. Topical application of 1.0, 10, or 20 micrograms serotonin provoked constriction of sinusoids and decreased sinusoidal and central venous perfusion, but no systemic hypotension. There was no significant difference in the magnitude of responses to these doses of serotonin alone or with 0.1 microgram lodoxamide; however, 100 micrograms phentolamine potentiated responses to 1.0 microgram serotonin. Given these results, and those of previous studies indicating that equivalent doses of these antagonists block mast cell degranulation or catecholamine-induced activation of alpha receptors, it is suggested that the vascular responses are mediated directly by serotonin and not indirectly by serotonin-evoked mast cell degranulation or alpha-adrenergic stimulation. The vascular receptor(s) triggered remain(s) to be elucidated.

Amino Acids↗
PubMed2004

Identification of the catalytic residues involved in the carboxyl transfer of pyruvate carboxylase.

To clarify the mechanism of carboxyl transfer from carboxylbiotin to pyruvate, the following conserved amino acid residues present in the carboxyl transferase domain of Bacillus thermodenitrificans pyruvate carboxylase were converted to homologous amino acids: Asp543, Glu576, Glu592, Asp649, Lys712, Asp713, and Asp762. The carboxylase activity of the resulting mutants, D543E, E576D, E576Q, E592Q, D649N, K712R, K712Q, D713E, D713N, D762E, and D762N, was generally less than that of the wild type from mutation, but it decreased the most to 5% or even less than that of the wild type with D543E, D576Q, D649N, K712R, and K712Q. The decrease in activity observed for Asp543, Asp649, and Lys712 mutants was not for structural reasons because their structures seemed to remain intact as assessed by gel filtration and circular dichroism. On the basis of these data, a mechanism is proposed where Lys712 and Asp543 serve as the key acid and base catalyst, respectively.

Acetyl-CoA Carboxylase↗
PubMed1979

The effect of lodoxamide ethyl [diethyl N,N'-(2-chloro-5-cyano-m-phenylene)dioxamate] on in vivo anaphylactic reactions.

Orally administered iodoxamide ethyl (U-42,718) inhibited anaphylactic reactions in a dose-related manner in the following test animals: (1) in the rat PCA reaction, excellent activity (75% inhibition at 0.1 mg/kg) was seen with a duration of activity of 30 min, (2) In the ascaris-sensitive primate (45% inhibition at 1.0 mg/kg) in lung parameters related to increased resistance and decreased compliance which persisted for up to 3 h, and (3) 50 mg/kg protected guinea pigs, sensitized to egg albumin, from lung function changes. Activity in these animal systems indicates that this orally active drug may hold promise in clinical asthma.

Aerosols↗
PubMed1981

Inhibition of oxidative enzymes by anti-allergy drugs.

Lodoxamide tromethamine and several other anti-allergy drugs, i.e. inhibitors of rat passive cutaneous anaphylaxis, are inhibitors of purified xanthine oxidase. Inhibition is noncompetitive with Ki's in the 1-13 micromolar range. Lodoxamide tromethamine had no effect on another flavoprotein, glucose oxidase. Other studies have shown several of these drugs are inhibitors of aldose reductase. It is speculated that the anti-allergy drugs inhibit mediator release from mast cells by blocking univalent electron transfers which are essential for release.

Aldehyde Reductase↗