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At least 883 records · Page 49Linked to original sources
PubMed1985

Blood loss following dental extractions in anticoagulated rabbits: effects of tranexamic acid and socket packing.

The present study demonstrates the feasibility of chronic anticoagulation in rabbits and of estimating the resulting increase in blood loss following extraction of four front teeth from labeled red cell disappearance curves. This setup proved useful for the evaluation of hemostatic techniques. Socket packing with oxidized cellulose soaked in thrombin solution or local application of cyanobutylacrylate reduced early blood loss; oral administration of tranexamic acid reduced both early and late bleeding; the combination of socket packing and oral tranexamic acid completely abolished the excessive blood loss that resulted from anticoagulation alone.

Administration, Oral↗
PubMed1996

Comparison of the uptake of [3H]-gabapentin with the uptake of L-[3H]-leucine into rat brain synaptosomes.

1. Gabapentin is a novel anticonvulsant with an unknown mechanism of action. Homogenate binding studies described elsewhere have suggested that [3H]-gabapentin binds to a site in brain similar to the large neutral amino acid (LNAA) uptake site, termed system-L. 2. This study describes an investigation into the uptake of [3H]-gabapentin into a crude synaptosomal preparation from cerebral cortex of rat brain. Characterization studies showed that [3H]-gabapentin is taken up into synaptosomes by a system that is similar to that responsible for the uptake of L-[3H]-leucine. This system is sodium-independent, temperature-sensitive and requires ATP for function. 3. Kinetic studies of [3H]-gabapentin uptake produced a Michaelis constant (KM = 160 microM) similar to that observed for L-[3H]-leucine (KM = 110.3 microM). Vmax values were 837.1 pmol mg-1 protein min-1 and 2.192 nmol mg-1 protein min-1 respectively. 4. Gabapentin and L-leucine mutually inhibit their uptake. Lineweaver-Burke plots of these data demonstrate that inhibition occurs by a competitive mechanism. Further to this the Dixon transformation of the data illustrates that these two substrates share a common uptake site by the similarity between their calculated Ki and KM values (gabapentin inhibition of L-[3H]-leucine uptake: Ki = 160 microM; L-leucine inhibition of [3H]-gabapentin uptake: Ki = 262 microM). 5. Studies into the effect of gabapentin, the system-L-specific ligand 2-(-)-endoamino-bicycloheptane-2-carboxylic acid (BCH), and the system-A-specific ligand alpha-(methyl-amino)-isobutyric acid (MeAIB), on the initial rate of uptake of [3H]-glycine, L-[3H]-glutamate, L-[3H]-glutamine, and L-[3H]-leucine were performed. At 100 microM, gabapentin significantly inhibited initial rate of uptake of [3H]-glycine (29%), L-[3H]-glutamate (22%) and L-[3H]-leucine (40%). 6. Gabapentin is taken up into synaptosomes by a system similar to system-L, responsible for the uptake of large neutral amino acids. Gabapentin will also inhibit the uptake of certain excitatory amino acids in this synaptosomal preparation. The implications of these findings for the mechanism of action for gabapentin are unclear. The data presented here may suggest an intracellular site for mechanism of action for this compound. Similarly changes in levels of amino acid pools may be involved in the mechanism of gabapentin's anticonvulsant action.

Acetates↗
PubMed1980

Abruptio placentae--treatment with the fibrinolytic inhibitor tranexamic acid.

Abruptio placentae is known to have a bad prognosis for the fetus. Pathologic proteolysis, e.g. a pathologic activation of the coagulation mechanism and/or the fibrinolytic system is known to be a common complication in such cases. Analysis of the coagulation factors and components of the fibronlytic system in the acute stage of 14 cases confirmed the earlier finding of mainly an activation of the fibrinolytic system, which argues for the use of a specific inhibitor. 73 consecutive cases of abruptio placentae were treated with tranexamic acid in the acute stage. 67 of the patients were immediately delivered by cesarean section. The remaining six patients were in early gestational age and were treated for a prolonged period. The perinatal mortality of the entire group was only 8 per cent and the maternal mortality nil. None of the cases were complicated by hemorrhagic diathesis or thromboses. We believe that routine immediate treatment with tranexamic acid can reduce the perinatal mortality in cases of abruptio placentae.

Abruptio Placentae↗
PubMedDate not supplied

Spectrofluorimetric determination of vigabatrin and gabapentin in dosage forms and spiked plasma samples through derivatization with 4-chloro-7-nitrobenzo-2-oxa-1,3-diazole.

A highly sensitive and specific method is proposed for the determination of vigabatrin (I) and gabapentin (II) in their dosage forms and spiked human plasma. The method is based on coupling the drugs with 4-chloro-7-nitrobenzo-2-oxa-1,3-diazole in borate buffer at pH 7.1 and measuring the resulting fluorescence at 532 nm after excitation at 465 nm. The fluorescence intensity was a linear function of the concentration of the drugs over the ranges of 1.3-6.5 and 1.7-8.5 microg/mL for I and II, respectively. Minimum detectability values were 0.54 microg/mL (4.2 x 10(-6)M) and 0.97 microg/mL (5.7 x 10(-6)M) for I and II, respectively, under the described conditions. The proposed method was successfully applied to the determination of the 2 drugs in their dosage forms, and the percent recoveries +/- standard deviation (SD) were 104.53 +/- 1.2 and 100.00 +/- 1.32 of the label claim for I and II, respectively. The method was further applied to the determination of vigabatrin in spiked plasma samples. The percent recovery +/- SD was 101.58 +/- 2.68. Interference from endogenous alpha-amino acids was overcome through selective complexation with freshly prepared Cu(OH)2. The interference likely to be encountered from co-administered drugs, such as carbamazepine, cimetidine, clonazepam, clopazam, phenobarbital, valproic acid, and lamotrigine, was also studied. A reaction pathway is suggested.

Acetates↗
PubMed1985

Determination of plasma tranexamic acid using cation-exchange high-performance liquid chromatography with fluorescence detection.

A procedure is described for the determination of plasma tranexamic acid concentrations using cation exchange high-performance liquid chromatography with fluorescence detection following post-column derivatisation with omicron-phthalaldehyde. The chromatographic conditions were optimised with respect to detector performance and the method applied to measuring the plasma tranexamic acid levels of patients in a double-blind trial.

Chromatography, High Pressure Liquid↗
PubMed1997

Contrasting nutrient effects on the plasma levels of an amino acid-like antiepileptic agent from jejunal administration in dogs.

The absorption of gabapentin was investigated by monitoring drug plasma levels as a function of time following midjejunal administration in mongrel dogs. From previous work, dose-dependent absorption had been postulated to be a consequence of carrier-mediated transport and a paracellular pathway had been postulated to contribute to the passive absorption component in mammalian small intestine. The potential for amino acid inhibition of the carrier-mediated absorption component was investigated by drug coinfusion with leucine and phenylalanine. The potential for monosaccharide-enhanced increases in drug absorption was studied by drug coinfusion with D-glucose and 3-O-methylglucose. While lower drug plasma levels were observed with amino acid coinfusion versus controls in each of the dogs studied, mean area under the plasma level time curves (AUC) were not statistically significantly different (p < or = 0.07). Monosaccharide coinfusion significantly increased gabapentin AUC over control studies (p < or = 0.014) and over coinfusion with L-system amino acids (p < or = 0.0025). Implications for the mechanisms of intestinal absorption of this amino acid-like antiepileptic drug in this canine model are discussed.

Acetates↗
PubMed1973

Derepression of anthranilate synthase in purified minicells of Escherichia coli containing the Col-trp plasmid.

Purified minicells of Escherichia coli K-12 containing the plasmid Col-trp(+) or Col-trpA2 could be derepressed for the synthesis of anthranilate synthase, the first enzyme encoded in the trp operon. Non-plasmid-containing, deoxyribonucleic acid-deficient minicells could not be derepressed. Derepressed enzyme synthesis was initiated by l-tryptophan starvation. The kinetics of derepression were studied with minicells containing the Col-trpA2 plasmid. The derepression curves were biphasic with a rapid initial rate of enzyme synthesis followed by a slower rate of synthesis. The presence of l-tryptophan (20 to 50 mug/ml) or chloramphenicol (200 mug/ml) abolished enzyme synthesis. The presence of rifamycin SV (280 mug/ml) partially inhibited enzyme synthesis after at least 3.5 min of exposure. The ratio of minicell-to-cell synthetic capacity was 1:2.4 when compared on the basis of derepressed enzyme activity per unit cell volume. This work demonstrates that plasmid-containing minicells are capable of considerable functional protein and messenger ribonucleic acid synthesis and that the regulation of at least the trp operon is similar in minicells to that observed in cells.

Chloramphenicol↗
PubMed1993

Toxicokinetics and biological monitoring in experimental exposure of humans to gaseous hexahydrophthalic anhydride.

Six healthy volunteers were exposed to gaseous hexahydrophthalic anhydride (HHPA) concentrations of 10, 40, or 80 micrograms.m-3 (65, 260 or 520 nmol.m-3, respectively) for 8 h. The respiratory uptake of the inhaled HHPA was almost complete. Rapid increases in plasma and urinary levels of hexahydrophthalic acid (HHP acid) were seen. During the first 4 h after the end of exposure, the half-time of HHP acid in plasma was about 2 h. A corresponding decay was seen in urine. The correlations (r > 0.90) between the air concentrations of HHPA and the levels of HHP acid in plasma and urine were close. They were even closer (r > 0.96) when the total respiratory uptake of HHPA was used. Urinary pH adjustment by intake of ammonium chloride or sodium hydrogen carbonate did not significantly alter the excretion of HHP acid. The results show that the analysis of HHP acid in plasma or urine is useful as a biological monitor for exposure to HHPA.

Adult↗
PubMed1978

Effects of cicloxilic acid on CCl4-induced liver injury.

The effects of cis-2-hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) on the liver injury produced by carbon tetrachloride poisoning were studied in rats. It was found that oral treatment counteracts the CCl4-induced increase in liver weight, rise of liver triglycerides, fall of plasma triglycerides and rise of serum transaminase and ornithine carbamoyl transferase activities. Further, cicloxilic acid, when administered alone, altered none of the parameters studied. Cicloxilic acid was found to be more effective at the lowest doses than any of the other antihepatotoxic and choleretic drugs used. When cicloxilic acid was administered at the highest doses, the plasma triglyceride level of the intoxicated animals was not significantly different from that of the controls. To find out whether cicloxilic acid was effective in maintaining a normal lipoprotein secretion after CCl4 poisoning, experiments were carried out with Triton WR-1339. The results indicate that cicloxilic acid maintains the output of triglycerides from the liver to the plasma compartment at near-normal level in CCl4 poisoned rats. Possible mechanisms for the effects of cicloxilic acid on the CCl4-induced liver damage are discussed.

Animals↗
PubMed1981

Influence of tranexamic acid on tumour blood flow.

The influence on the intratumour blood flow distribution in a transplantable rat sarcoma by a potent antifibrinolytic drug, tranexamic acid, administered intraperitoneally for 3 or 10 days was studied by the intratumour distribution of intravenously injected 86Rb. A local Xenon clearance technique was used to study the direct effect of tranexamic acid on local tumour blood flow. local tumour blood flow and the intratumour blood flow distribution after administration of tranexamic acid for 3 days were unchanged compared to controls. Prolonged administration of tranexamic acid changed the intratumour blood flow distribution significantly towards low flow values. This might be one mechanism behind the inhibiting effect of tranexamic acid in tumour growth rate, previously observed in both experimental and clinical studies.

Animals↗
PubMed1990

Effect of helium and heliox on glutamate decarboxylase activity.

The activity of glutamate decarboxylase (GAD) in pure helium at 6.8 MPa was significantly enhanced when compared to GAD activity in air at 0.1 MPa (906 vs. 602 nmol.h-1.mg-1 protein, respectively). No significant difference was found between GAD activities in heliox at 6.8 MPa (0.87% O2 at 6.8 MPa) and in air at 0.1 MPa. On the other hand, the activities in heliox at 0.1 MPa (0.87% O2 at 0.1 MPa) and air at 0.1 MPa were significantly different (655 and 446 nmol.h-1.mg-1 protein, respectively). These data indicate that pressures up to 6.8 MPa do not affect the GAD-catalyzed synthesis of gamma-aminobutyric acid, but that the enzyme, as previously reported, is sensitive to low levels of oxygen.

Animals↗
PubMed1985

Effects of tranexamic acid on the conversion of Glu-plasminogen I and II to its Lys-forms.

Glu-plasminogen (Glu-plg) was incubated with plasmin. It took more than 2 hr incubation for the conversion of Glu-plg to a modified form (Lys-plg) to take place. Especially the conversion of Glu-plg II to Lys-plg II by plasmin took place very slowly. On the other hand, the conversion of Glu-plg I to Lys-plg I took place faster than that of Glu-plg II. In the presence of 1 mM tranexamic acid, the conversion of both Glu-plg I and II to their Lys-forms by plasmin was accelerated and completed in 30 min incubation. Fifty percent increase in the rate of the conversion of Glu-plg I to Lys-plg I was observed in the presence of 0.18 mM tranexamic acid. For the conversion of Glu-plg II to Lys-plg II, larger concentration of tranexamic acid was needed. Another observation was that tranexamic acid protected the degradation of plasminogen by plasmin, indicating the involvement of the lysine binding sites (LBS) of plasmin in the proteolytic attack against plg.

Catalysis↗