RESUMEN
The sphincters failure is a part of NSAIDs-toxicity that can be accordingly counteracted. We used a safe stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419), LD1 not achieved, since successful in inflammatory bowel disease trials, and counteracts esophagitis, sphincters failure, gastrointestinal ulcer and skin ulcer, external and internal fistulas in rats, and particularly counteracts all NSAIDs-lesions. We assessed lower esophageal sphincter and pyloric sphincter pressure (cmH2O) in rats treated with various NSAIDs regimens, at corresponding time points, known to produce stomach, small intestine lesions, hepatotoxicity and encephalopathy. Assessment was after diclofenac (12.5 mg/kg, 40 mg/kg intraperitoneal challenge), ibuprofen (400 mg/day/kg intraperitoneally for 4 weeks), paracetamol (5.0 g/kg intraperitoneal challenge), aspirin (400 mg/kg intraperitoneally or intragastrically), celecoxib (0.5 mg/kg, 1.0 mg/kg intraperitoneally). BPC 157 (10 µg/kg, 10 ng/kg) was given immediately after NSAIDs (intraperitoneally or intragastrically) or given in drinking water. Regularly, in all control NSAIDs fall of pressure occurred in both sphincters rapidly and then persisted. By contrast, in all NSAIDs-rats that received BPC 157, initial fall of pressure was minimized and pressure values restored to normal values. All tested NSAIDs decrease pressure in both sphincters, whilst BPC 157 counteracts their effects and restored both sphincters function.
Asunto(s)
Antiinflamatorios no Esteroideos/toxicidad , Antiulcerosos/farmacología , Esfínter Esofágico Inferior/efectos de los fármacos , Fragmentos de Péptidos/farmacología , Proteínas/farmacología , Píloro/efectos de los fármacos , Acetaminofén/toxicidad , Animales , Aspirina/toxicidad , Celecoxib/toxicidad , Diclofenaco/toxicidad , Ibuprofeno/toxicidad , Masculino , Presión , Ratas WistarRESUMEN
Sets containing of four specimens of intact human enamel of 18 teeth were inserted into volunteers' partial prostheses. The specimens were exposed to the action of oral cariogenic factors during 7, 14, 21 or 28 days. Electron microanalysis was employed to assess the demineralizing loss of calcium and phosphorus concentrations in experimental specimens, in relation to the original enamel of control specimens. Results showed a significant and steady decrease in Ca and P concentrations in all specimens, which was directly proportional to the duration of specimen exposure to oral cavity conditions. In four specimens with a 28-day oral exposure, an increase in Ca and P concentrations was observed in the most superficial enamel layer, which was explained as activation of the process of remineralization.