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PubMed1976

Effects of calcium antagonist, 6-(N, N-diethylamino) hexyl-3, 4, 5-trimethoxybenzoate, on digitalis-induced arrhythmias and cardiac contractions.

6-(N, N-Diethylamino) hexyl-3, 4, 5-trimethylbenzoate (TMB-6) and lidocaine were equipotent (1 mg/kg) in the conversion of ectopic rhythms to normal rhythms in digoxin-toxic dogs. However, TMB-6 had fewer side effects on heart rates and dp/dt than lidocaine. TMB-6 inhibited the contractile force of electrically stimulated dog and guinea-pig atria and ventricles at concentrations ranging from 2.5 X 10(-5) to 1.7 X 10(-4) M. Elevation of extracellular Ca++ concentrations from 2.7 to 5.4 mM produced a significant increase in the ID50 of TMB-6 in atria (from 2.5 X 10(-5) to 5.0 X 10(-5) M in dogs and from 7.2 X 10(-5) to 1.0 X 10(-4) M in guinea pigs). TMB-6 (7.3 X 10(-5) to 2.4 X 10(-4) M) depressed the amplitude of Ca++-dependent action potentials in depolarized dog cardiac Purkinje fibers. These results are discussed with regard to the antagonism of TMB-6 on Ca++ availability in the myocardium which leads to the conversion of cardiac arrhythmias.

Action Potentials↗
PubMed1991

Cardiotonic drugs inhibit purified mammalian acetylcholinesterase.

Oxime- and non-oxime-related drugs, as well as cardiotonic drugs (CDs), have been used to treat the effects of organophosphorus (OP) poisoning. We conducted our experiments to determine what effects CDs may have on acetylcholinesterase (AChE), and how CDs interact with other treatment drugs as well as with OP-inhibited AChE. True AChE (EC 3.1.1.7) was purified from fetal bovine serum, and enzyme activity was measured according to Ellman et al. The CDs coumingine, cassaine, proscillaridin and convallatoxin were incubated with AChE at 550 microM at pH 7.6 and 25 degrees C. The CD ouabain was incubated with AChE at 500 microM. The CDs inhibited AChE by 97%, 89%, 10%, 7% and 6%, respectively. The mean AChE activities for these experiments, except for ouabain, were significantly different (P = 0.05) from their controls, as determined by the two-tailed Student's t-test. In a separate experiment, the oxime TMB-4.2Br (100 microM), which did not inhibit AChE, increased the inhibitory effect of proscillaridin from 4% to 11% (a 3.7-fold increase). When AChE was inhibited 39% with 37 nM VX, the addition of proscillaridin increased the inhibition to 51% (a 1.3-fold increase). When TMB-4 was added to the proscillaridin- and VX-inhibited AChE mixture, the inhibition decreased from 50% to 32% (a 0.37-fold decrease), whereas TMB-4 alone added to VX-inhibited AChE decreased the inhibition from 39% to 24% (a 0.38-fold decrease). The results show that TMB-4 increases the inhibition of AChE by proscillaridin. However, TMB-4 decreases the inhibition of AChE by VX and proscillaridin combined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Stability studies of bis(pyridiniumaldoxime) reactivators of organophosphate-inhibited acetylcholinesterase.

Relative stability studies of three organophosphate-inhibited acetylcholinesterase reactivators, 1-(2-hydroximinomethyl-1-pyridinium)-3-(4-carbamoyl-1-pyridinium)- 2-oxapropane dichloride (HI-6), 1,1'-methylenebis(4-hydroximinomethylpyridinium) dichloride (MMB-4), and 1,1'-trimethylenebis(4-hydroximinomethylpyridinium) dibromide (TMB-4) were carried out by semiquantitative TLC and NMR methods. TMB-4 appears to be the most, and HI-6 the least stable of the three compounds. The extent of hydrolysis of HI-6, MMB-4, and TMB-4 in 0.05 M, pH 7 phosphate buffer was approximately 50, 25, and less than 1%, respectively, after 20 d at room temperature. The hydrolysis products of HI-6 were identified by NMR and MS (electron impact) as 2-pyridinealdoxime, picolinamide, and isonicotinamide, whereas that of MMB-4 was identified as 4-pyridinealdoxime. The stability of these reactivators decreases with increasing pH. TMB-4 was stable under both neutral and basic conditions at room temperature. Deuterium exchange of the methylene protons of MMB-4 in D2O and of the protons at the 2- and 6-positions of the pyridinium ring of TMB-4 in NaOD/D2O were observed.

Acetylcholinesterase↗
PubMed1994

Conversion of lignin peroxidase compound III to active enzyme by cation radicals.

It has been previously reported that the catalytically inactive compound III form of lignin peroxidase is formed during the oxidation of certain chemicals such as phenols (P.J. Harvey and J.M. Palmer, 1990, J. Biotechnol. 13, 169-179). Here we provide evidence that the cation radicals of methoxybenzenes such as 1,2,4,5-tetramethoxybenzene (TMB) and veratryl alcohol promote the oxidative conversion of compound III back to ferric enzyme. Two kinetic phases were observed during the oxidation of TMB by lignin peroxidase. In the first phase the formation of TMB cation radical and compound III were observed simultaneously. The second phase involved a rapid disappearance of compound III and the TMB cation radical. Ferric enzyme appeared concomitantly with the disappearance of compound III. The TMB cation radical, generated electrochemically, was able to convert compound III to ferric enzyme. Comparative studies using veratryl alcohol were performed and supported the idea that the cation radical of these chemicals are capable of reactivating compound III. The significance of these reactions with respect to lignin peroxidase catalysis are discussed.

Anisoles↗
PubMed1984

Role of intracellular calcium in histamine release from rat mast cells.

Compound 48/80-induced histamine release may utilize both intracellular and extracellular calcium. The release is inhibited by La3+ and TMB-8 both in the presence and absence of calcium. The observations are consistent with a mobilization of calcium from the inner surface of the plasma membrane supporting the release. TMB-8 probably acts at more than one site. It has been shown to inhibit skeletal muscle contraction and this has been correlated to its inhibitory effect on the release of Ca2+ from the sarcoplasmic reticulum. TMB-8 also inhibits resting cellular influx and efflux of calcium in the ileum. Anaphylactic and dextran-induced histamine release is dependent on extracellular calcium; the inhibition of the release by TMB-8 seems to be primarily due to an interference with calcium transport across the plasma membrane. In the absence of extracellular calcium the inhibition of compound 48/80-induced histamine release by TMB-8 seems to be due to stabilization of Ca2+ binding to cellular stores.

Animals↗
PubMed1998

Ultrastructural and permeability features of microvessels in the olfactory bulbs of SAM mice.

The ultrastructural features of microvessels showing increased permeability to intravenously injected horseradish peroxidase (HRP) were examined in the olfactory bulbs of senescence-accelerated prone mice (SAMP8), which showed age-related deficits in learning and memory, and senescence-accelerated resistant mice (SAMR1), which did not show the age-related deficits. HRP was visualized with tetramethyl benzidine (TMB) and diaminobenzidine (DAB) for light and electron microscopic examination, respectively. In the olfactory bulbs of 13-month-old SAMP8 mice, the staining reaction with TMB for HRP appeared in the neuropil of central area (granule cell layer and subependymal layer), in the pia mater and in the vascular wall. Some vessels located in the central area showed several changes observed at the ultrastructural level. The cytoplasm of the endothelial cells, especially in the arterioles, was segmentally thickened and contained numerous vesicles and vacuoles, some of which were HRP positive. The endothelial cell surface was occasionally undulated with microvillous protrusions. Membranous inclusions within the basal lamina, suggesting the cellular (presumably pericytal) degeneration, were frequently observed, especially in venules. The collagen deposits were occasionally observed in the subendothelial space of some vessels. Perivascular cells with vacuolated inclusions or lipid-like droplets were present around some vessels in the central area of the olfactory bulbs of aged SAMP8 mice. On the other hand, in the microvessels located in the areas negative for HRP-TMB reaction, except the vessel walls, the cytoplasm of the endothelial cells with smooth luminal surface was flattened and some vesicles located there contained HRP-DAB reaction product. Weak staining reaction with TMB for HRP appeared also in the central area of the olfactory bulbs of 3-month-old SAMP8 mice and 3- and 13-month-old SAMR1 mice. The cytoplasm of the endothelial cells in the olfactory bulbs of these mice was focally thickened and contained some cytoplasmic vesicles. Occasionally, the endothelial cell surface was moderately undulated with few microvillous protrusions. Membranous inclusions within the basal lamina were not observed in these animals. These findings indicate that the endothelial cells and pericytes in some vessels located in the central area of the olfactory bulb of aged SAMP8 mice, which show staining reaction with TMB for HRP, are ultrastructurally changed, suggesting their altered functions.

Age Factors↗
PubMed1978

The activation by Ca2+ of platelet phospholipase A2. Effects of dibutyryl cyclic adenosine monophosphate and 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate.

Thrombin-induced release of arachidonic acid from human platelet phosphatidylcholine is found to be more than 90% impaired by incubation of platelets with 1 mM dibutyryl cyclic adenosine monophosphate (Bt2 cyclic AMP) or with 0.6 mM 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8), an intracellular calcium antagonist. Incorporation of arachidonic acid into platelet phospholipids is not enhanced by Bt2 cyclic AMP. The addition of external Ca2+ to thrombin-treated platelets incubated with Bt2 cyclic AMP or TMB-8 does not counteract the observed inhibition. However, when divalent cation ionophore A23187 is employed as an activating agent, much less inhibition is produced by Bt2 cyclic AMP or TMB-8. The inhibition which does result can be overcome by added Ca2+. Inhibition of arachidonic acid liberation by Bt2 cyclic AMP, but not by TMB-8, can be overcome by high concentrations of A23187. When Mg2+ is substituted for Ca2+, ionophore-induced release of arachidonic acid from phosphatidylcholine of inhibitor-free controls is depressed and inhibition by Bt2 cyclic AMP is slightly enhanced. The phospholipase A2 activity of platelet lysates is increased by the presence of added Ca2+, however, the addition of either A23187 or Bt2 cyclic AMP is without effect on this activity. We suggest that Bt2 cyclic AMP may promote a compartmentalization of Ca2+, thereby inhibiting phospholipase A activity. The compartmentalization may be overcome by ionophore. By contrast, TMB-8 may immobilize platelet Ca2+ stores in situ or restrict access of Ca2+ to phospholipase A in a manner not susceptible to reversal by high concentrations of ionophore.

Arachidonic Acids↗
PubMed1982

Requirements for different Ca2+ pools in the activation of rabbit platelets. I. release reaction and protein phosphorylation.

We examined the role of Ca2+, both extracellular and intracellular in origin, in the release reaction and protein phosphorylation in rabbit platelets stimulated with platelet activating factor (acetylglyceryl ether phosphorylcholine), thrombin, or ionophore A23187. In the presence of extracellular Ca2+, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), a putative antagonist of intracellular Ca2+ transport, blocked platelet activating factor-initiated serotonin release at a half-maximal inhibitor concentration of 40 microM, compared to 350 microM for thrombin-induced release and greater than 500 microM, for A23187-induced release. Platelet activating factor-induced phosphorylation of two platelet proteins of Mr = 41,000 (P7P) and 20,000 (P9P) was inhibited by TMB-8, an effect which was additive to that caused by removing extracellular Ca2+. TMB-8 demonstrated only minor to non-existent inhibitory effect on phosphorylation in thrombin- or A23187-stimulated platelets. In contrast to P9P phosphorylation, phosphorylation of P7P caused by platelet activating factor was more dependent on a TMB-8 sensitive step than on the availability of extracellular Ca2+. Experiments with buffers containing fixed concentrations of free Ca2+ revealed that both processes (release and phosphorylation), when stimulated by platelet activating factor and thrombin, had the same threshold requirement (1-3 microM) for extracellular free Ca2+. These studies provide evidence tht stimulation of rabbit platelets by platelet activating factor is more dependent on a TMB-8-sensitive intracellular Ca2+ source than is stimulation caused by thrombin. Furthermore, our data indicate that activation of different intracellular processes involved in platelet secretion (such as P7P and P9P phosphorylation) may require Ca2+ from different pools.

Animals↗
PubMed1982

Requirement for different Ca2+ pools in the activation of rabbit platelets II. Phospholipase activity.

The effects of extracellular Ca2+ concentration and the putative antagonist of intracellular Ca2+ movement, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) on platelet phospholipase activity and thromboxane B2 synthesis were examined in rabbit platelets stimulated by platelet activating factor, thrombin and ionophore A23187. TMB-8 markedly inhibited the platelets stimulated by platelet activating factor, thrombin and ionophore A23187. TMB-8 markedly inhibited the platelet activating factor-induced decrease in [14C]arachidonate content in platelet phosphatidylcholine and phosphatidylinositol, while showing minimal effects on thrombin-induced phospholipase activation. A23187 stimulation of these processes was inhibited to an intermediate degree by TMB-8. In contrast, extracellular Ca2+ removal inhibited phospholipase activity to a similar degree with all three stimuli. Moreover, the threshold concentration of extracellular Ca2+ for phospholipase activation, as measured by thromboxane B2 synthesis, was similar for platelet activating factor- and thrombin-stimulated platelets. These data provide evidence that, while platelet activating factor and thrombin may, to some extent, have similar requirements for extracellular Ca2+, they utilize a TMB-8 sensitive step to different degrees during activation of platelet phospholipase.

Animals↗
PubMed1994

Effect of trimebutine maleate on the contractile response of the isolated ileum from diabetic rats.

1. Tension of the isolated ileum from diabetic rats induced by streptozotocin was measured isometrically to study the mode of action of trimebutine maleate (TMB). 2. The hyperreactivity of contractile response to KCl was observed in the isolated ileum from diabetic rats. TMB inhibited the contraction induced by KCl and acetylcholine (ACh) in normal solution. 3. In Ca2+ free solution, the hyperreactivity of contractile response to KCl was attenuated, and TMB did not inhibit the contraction induced by KCl. In contrast, TMB inhibited the contraction induced by ACh even in Ca2+ free solution. 4. These results suggest that the hyperreactivity of contractile response to KCl in the ileum from diabetic rats is due to the enhancement of Ca2+ influx through voltage-dependent Ca2+ channel and that TMB inhibits the hyperreactivity of contractile response through the inhibition of Ca2+ movement by the cell.

Animals↗
PubMed2006

Pharmacokinetic and bioequivalence evaluation of two formulations of 100 mg trimebutine maleate (Recutin and Polybutin) in healthy male volunteers using the LC-MS/MS method.

BACKGROUND: Trimebutine maleate is a prokinetic agent that acts directly on the smooth muscle of the GI tract. A bioequivalence (BE) study of 2 oral formulations of 100 mg trimebutine maleate (TMB) was carried out in 24 healthy male Korean volunteers according to a crossover-randomized design. METHODS: Subjects were given a single dose of 2 100 mg tablets of each formulation. The test and reference formulations were Recutin (Hutax Co., South Korea) and Polybutin (Samil Co., South Korea), respectively. Each set of tablets was administered with 240 ml of water to subjects after 10 h overnight fasting on 2 treatment days separated by a 1 week washout period. After dosing, serial blood samples were collected for a period of 36 h. Plasma was analyzed for the main metabolite of TMB, N-monodesmethyl trimebutine (nor-TMB), by a validated LC with MS/MS detection capacity for nor-TMB in the range 5-1500 ng/ml, with a lower limit of quantification (LLOQ) of 5 ng/ml. Several pharmacokinetic (PK) parameters (including AUC(t), AUC(infinity), C(max), T(max), T(1/2), and K(e)) were determined from the plasma concentrations of nor-TMB of both formulations. AUC(t), AUC(infinity), and C(max) were tested for BE after log-transformation of the data. RESULTS: No significant difference was found based on ANOVA; 90% confidence intervals (98.98%112.03% for AUC(t); 98.60%-113.20% for AUC(infinity); 90.85%-107.87% for C(max)) for the test and reference were found within KFDA acceptance range of 80-125%. CONCLUSIONS: Based on these statistical inferences, it was concluded that Recutin is bioequivalent to Polybutin and can be used interchangeably in a clinical setting.

Adult↗
PubMed2005

Effect of methyl substitution of benzene on the percutaneous absorption and skin irritation in hairless rats.

The permeation rate and skin retention of benzene and methylbenzenes were assessed in vitro using hairless rat skin. The effects of unocclusive dermal exposures of these chemicals (15 microl every 2h for 8h a day for 4 days) on the transepidermal water loss (TEWL), erythema and skin histopathology were measured in CD hairless rats. The expression of IL-1 alpha and TNF-alpha in the skin and blood were measured at the end of dermal exposures. The flux of benzene was about 1.5-, 2.5- and 80-fold higher than toluene, xylene and tetramethyl benzene isomers (TMB), respectively, and the values were inversely correlated with molecular weight (r(2)=0.7455) and logoctanol-water partition coefficient (r(2)=0.7831). The retention of chemicals in stratum corneum (SC) was in the order of TMB>xylene>toluene approximately benzene. The TEWL and erythema data demonstrated that the irritation was in the following order: TMB>xylene>benzene. The histo-pathological examination showed that xylene and TMB induced granulocyte infiltration, swelling of the epidermis, and extensive disruption and damage of stratum corneum. Likewise, the expression of IL-1 alpha in the blood and TNF-alpha in the skin after dermal exposures was higher for TMB followed by xylene and benzene compared to control. In conclusion, the aromatic hydrocarbon chemicals induced cumulative irritation upon low-level repeat exposures for a 4-day period and the irritation increased with the number of methyl groups of benzene. The affinity of the chemical to SC and their gradual accumulation in the skin in the present study is the reason for the differences in the skin irritation profiles of different aromatic chemicals. Our ultimate goal is to develop a biologically based model that connects skin retention of chemical to the skin irritation response. The findings of the present study will be helpful in understanding the role of these chemicals in the jet fuel and various petroleum based fuels in inducing skin irritation response.

Animals↗
PubMed2000

A stable and highly sensitive 3,3',5,5'-tetramethylbenzidine-based substrate reagent for enzyme-linked immunosorbent assays.

3,3',5,5'-Tetramethylbenzidine (TMB) is a widely used chromogen for horseradish peroxidase-based detection systems because it yields reaction products with high absorption coefficients and lacks carcinogenicity. Unfortunately, TMB is labile and poorly soluble in aqueous buffers and such solutions must be freshly prepared before each experiment. Moreover, substrate depletion can occur under assay conditions. To overcome these problems we have developed a two-component TMB substrate system which has a lower detection limit and is more sensitive than many commercially available TMB reagents when compared in microtiter plate enzyme-linked immunosorbent assays. Both components of the substrate system are stable for at least 1 year at 4 degrees C and the usual discoloration of TMB stock solutions is prevented by the addition of a stabilizer that decomposes upon mixing of the two components.

Animals↗
PubMed1999

High-performance liquid chromatographic determination of trimebutine and its major metabolite, N-monodesmethyl trimebutine, in rat and human plasma.

A rapid, selective and very sensitive ion-pairing reversed-phase HPLC method was developed for the simultaneous determination of trimebutine (TMB) and its major metabolite, N-monodesmethyltrimebutine (NDTMB), in rat and human plasma. Heptanesulfonate was employed as the ion-pairing agent and verapamil was used as the internal standard. The method involved the extraction with a n-hexane-isopropylalcohol (IPA) mixture (99:1, v/v) followed by back-extraction into 0.1 M hydrochloric acid and evaporation to dryness. HPLC analysis was carried out using a 4-microm particle size, C18-bonded silica column and water-sodium acetate-heptanesulfonate-acetonitrile as the mobile phase and UV detection at 267 nm. The chromatograms showed good resolution and sensitivity and no interference of plasma. The mean recoveries for human plasma were 95.4+/-3.1% for TMB and 89.4+/-4.1% for NDTMB. The detection limits of TMB and its metabolite, NDTMB, in human plasma were 1 and 5 ng/ml, respectively. The calibration curves were linear over the concentration range 10-5000 ng/ml for TMB and 25-25000 ng/ml for NDTMB with correlation coefficients greater than 0.999 and with within-day or between-day coefficients of variation not exceeding 9.4%. This assay procedure was applied to the study of metabolite pharmacokinetics of TMB in rat and the human.

Animals↗
PubMed2006

Synthesis of large-pore micelle-templated silico-aluminas at different alumina contents.

The EPR spectra of radical surfactant probes embedded in cetyltrimethylammonium bromide (CTAB) and trimethylbenzene (TMB) stable water emulsions (TMB/CTAB = 13) were analyzed to provide information on the kinetics of formation of micelle-templated silicoaluminas (MTSA) at 343 K, obtained by means of silica and alumina, solved in alkaline solutions, at different Si/Al ratios. Textural (surface area, pore volume, pore size, surfactant content) and structural characterization of both as-synthesized and calcined MTSA were performed by means of nitrogen sorption isotherms, TEM, and chemical analysis. This analysis showed that TMB worked as a swelling agent of the CTAB micelles, providing large-pore homogeneous and stable MTSA at TMB/CTAB = 13 for Si/Al from infinity to 10. A demixing of the emulsion occurs at Si/Al < 10: at Si/Al = 7, a double wide-and-narrow pore structure was formed; then, at Si/Al = 5, an amorphous material was obtained. At Si/Al > or = 10, the computer-aided analysis of the EPR spectra as a function of the synthesis time indicated the distribution of the probes in two different environments: "micellar" probes inserted in the surfactant aggregates, whose mobility decreases over the synthesis time, thus reporting on the progressive modification of the surfactant aggregates structure and the solid condensation, and "interacting" probes due to probe-surfactant heads electrostatically interacting with the charged surface sites induced by alumina incorporation in the silica network. This last fraction increases its relative amount over the synthesis time, informing about the condensation and structuration of the MTSA. Without alumina, the "interacting" component is absent in the EPR spectra because TMB preferentially interacts with the surfactant headgroups by cation-pi interactions, thus preventing the interactions of these headgroups with silanols. When alumina is added, the negatively charged silicoaluminate at the surface promotes the interaction of the ammonium headgroups with the surface, and some Na+ cations also interact with TMB by cation-pi interaction and contribute to decreasing the interaction of the headgroups with TMB. Therefore, increasing alumina contents promote electrostatic interactions between the positively charged surfactant heads and the negatively charged silicoaluminate groups. The strong interaction of the surfactants with the silicoaluminate surface allows the formation of a monolayerlike structure of surfactant, which is not observed in the absence of alumina. The synthesis is slowed by increasing alumina contents due to a destructuration effect of alumina in the MTSA formation.

Journal Article↗
PubMed2006

Interaction of 2-(2'-pyridyl)benzimidazolyl derivative ligands with group 12 metal ions: coordination, structures and luminescence.

The coordination chemistry of the group 12 metal ions with two 2-(2'-pyridyl)benzimidazolyl derivative ligands 1,3,5-tris[2-(2'-pyridyl)benzimidazolyl]benzene (tmb) and 2-(2'-pyridyl)benzimidazolylbenzene (mb) has been investigated. The crystal structures of two coordination compounds (HgCl(2))(2)(tmb) and [Zn(mb)(2)(H(2)O)][ClO(4)](2) have been determined by single-crystal X-ray diffraction analysis which established the chelate bonding mode by the group 12 metal ions to the tmb or mb ligand. The luminescent response of tmb and mb toward group 12 metal ions, Zn(II), Cd(II) and Hg(II) has been examined by fluorescent titration experiments which established that the three group 12 metal ions have distinct luminescent response toward the tmb or mb ligand. The addition of the Hg(II) ion resulted in fluorescence quenching. In contrast, the addition of Zn(II) or Cd(II) led to a red shift and dramatic intensity increase of the emission spectrum of the ligand.

Journal Article↗
PubMed2004

A simple spectrophotometric method for the quantification of residual haemoglobin in platelet concentrates.

BACKGROUND AND OBJECTIVES: High levels of residual haemoglobin (Hb 0.1 g/l) are known to decrease the efficiency of pathogen-inactivation systems. We evaluated three separate methods to quantify Hb in platelet concentrates (PC). MATERIALS AND METHODS: Nine PC prepared in platelet additive solution (PASIII) (median platelet yield of 283 x 10(9)/unit, range 46-353) were spiked to known Hb concentrations with whole blood and the samples were measured by using each of three methods: the 3,3',5,5'-tetramethylbenzidine (TMB) oxidation method (Sigma Diagnostics, 527-A); the Harboe spectrophotometric method; and the HemoCue plasma low-Hb photometer (PLHP). RESULTS: The TMB and Harboe methods showed linear results compared to expected Hb (r2 > or = 0.981, P < 0.001) over the range tested (0.09-0.28 g/l) when the samples were haemolysed. The TMB method underestimated by an average of 6%, at and around 0.1 g/l Hb, compared to a 4% overestimation by the Harboe method and a threefold overestimation by the PLHP. The Harboe intra-assay coefficient of variation was < or = 1.85% across all concentrations, which contrasted with 30% at and around 0.1 g/l for the TMB method. CONCLUSIONS: The Harboe spectrophotometric method is convenient, safe, accurate and reproducible, and outperforms the TMB and PLHP methods for quantification of residual Hb in PC.

Blood Preservation↗
PubMed1987

Interactions of trimebutine with guinea-pig opioid receptors.

Affinities of trimebutine (TMB) and N-desmethyl trimebutine (NDTMB) for mu, delta and kappa opioid receptor subtypes have been examined using specific 3H-ligands and guinea-pig membrane. TMB and NDTMB showed a relative higher affinity for the mu receptor subtype although they were, respectively, 30- and 48-fold less active than morphine. The receptor selectivity index for mu, delta and kappa were 100:12:14.4 for TMB, 100:32:25 for NDTMB and 100:5:5 for morphine. The sodium shift ratio was 14 for TMB, 10 for NDTMB and 37 for morphine. These data show that (unlike morphine, a pure mu agonist) TMB and NDTMB can be classified as weak opioid agonists and confirm that peripheral opioid receptors mediate their gastrointestinal motility effects.

Animals↗