Nandrolone decanoate impairs gastrointestinal motility and duodenal morphometry in moderately exercised rats.

The misuse of anabolic androgenic steroid associated or not with physical workouts disrupts gastrointestinal (GI) function homeostasis. Our goal was to investigate the effects of nandrolone decanoate (ND) and moderate swimming on the GI transit of solid meals, GI motor contractility, and intestinal histology in rats. Male Wistar rats were allocated to four groups that received intramuscular injections of ND (5.0 mg/kg) or vehicle (60.0 µL) and were submitted or not to swimming sessions (60 min, 5% body weight overload) for 4 weeks. Gastric emptying, intestinal transit, in vitro GI contractility, intestinal morphometry, and duodenal mucosal mast cells were evaluated in all experimental groups. ND treatment accelerated gastric emptying, slowed small intestine transit time, enhanced gastric carbachol-mediated reactivity, decreased crypt depth and villus height, reduced mucosal thickness, and increased the circular and longitudinal muscle layer thickness of the duodenum in sedentary rats. Moderate exercise accelerated intestinal transit time and reduced submucosa thickness. In vehicle-treated animals, a strong negative correlation was found between intestinal transit and mucosal mast cells, which was reversed by ND treatment. Combining ND treatment and swimming accelerated gastric emptying, increased duodenal cholinergic reactivity, inhibited the sodium nitroprusside relaxing response, increased the number of duodenal mast cells, decreased villus height, and increased the thickness of all muscle layers. ND changed the morphological and functional properties of the GI tract over time, with intense dysmotility, especially in sedentary animals, but moderate exercise seemed to have played a compensatory role in these harmful effects in the gut.

Nandrolone decanoate impairs gastrointestinal motility and duodenal morphometry in moderately exercised rats

The misuse of anabolic androgenic steroid associated or not with physical workouts disrupts gastrointestinal (GI) function homeostasis. Our goal was to investigate the effects of nandrolone decanoate (ND) and moderate swimming on the GI transit of solid meals, GI motor contractility, and intestinal histology in rats. Male Wistar rats were allocated to four groups that received intramuscular injections of ND (5.0 mg/kg) or vehicle (60.0 µL) and were submitted or not to swimming sessions (60 min, 5% body weight overload) for 4 weeks. Gastric emptying, intestinal transit, in vitro GI contractility, intestinal morphometry, and duodenal mucosal mast cells were evaluated in all experimental groups. ND treatment accelerated gastric emptying, slowed small intestine transit time, enhanced gastric carbachol-mediated reactivity, decreased crypt depth and villus height, reduced mucosal thickness, and increased the circular and longitudinal muscle layer thickness of the duodenum in sedentary rats. Moderate exercise accelerated intestinal transit time and reduced submucosa thickness. In vehicle-treated animals, a strong negative correlation was found between intestinal transit and mucosal mast cells, which was reversed by ND treatment. Combining ND treatment and swimming accelerated gastric emptying, increased duodenal cholinergic reactivity, inhibited the sodium nitroprusside relaxing response, increased the number of duodenal mast cells, decreased villus height, and increased the thickness of all muscle layers. ND changed the morphological and functional properties of the GI tract over time, with intense dysmotility, especially in sedentary animals, but moderate exercise seemed to have played a compensatory role in these harmful effects in the gut.

Myenteric neuroprotective role of aspirin in acute and chronic experimental infections with Trypanosoma cruzi.

BACKGROUND: Experimental and clinical studies have shown that myenteric neuron cell death during infection with Trypanosoma cruzi mainly occurs in the esophagus and colon, resulting in megaesophagus and megacolon, respectively. Evidence suggests that the cyclooxygenase enzyme (COX) is involved in the T. cruzi invasion process. The use of low-dose aspirin (ASA), a COX-1/COX-2 inhibitor, has been shown to reduce infection with T. cruzi. Therefore, in this study, we evaluated the effects of treatment with low-dose ASA on myenteric colonic neurons during murine infection with T. cruzi. METHODS: Swiss mice were assigned into groups treated with either phosphate-buffered saline or low doses of ASA during the acute phase (20 mg/kg ASA) and chronic phase (50 mg/kg ASA) of infection with the Y strain of T. cruzi. Seventy-five days after infection, colon samples were collected to quantify inflammatory foci in histological sections and also general (myosin-V+ ), nitrergic, and VIPergic myenteric neurons in whole mounts. Gastrointestinal transit time was also measured. KEY RESULTS: Aspirin treatment during the acute phase of infection reduced parasitemia (P<.05). Aspirin treatment during the acute or chronic phase of the infection reduced the intensity of inflammatory foci in the colon, protected myenteric neurons from cell death and plastic changes, and recovered the gastrointestinal transit of mice infected with T. cruzi (P<.05). CONCLUSION & INFERENCES: Early and delayed treatment with low-dose ASA can reduce the morphofunctional damage of colonic myenteric neurons caused by murine T. cruzi infection.