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.

[Autonomic nervous system and gastric stress in rats]. / Sistema nervioso autónomo y estres gástrico, en ratas.

The role of the autonomic nervous system on gastric stress was studied in different groups of Wistar rats (n = 10). The experimental stress model consisted of immobilization and immersion in 15 degrees C water during 6 hours. The percentage of the gastric mucosa macroscopic lesional area was tabulated, and at the same time cortisol, melatonin, noradrenaline, adrenaline, dopamine and serotonin blood levels were measured. The stress control showed a necrotic area (80%) and in blood there was only and increase in noradrenaline and adrenaline. The following dose dependent drugs were studied: beta adrenergics agonists and antagonists, alpha 1 postsinaptical adrenergic antagonists, anticholinergics and cholinergics, endorphin and GABA receptors. Isoproterenol, prazosim, doxasine, tramadol and vigabatrin yielded a remarkable gastric mucosa protection in stress with an area close to 0% (p < 0.001). In contrast, propanolol, acetylholine, atropine, naloxone and flumazenil showed no difference in control stress (p > 0.5). All the drugs under study yielded similar vasoactive amines than the control stress. It is concluded that the protective gastric mechanism of the autonomic nervous system in stress, could be linked to its receptors with an increase in the splanchnic microcirculation.

Sistema nervioso autónomo y estres gástrico, en ratas / Autonomic nervous system and gastric stress in rats

En grupos diferentes de ratas Wistar (n=10), se estudió el efecto fisiopatológico del sistema nervioso autónomo en el estrés gástrico, en el modelo experimental de estrés, por inmovilización e inmersión en agua a 15 grados Celsius durante 6 hs., en el que se tabuló el por ciento lesional macroscópica de la mucosa gástrica y en sangre se midió el cortisol, malatonina, nor-adrenalina, adrenalina, dopamina y serotonina. En estrés testigo se encontró un área necrótica gástrica de un 80 por ciento en sangre solo se halló aumento de nor-adrenalina y adrenalina. Se estudiaron fármacos en dosis dependientes, agonistas y antagonistas de los receptores Beta adrenérgicos, antagonistas alpha adrenérgicos postinápticos; colinérgicos y anticolinérgicos, de los receptores endorfínicos y de los GABA. Se encontró que Isoproterenal, Prazosim, Doxazosina, Tramadol y Vgabatrin dieron marcada protección de la mucosa gástrica en el estrés, con un área necrótica cercana al 0 por ciento (P<0.001); en contraste, Propanolol, Acetilcolina, Atropina, Naloxona y Flumazenil no se diferenciaron del estrés testigo (P>0.5). Todos los fármacos estudiados dieron similares aminas vasoactivas que el estrés testigo. Se concluyó que el sistema nervioso autónomo en su vinculado a sus receptores con incremento de la microcirculación esplácnica.

Sistema nervioso autónomo y estres gástrico, en ratas / Autonomic nervous system and gastric stress in rats

En grupos diferentes de ratas Wistar (n=10), se estudió el efecto fisiopatológico del sistema nervioso autónomo en el estrés gástrico, en el modelo experimental de estrés, por inmovilización e inmersión en agua a 15 grados Celsius durante 6 hs., en el que se tabuló el por ciento lesional macroscópica de la mucosa gástrica y en sangre se midió el cortisol, malatonina, nor-adrenalina, adrenalina, dopamina y serotonina. En estrés testigo se encontró un área necrótica gástrica de un 80 por ciento en sangre solo se halló aumento de nor-adrenalina y adrenalina. Se estudiaron fármacos en dosis dependientes, agonistas y antagonistas de los receptores Beta adrenérgicos, antagonistas alpha adrenérgicos postinápticos; colinérgicos y anticolinérgicos, de los receptores endorfínicos y de los GABA. Se encontró que Isoproterenal, Prazosim, Doxazosina, Tramadol y Vgabatrin dieron marcada protección de la mucosa gástrica en el estrés, con un área necrótica cercana al 0 por ciento (P<0.001); en contraste, Propanolol, Acetilcolina, Atropina, Naloxona y Flumazenil no se diferenciaron del estrés testigo (P>0.5). Todos los fármacos estudiados dieron similares aminas vasoactivas que el estrés testigo. Se concluyó que el sistema nervioso autónomo en su vinculado a sus receptores con incremento de la microcirculación esplácnica. (AU)