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Using a previously described technique, "in vitro" determinations were carried out for faecal fermentation (FF): basal faecal fermentation (BFF), i.e, only with faeces, with faeces and lactulose (LFF) and with faeces, lactulose and bismuth subsalicylate (BiLFF) in 34 patients with flatulence. The media+d.s. of the difference between the LFFand BFF levels (LFF-BFF) in patients with flatulence was significant and markedly higher than the respective media +d.s. in 30 normal control patients previously studied (9.1+4.7 vs. 3.9+3.2 ml gas/24 hrs; p<0.000001 respectively). And, although FF was reduced by adding bismuth salicylate in only 24% (70.6%) of the patients with flatulence but not in the remaining 10 (29.4%), in total the media+d.s. of the differences between the levels BiLFF and BFF (BiLFFBFF) was significantly lower that the media+d.s. of the differences between the LFF and BFF levels (LFF-BFF) (6.0+4.2 vs 9.1+4.7 ml gas/24 hrs; p<0.01 respectively). These results confirm that: 1) The fermentative capacity of the colonic bacteriae is most likely to be abnormally intense in peoples with flatulence and 2) Bismuth subsalicylate can be useful in the control of excessive colonic fermentation and flatulence; they raise, furthermore, the interesting possibility that we may have found the way to predict when the use of bismuth subsalicylate could be effective in the treatment of a patient with flatulence.

Aspirin reduces the size of infarcts after ischaemic stroke. Although this fact has been attributed to its antiplatelet actions, direct neuroprotective effects have been also reported. We have demonstrated that aspirin is neuroprotective by inhibiting glutamate release in "in vitro" models of brain ischaemia. A pharmacological dissection of the components involved, using cell cortical culture exposed to oxygen-glucose deprivation, indicated that aspirin selectively inhibits the increase in extracellular glutamate concentration which results from reversal of the glutamate transporter, a component of release which is due to ATP depletion. Moreover, the neuroprotection afforded by aspirin occurred in parallel to a lesser decay in ATP levels after OGD. Aspirin not only elevated ATP levels in intact cortical neurones, but also in isolated brain mitochondria. On the other hand, using a whole-animal model of permanent focal brain ischaemia (MCAO; middle cerebral artery occlusion), wed have also demonstrated that aspirin (30 mg/Kg i.p. administered 2 h before the occlusion) produced a significant reduction in infarct volume, effect that correlated with the inhibition caused by aspirin on ischaemia-induced increase in brain and serum glutamate concentrations after the onset of the ischaemia. Aspirin also inhibited ischaemia-induced decrease in brain ATP levels. Finally, clinical studies showed that prior treatment with aspirin was associated with a lower risk of neurological deterioration after acute ischemic stroke which was related to a reduction of glutamate release. Our present findings show a novel mechanism for the neuroprotective effects of aspirin, that takes place at concentrations in the antiaggregant-analgesic range, useful in the management of patients with risk of ischaemic events.

Introduction and Aims: The thrombotic process is a multicellular phenomenon in which not only platelets are involved but also neutrophils are involved. Recent in vitro studies performed in our laboratory have demonstrated that triflusal reduced platelet aggregation by stimulating nitric oxide (NO) production by neutrophils. The aim of the present study was to evaluate whether the in vivo treatment with triflusal could also modify the ability of neutrophils to produce NO. Furthermore, the role of NO released by neutrophils on platelet aggregation and secretion was also tested., Methods: The study was performed in 12 healthy volunteers of 32 +/- 6 years of age. The volunteers were treated with triflusal (600 mg/day) for 5 days and platelets and neutrophils were isolated before and after treatment. The ability of neutrophils to produce NO and the capacity of inhibiting platelet aggregation and secretion of transforming growth factor-beta (TGF-beta) were assessed., Results: After the treatment with triflusal we obtained the following results: a) an increase in NO production by neutrophils; b) potentiation of the inhibition of platelet aggregation by neutrophils, an effect that was reverted by incubating neutrophils with an L-arginine antagonist, L-NAME, and c) the presence of neutrophils reduced the release of TGF-beta by platelets measured as index of platelet secretion by a NO-independent mechanism., Conclusions: Triflusal (600 mg/day/5 days) stimulated NO production by neutrophils. After the treatment with triflusal, neutrophils inhibited both platelet aggregation and secretion. The antiaggregating effect of neutrophils was an NO-dependent mechanism while the inhibition of platelet secretion mediated by neutrophils after the treatment with triflusal was an NO-independent mechanism.

Background: Different antibiotics, antagonist H2 and others have been used for elimination and/or eradication of Helicobacter pylori., Aims: Evaluate elimination of Helicobacter pylori with amoxicillin, bismuth subsalicylate and ranitidine; and the improvement of recurrent abdominal pain., Method: 20 children with recurrent abdominal pain associated to gastritis and histologic identification of Helicobacter pylori were studied under a period of 18 months (January 1992 to June 1993), at Instituto Nacional de Pediatría, México, D.F. All children were treated simultaneously with: Amoxicillin, 15 days, plus ranitidine and bismuth subsalicylate for one month., Results: Helicobacter pylori was eliminated in 14 of 20 children studied. All these children had an important improvement of recurrent abdominal pain., Conclusion: Elimination of Helicobacter pylori and clinical improvement was present in 14 of 20 children studied (70%).

In order to study the in vitro behavior of the drug used according to our formula cultures of Trichophyton mentagrophytes. Trichophyton rubrum, Trichophyton verrucosum, Trichophyton tonsurans, Microsporum canis, Microsporum gallinae, Microsporum audouinii, Microsporum gypseum and Epidermophyton floccosum were prepared in order to prove its efficacy. It was found no growth in cultures to which the drug was added in different concentrations thus proving its efficacy as a fungistatic element. The inocula obtained were re-cultured in the same medium having no drug and no growth was evidenced; this would suggest its efficacy as a fungicide. This efficacy was proved for the different concentrations, that is, from the minimal coinentration (0.1 ml) up to the 1 ml concentration the drug disclosed fungicide power. The untreated controls which were recultured from the original strains grew according to their common development rhythm.

An investigation was done on the action in vitro of two pharmaceutical preparations containing Bi, De Nol and Pepto Bismol, on the fermentative capacity of intestinal bacteria. For the purpose, using an instrument and a technique previously described, fecal fermentation (FF) was measured in 21 stool samples, to which lactose was added to assure appreciable levels of fermentation. In 11 of the samples, FF was measured without and with addition of De Nol; and in the 10 remaining samples, without and with addition of Pepto Bismol. In 7 of the samples with which the action of De Nol was studied, this preparation significantly reduced FF from 10.9 not equal to 4.3 (mean not equal to s. d.) to 4.9 not equal to 5.0 ml of gas/24 h (p less than 0.02); on the contrary, in the 4 remaining samples, it increased FF, although not significantly, from 8.7 not equal to 4.8 to 16.7 not equal to 8.8 ml of gas/24 h (N.S.). Pepto Bismol significantly reduced FF, in all the 10 samples with which the action of that pharmaceutical - preparation was investigated, from 11.7 not equal to 6.1 to 3.0 not equal to 2.1 ml of gas/24 L (p less than 0.0001). A discussion was done on the possible mechanisms of the antifermentative action of Bi, as well as on the probable usefulness of De Nol and Pepto Bismol for the control of exaggerated intestinal fermentation and the flatulence it frequently causes.