[Protective effect of thiopreperazine and of tranxenemic acid (AMCHA) on gastric vasomotor response induced by polymyxin B in the rat].
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Glial fibrillary acidic protein (GFAP)-positive astrocytes in preconfluent cultures derived from postnatal rat cerebellum have been previously shown to display two distinct morphologies, one stellate and the other irregularly epithelioid. The immunofluorescence studies described here showed that these cells also possess unique surface characteristics. In cultures derived from 8-day-old animals stellate cells bound the monoclonal antibody A2B5 whereas the epithelioid cells bound another monoclonal antibody against rat neural antigen-2 (RAN2). Some stellate cells derived from 2-day-old animals also bound tetanus toxin. The A2B5 labelling of the stellate cells made it possible to follow their fate in vitro. In confirmation of previous time-lapse studies, they underwent a shape transformation as confluence was approached, ultimately attaining a form resembling that of the epithelioid cells. Autoradiographic transport studies using two tritiated gamma-aminobutyric acid (GABA) analogues cis-1,3-aminocyclohexane carboxylic acid (ACHC) and beta-alanine revealed further differences between the two types of astrocytes. Whereas [3H]ACHC was taken up solely by the stellate cells [3H]beta-alanine was transported by both cell types. In other experiments in which various inhibitors of [3H]GABA transport were used ACHC virtually eliminated uptake into the stellate astrocyte, but had little effect on the epithelioid ones. The 'neuron-like' [3H]GABA transport process in the stellate astrocytes was confirmed in experiments comparing the effect of another compound which has been proposed as an astrocyte-selective GABA transport inhibitor, 4,5,6,7-tetrahydroisoxazolo-(4,5-C)pyridin-3-ol (THPO). No discrimination was found in its effect on the uptake of [3H]GABA into either neurons or stellate astrocytes. Further autoradiographic studies following the uptake of [3H]GABA by postnatal cerebellar slices showed that astrocytes in all layers of the cerebellar cortex and white matter transported [3H]GABA in contrast to the situation in culture where the amino acid is taken up predominantly by the stellate astrocytes. The possibility is discussed that the stellate astrocytes represent a population of cerebellar fibrous astrocytes whereas the identity of the epithelioid astrocytes is less certain.
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An automated high-performance liquid chromatographic method for the determination of gabapentin, 1-(amino-methyl)cyclohexaneacetic acid, in serum is described. The procedure involves protein precipitation with methanol followed by using a robotized derivatization with o-phthaldialdehyde reagent and automated high-performance liquid chromatography. The analog of gabapentin, 1-(aminomethyl)cycloheptaneacetic acid, was used as the internal standard. Blank serum was fortified with gabapentin (0.1-10.0 microg/ml) and internal standard. Separation was achieved on a Waters 5-microm reversed-phase column (10 cmx4.6 mm) with mobile phase consisting of 0.02 M phosphate buffer (pH 4.5)-acetonitrile (50:50, v/v). Eluents were monitored by fluorescence spectroscopy with excitation and emission wavelengths of 230 and 420 nm, respectively. The calibration curve for gabapentin in serum was linear (r=0.999) over the concentration range 0.1-10.0 microg/ml. The inter- and intraassay variations for three different gabapentin concentrations were < or =10% throughout. The lower limit of quantitation was found to be 0.1 microg/ml. Chromatography was unaffected by a range of commonly employed antiepileptic drugs or selected amino acids.
A double-blind study of the influence of systemic tranexamic acid on the central corneal thickness after cataract extraction was performed in 17 pairs of patients. Apart from the cataract, no were present. A sequential statistics was used to show that the increase in central corneal thickness after operation was significantly less in the tranexamic acid treated group than in the placebo group. There was no significant difference in intraocular pressure between the tranexamic acid and the placebo treated group. The possible influence of tranexamic acid on the thickness controlling mechanism of the cornea is discussed, and studies concerning the fibrinolytic system, the complement system and the aqueous humour amino acid treated patients are mentioned.
The effects of intravenous tranexamic acid were compared with placebo in 64 patients with subarachnoid hemorrhage. A double-blind procedure was used. One gram of tranexamic acid was given intravenously every 4 hours up to the time of operation on an intracranial arterial aneurysm or for up to 21 days after the first bleeding if operative treatment was not feasible. There were no differences in re-bleeds, morbidity or mortality between the tranexamic and placebo-treated groups. No thromboembolic complications were noted in either group. Our results do not support the use of tranexamic acid in subarachnoid hemorrhage in daily doses of 6 g.
Tranexamic acid (Cyklokapron, Kabi, Stockholm) in a dose of 10 mg per kg body weight was given i.v. to 17 patients at various intervals before operation on the knee joint, in order to elucidate the diffusion of the drug to the joint fluid and the synovial membrane. The acid diffused rapidly to both the above tissues, and in the joint fluid it reached the same concentration as in the serum. The biologic half-time in the joint fluid was about 3 hours. In the treatment of joint bleedings in hemophiliacs and in association with intra-articular operations on such patients tranexamic acid is a suitable supplement to conventional substitution therapy.
Tranexamic acid in a dose of 50 mg/kg b.w. was unable to alter the ellagic acid induced hypercoagulable state. No change in the hypercoagulability pattern was observed regardless of the time of administration of the compound (before or after the ellagic infusion). The silicone clotting times after the infusion of ellagic acid were markedly shortened and remained so for about 60 minutes. The results observed in two control groups treated with saline were similar. The euglobulin lysis times were clearly prolonged after the administration of tranexamic acid, whereas no changes were observed after the administration of saline. These results indicate that tranexamic acid has no anti-factor XII activity.
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