Bioflora probiotic in immunomodulation and prophylaxis of intestinal bacterial translocation in rats.

UNLABELLED: The immunomodulator effect of Bioflora probiotic on T (CD4+) and B (CD20) lymphocytes in gastrointestinal mucosa and intestinal bacterial translocation was studied using Wistar rats (n = 10 per group). Two experiments were used: (I) stress with immobilization and water immersion at 22 degrees C for 7 h plus the application of indomethacin (Indo) 10 mg/kg SC every 24 h for 3 days (comparator group), and (II) stress experiment I with the addition of 1 mL of Bioflora applied through a orogastric tube every 12 h for 3 days. At the 4th day, in asepsis, a dissection laparotomy of liver, spleen, mesenteric lymphatic nodes, and cecum was performed for microbiological culture, and stomach, ileum, and colon were also dissected for immunohistochemical and quantification of CD4+ and CD20. Findings in experiment I revealed cecum bacterial overdevelopment of 6 x 10(10) +/- 2.3 x 10(9) colony-forming units (CFU) (P < 0.01) and positive cultures in liver, spleen, and all mesenteric lymphatic nodes. On the other hand, in the group treated with Probiotic Bioflora, cecum without overdevelopment (3 x 10(6) +/- 1.3 x 10(5) CFU), negative cultures in liver and spleen, and in lymphatic nodes two positive and eight negative cultures for E. coli and P. vulgaris (P < 0.01) were observed. Immunohistochemistry revealed a relevant increase of T lymphocytes (CD4+) in ileum and colon. CONCLUSIONS: Bioflora probiotic was shown to be an intestinal immunomodulator that induced increased T (CD4+) lymphocytes that also offer prophylaxis of intestinal bacterial translocation in a stressed rat model.

[Mechanism of inhibition OF COX-2 and COX-3 in gastrointestinal damage induced by NSAID in rats ]. / Mecanismo inhibidor COX-2 y COX-3 en el daño gastrointestinal inducido por AINEs, en ratas.

In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.

Mecanismo inhibidor COX-2 y COX-3 en el daño gastrointestinal inducido por AINE en ratas / Mechanism of inhibition OF COX-2 and COX-3 in gastrointestinal damage induced by NSAID in rats

In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.(AU)

Mecanismo inhibidor COX-2 y COX-3 en el daño gastrointestinal inducido por AINE en ratas / Mechanism of inhibition OF COX-2 and COX-3 in gastrointestinal damage induced by NSAID in rats

In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.

Mecanismo inhibidor COX-2 y COX-3 en el daño gastrointestinal inducido por AINEs, en ratas. / [Mechanism of inhibition OF COX-2 and COX-3 in gastrointestinal damage induced by NSAID in rats ]

In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.

[Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats]. / Dexketoprofeno. Aine preferencial inhibidor COX-1, sin lesión gastrointestinal, en ratas.

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition.

Dexketoprofeno: aine preferencial inhibidor COX-1, sin lesión gastrointestinal, en ratas / Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition

Dexketoprofeno: aine preferencial inhibidor COX-1, sin lesión gastrointestinal, en ratas / Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition (AU)

Dexketoprofeno. Aine preferencial inhibidor COX-1, sin lesión gastrointestinal, en ratas. / [Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats]

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition.

Gastrointestinal damage induced by celecoxib and rofecoxib in rats.

Five experimental models were developed in different groups of Wistar rats (N = 15) to study selective COX-2-inhibitor NSAIDs such as celecoxib and rofecoxib, as follows: (1) dose-dependent oral Celecoxib and Rofecoxib for 5 days, and 24 hr after oral indomethacin; (2) Same as 1 but subcutaneously; (3) gastric ulcer induced by glacial acetic acid; (4) duodenal ulcer induced by cysteamine; and (5) stress by immobilization and immersion in water at 15 degrees C for 6 hr. Celecoxib and Rofecoxib, either orally or subcutaneously, did not produce necrotic lesions in healthy gastrointestinal mucosa (0%), showing normal histology. In contrast, previously indomethacin-induced lesions were aggravated (90%, P < 0.001). Total necrosis in the small intestine as well as increased ulcers and perforation of gastric and duodenal ulcers induced by acetic acid and cysteamine were observed. There was also aggravation of the necrotic gastric area in stress (60-90%, P < 0.05). Celecoxib and rofecoxib showed neutrophilia (5000/mm3) similar to that with indomethacin. In contrast, there was no leukocyte infiltration in the gastric múcosa; thus, we can consider it a selective COX-2 NSAID. In conclusion, celecoxib and rofecoxib at doses causing COX-2 but not COX-1 inhibition did not produce toxic lesions in healthy gastrointestinal mucosa, yielding a broad therapeutic margin. In contrast, when administered in altered gastrointestinal mucosa, they aggravated and complicated gastric ulcers as well as necrosis in the small intestine, consequently restricting their clinical use.

[Celecoxib vs indomethacin and acute gastric lesions in rats]. / Celecoxib vs indometacina y lesiones gástricas agudas en ratas.

In 5 random groups of Wistar rats (n = 15 for each group), ulcerogenic doses of NSAIDs COX-1-COX-2 inhibitors such as indomethacin were compared with Celecoxib (COX-2 inhibitor); the production of antrum gastric ulcers and bowel and colon necrotic areas was studied. Celecoxib was given each 12 hs orally and subcutaneously during 5 days and gastrointestinal lesions were not found; in contrast, Celecoxib given after indomethacin aggravated antrum gastric ulcers (p < 0.001); intestinal massive necrosis and death were observed in all the rats. We conclude that Celecoxib does not induce gastrointestinal lesions in healthy mucosa; in contrast, Celecoxib amplifies the gastrointestinal lesions induced by indomethacin.

In vivo selectivity of nonsteroidal antiinflammatory drugs and gastrointestinal ulcers in rats.

The aim of the present work was to study in vivo COX-2-COX-1 selectivity of 16 nonsteroidal anti-inflammatory drugs (NSAIDs) in equipotent ulcerogenic doses in two in vivo experimental models. Indomethacin, ibuprofen, nimesulide, aceclofenac, aspirin, sodium diclofenac, meloxicam, naproxene, paracetamol, piroxicam, tenoxicam, nabumetone, ketoprofen, mefenamic acid, etodolac, and ketorolac were administered to female Wistar rats (N = 10 each group). In experiment I, solid food plus subcutaneous NSAIDs were given. In experiment II, NSAIDs were given by oral gavage and in bolus. Macroscopic gastric antral ulcer area (30%) and intestinal erosiva area (295 mm2) in experiment I and necrotic gastric fundus area (65%) and erosive intestinal area (182 mm2), "in vivo" the NSAIDs COX-1 was showed. Neutrofilia assessed in gastric intestinal mucosa where also ibuprofen and paracetamol not given neotrophilic infiltration. In conclusion, COX-2-COX-1 selectivity was demonstrated in vivo with the drugs aceclofenac, nabumetone, meloxicam, nimesulide, and paracetamol.

[Gastrointestinal damage induced by celecoxib and rofecoxib in rats]. / Daño gastrointestinal inducido por celecoxib y rofecoxib, en ratas.

UNLABELLED: Five experimental models were carried out in different groups of Wistar rats (n = 15) in order to study selective (cyclo-oxygenase) COX-2 non-steroid antiinflammatory inhibitors, such as celecoxib and rofecoxib, as follows: 1) Dose-dependent oral celecoxib and rofecoxib for 5 days, and 24 hours after oral indomethacin. 2) Same as 1, but subcutaneously. 3) Gastric ulcer induced by means of glacial acetic acid. 4) Duodenal ulcer induced by means of cysteamine. 5) Stress due to being kept under restraint and immersion in water at 15 degrees C for 6 hours. Celecoxib and rofecoxib, either orally or subcutaneously, did not produce necrotic injuries in healthy gastrointestinal mucosa (0%), showing normal histology. On the other hand, the injuries previously induced by indomethacin worsened (90%, p < 0.001). Total necrosis of small intestine as well as increased ulcer and perforation of gastric and duodenal ulcers induced by acetic acid and cysteamine were observed. There was also worsening of gastric necrotic area with stress (60-90%, p < 0.05). Celecoxib and rofecoxib showed neutrophilia (5,000/mm3) similar to that presented by indomethacin, but there was no leukocyte infiltration in the gastric mucosa; thus we can consider it a COX-2 selective NSAID (non-steroidal anti-inflammatory drug). CONCLUSION: Dose-dependent administration of celecoxib and rofecoxib as COX-2 inhibitors and non-COX-1 inhibitors, respectively, did not produce toxic injuries on healthy gastrointestinal mucosa, thus providing a broad therapeutic spectre. On the other hand, when administered in presence of altered gastrointestinal mucosa, they worsened and complicated gastric ulcers, and also induced necrosis in the small intestine, thereby restricting their clinical use.

Daño gastrointestinal inducido por celecoxib y rofecoxib, en ratas / Gastrointestinal damage induced by celecoxib and rofecoxib in rats

En diferentes grupos de ratas Wistar (n=15), se estudiaron AINEs inhibidores selectivos de la COX-2, como delecoxib y refecoxib, en cinco modelos experimentales: 1) Celecoxib y rofecoxib por vía oral y dosis dependiente durante 5 días y 24 hs. Después de indometacina oral. 2) Similar a 1, pero subcutáneo. 3) Ulcera gástrica inducida por ácido acético glacial. 4) Ulcera duodenal por cisteamina. 5) Estrés por inmovilización e inmersión en agua a 15 grados Celsius durante 6 horas. Celecoxib y rofecoxib por vía oral o SC en mucosa gastrointestinal sana no provaron lesiones necróticas en una superficie del 0 grados Celsius, presentanto histología normal; en cambio, agravaron y complicaron lesiones inducidas en forma previa por indometacina en más del 90 por ciento (p<0,001), con necrosis masiva del intestino delgado, así como ampliaron y causaron perforaciones en las úlceras gástricas y duodenales inducidas por ácido acético y cisteamina. Se produjo asimismo agravación de la zona necrótica gástrica por estrés en un 60-90 por ciento (p<0,05). Celecoxib y rofecoxib condujeron a una neutrofilia de 5000/mm3, similar a la inducida por la indometacina; en cambio, no produjeron infiltración leucocitaria en mucosa gástrica (MPO), siendo un marcador de AINE selectivo COX-2. Se concluyó que celecoxib y rofecoxib, administrados en dosis dependiente como inhibidores de COX-2 y no COX-1, no provocaron en mucosa gastrointestinal sana ninguna lesión por toxicidad, observándose un amplio margen terapéutico. En cambio, suministrados en mucosa gastrointestinal dañada agravaron y complicaron las lesiones ulcerosas gástricas y necróticas intestinales, limitando su uso en clínica.

Daño gastrointestinal inducido por celecoxib y rofecoxib, en ratas / Gastrointestinal damage induced by celecoxib and rofecoxib in rats

En diferentes grupos de ratas Wistar (n=15), se estudiaron AINEs inhibidores selectivos de la COX-2, como delecoxib y refecoxib, en cinco modelos experimentales: 1) Celecoxib y rofecoxib por vía oral y dosis dependiente durante 5 días y 24 hs. Después de indometacina oral. 2) Similar a 1, pero subcutáneo. 3) Ulcera gástrica inducida por ácido acético glacial. 4) Ulcera duodenal por cisteamina. 5) Estrés por inmovilización e inmersión en agua a 15 grados Celsius durante 6 horas. Celecoxib y rofecoxib por vía oral o SC en mucosa gastrointestinal sana no provaron lesiones necróticas en una superficie del 0 grados Celsius, presentanto histología normal; en cambio, agravaron y complicaron lesiones inducidas en forma previa por indometacina en más del 90 por ciento (p<0,001), con necrosis masiva del intestino delgado, así como ampliaron y causaron perforaciones en las úlceras gástricas y duodenales inducidas por ácido acético y cisteamina. Se produjo asimismo agravación de la zona necrótica gástrica por estrés en un 60-90 por ciento (p<0,05). Celecoxib y rofecoxib condujeron a una neutrofilia de 5000/mm3, similar a la inducida por la indometacina; en cambio, no produjeron infiltración leucocitaria en mucosa gástrica (MPO), siendo un marcador de AINE selectivo COX-2. Se concluyó que celecoxib y rofecoxib, administrados en dosis dependiente como inhibidores de COX-2 y no COX-1, no provocaron en mucosa gastrointestinal sana ninguna lesión por toxicidad, observándose un amplio margen terapéutico. En cambio, suministrados en mucosa gastrointestinal dañada agravaron y complicaron las lesiones ulcerosas gástricas y necróticas intestinales, limitando su uso en clínica. (AU)

Daño gastrointestinal inducido por celecoxib y rofecoxib, en ratas. / [Gastrointestinal damage induced by celecoxib and rofecoxib in rats]

Five experimental models were carried out in different groups of Wistar rats (n = 15) in order to study selective (cyclo-oxygenase) COX-2 non-steroid antiinflammatory inhibitors, such as celecoxib and rofecoxib, as follows: 1) Dose-dependent oral celecoxib and rofecoxib for 5 days, and 24 hours after oral indomethacin. 2) Same as 1, but subcutaneously. 3) Gastric ulcer induced by means of glacial acetic acid. 4) Duodenal ulcer induced by means of cysteamine. 5) Stress due to being kept under restraint and immersion in water at 15 degrees C for 6 hours. Celecoxib and rofecoxib, either orally or subcutaneously, did not produce necrotic injuries in healthy gastrointestinal mucosa (0

), showing normal histology. On the other hand, the injuries previously induced by indomethacin worsened (90

, p < 0.001). Total necrosis of small intestine as well as increased ulcer and perforation of gastric and duodenal ulcers induced by acetic acid and cysteamine were observed. There was also worsening of gastric necrotic area with stress (60-90

, p < 0.05). Celecoxib and rofecoxib showed neutrophilia (5,000/mm3) similar to that presented by indomethacin, but there was no leukocyte infiltration in the gastric mucosa; thus we can consider it a COX-2 selective NSAID (non-steroidal anti-inflammatory drug). CONCLUSION: Dose-dependent administration of celecoxib and rofecoxib as COX-2 inhibitors and non-COX-1 inhibitors, respectively, did not produce toxic injuries on healthy gastrointestinal mucosa, thus providing a broad therapeutic spectre. On the other hand, when administered in presence of altered gastrointestinal mucosa, they worsened and complicated gastric ulcers, and also induced necrosis in the small intestine, thereby restricting their clinical use.

Celecoxib vs indometacina y lesiones gástricas agudas en ratas. / [Celecoxib vs indomethacin and acute gastric lesions in rats]

In 5 random groups of Wistar rats (n = 15 for each group), ulcerogenic doses of NSAIDs COX-1-COX-2 inhibitors such as indomethacin were compared with Celecoxib (COX-2 inhibitor); the production of antrum gastric ulcers and bowel and colon necrotic areas was studied. Celecoxib was given each 12 hs orally and subcutaneously during 5 days and gastrointestinal lesions were not found; in contrast, Celecoxib given after indomethacin aggravated antrum gastric ulcers (p < 0.001); intestinal massive necrosis and death were observed in all the rats. We conclude that Celecoxib does not induce gastrointestinal lesions in healthy mucosa; in contrast, Celecoxib amplifies the gastrointestinal lesions induced by indomethacin.

Automedicación en adolescentes universitarios / Self medication among university adolescents

El objetivo de este trabajo fue conocer el autoconsumo de medicamentos en alumnos menores de 20 años, ingresantes al 1er. año de la carrera de medicina. Sobre un total de 2049 alumnos ingresantes en forma directa (año 1996), fueron encuestados 330 en forma voluntaria. El cuestionario contenía 52 preguntas abiertas y cerradas y recababa datos identificatorios, socieconómicos, culturales y relacionados con el consumo y conocimiento de medicamentos. Se obtuvo entre los resultados: que de los 330 encuestados, 300 son menores de 20 años y 102 de ellos declaran automedicarse. De éstos (56 por ciento sexo femenino y 44 por ciento sexo masculino) y el 30 por ciento admitió haber obtenido información para hacerlo de médicos, el 22 por ciento de algún familiar y el 18 por ciento del farmacéutico. Reconocen efectos colaterales y contraindicaciones. Los medicamentos más frecuentemente utilizados son: analgésicos (90 por ciento), antibíoticos (22 por ciento), y vitaminas (17 por ciento), obteniéndolos en farmacias (87 por ciento), en laboratorios de productos medicinales (25 por ciento) y en kioscos (18 por ciento). El 29 por ciento de los encuestados declara, además, consumir medicamentos caseros. Se concluyó que, siendo una población joven, un alto porcentaje de alumnos consume medicamentos y sobre todo sin prescripción médica, a pesar de que la mayoría de los mismos son de venta bajo receta, así como resultó llamativo el reconocimiento de efectos colaterales y contraindicaciones y sin embargo la escasa gravedad que los alumnos le otorgan a los mismos

Automedicación en adolescentes universitarios / Self medication among university adolescents

El objetivo de este trabajo fue conocer el autoconsumo de medicamentos en alumnos menores de 20 años, ingresantes al 1er. año de la carrera de medicina. Sobre un total de 2049 alumnos ingresantes en forma directa (año 1996), fueron encuestados 330 en forma voluntaria. El cuestionario contenía 52 preguntas abiertas y cerradas y recababa datos identificatorios, socieconómicos, culturales y relacionados con el consumo y conocimiento de medicamentos. Se obtuvo entre los resultados: que de los 330 encuestados, 300 son menores de 20 años y 102 de ellos declaran automedicarse. De éstos (56 por ciento sexo femenino y 44 por ciento sexo masculino) y el 30 por ciento admitió haber obtenido información para hacerlo de médicos, el 22 por ciento de algún familiar y el 18 por ciento del farmacéutico. Reconocen efectos colaterales y contraindicaciones. Los medicamentos más frecuentemente utilizados son: analgésicos (90 por ciento), antibíoticos (22 por ciento), y vitaminas (17 por ciento), obteniéndolos en farmacias (87 por ciento), en laboratorios de productos medicinales (25 por ciento) y en kioscos (18 por ciento). El 29 por ciento de los encuestados declara, además, consumir medicamentos caseros. Se concluyó que, siendo una población joven, un alto porcentaje de alumnos consume medicamentos y sobre todo sin prescripción médica, a pesar de que la mayoría de los mismos son de venta bajo receta, así como resultó llamativo el reconocimiento de efectos colaterales y contraindicaciones y sin embargo la escasa gravedad que los alumnos le otorgan a los mismos (AU)

[In vivo selectivity of nonsteroidal anti-inflammatory drugs on COX-1-COX-2 and gastrointestinal ulcers, in rats]. / Selectividad "in vivo" de daines COX-1-COX-2 y úlceras gastrointestinales, en ratas.

UNLABELLED: This work was aimed to study COX-1 and COX-2 selectivity in 16 non-steroidal anti-inflammatory drugs (NSAIDs), at ulcerogenic doses in 2 experimental models: 1) provided subcutaneously (sc), after solid food(SF), (antrum ulcers and intestinal erosions); and 2) orally (O) (fundic and intestinal erosions). METHODS: 17 groups of female Wistar rats (n = 7 each group), weighing 200 g, 36 h fasting with water ad libitum, were submitted to the following experiments: 1. SF (Cargill chow) during 1 h, and then sc: 1.1 ml saline; 2. diclofenac (Di); 3. indomethacine (Indo); 4. Ketorolac (Ke); 5. meloxicam (Mel); 6. Pyroxicam (P); 7. tenoxicam (T). The dose for the aforementioned drugs was 60 mg/kg; 8. aceclofenac (Ace); 9. 200 mg/kg nimesulide (Ni); 10. mefenamic acid (Mac); 11. aspirin (A); 12. etodolac (E); 13. ibuprophen (Ibu); 14. nabumetone (Na); 15. naproxene (Nap); 16. ketoprophen (Ket); 17. paracetamol (Pa), 500 mg/kg. II. The drugs where administered by orogastric tubing to the same groups of fasting animals. After 24 h the animals were killed by ether overdose. Laparotomy was performed and the stomach and the small intestine was removed. The percentage of antum ulcer, and fundic and intestinal erosion (mm2) was tabulated by planimetry. Blood and histological samples were obtained. RESULTS: The NSAIDs Indo, Ibu, Ke, Ket, P and Te yielded an antrum ulcer area: 5-29% and intestinal erosion, 101-395 mm2, similar to Indo (p > 0.50). In contrast there were neither ulcers nor intestinal erosions with Mac, A, Di, E and Nap (p > 0.50). While there were absence of ulcers with Ace, Me, Na, Ni and Pa and slight intestinal erosion (0-23 mm2; p < 0.01). II. There were differences in the following oral (NAIDs: Ace, Me, NA, Ni and Pa, yielding 0-5% fundic erosion and 0-22 mm2 intestinal erosion (p < 0.001). The other NSADs yielded 33-90% fundic erosion and 116-550 mm2 intestinal erosion, similarly to Indo (p > 0.50). HISTOLOGY: Leukocyte infiltrate in the gastrointestinal mucosa with all the NSADs, except Ibu and Pa. There was also neutrophilia (5000-20,000), but not with Ibu and Pa (700-1200). CONCLUSIONS: COX-2-COX-1 selectivity was demonstrated "in vivo" in aceclofenac, meloxicam, nabumetone, nimesulide and paracetamol.