We evaluated the effects of cyclooxygenase-2 (COX-2) selective inhibitors, COX-1 selective inhibitor, or COX non-selective inhibitor on gastric emptying and intestinal transit of liquids, and evaluated the effect of a COX-2 selective inhibitor on gastric tonus (GT). Male Wistar rats were treated per os with saline (control), rofecoxib, celecoxib, ketorolac, rofecoxib + ketorolac, celecoxib + ketorolac, or indomethacin. After 1 h, rats were gavage-fed (1.5 mL) with the test meal (5% glucose solution with 0.05 g mL(-1) phenol red) and killed 10, 20 or 30 min later. Gastric, proximal, medial or distal small intestine dye recovery (GDR and IDR, respectively) were measured by spectrophotometry. The animals of the other group were treated with i.v. valdecoxib or saline, and GT was continuously observed for 120 min using a pletismomether system. Compared with the control group, treatment with COX-2 inhibitors, alone or with ketocolac, as well as with indomethacin increased GDR (P < 0.05) at 10-, 20- or 30-min postprandial intervals. Ketorolac alone did not change the GDR, but increased the proximal IDR (P < 0.05) at 10 min, and decreased medial IDR (P < 0.05) at 10 and 20 min. Valdecoxib increased (P < 0.01) GT 60, 80 and 100 min after administration. In conclusion, COX-2 inhibition delayed the gastric emptying of liquids and increased GT in rats.
Sildenafil slows down the gastric emptying of a liquid test meal in awake rats and inhibits the contractility of intestinal tissue strips. We studied the acute effects of sildenafil on in vivo intestinal transit in rats. Fasted, male albino rats (180-220 g, N = 44) were treated (0.2 mL, iv) with sildenafil (4 mg/kg) or vehicle (0.01 N HCl). Ten minutes later they were fed a liquid test meal ( 99m 99m 99m 99m 99m technetium-labeled saline) injected directly into the duodenum. Twenty, 30 or 40 min after feeding, the rats were killed and transit throughout the gastrointestinal tract was evaluated by progression of the radiotracer using the geometric center method. The effect of sildenafil on mean arterial pressure (MAP) was monitored in a separate group of rats (N = 14). Data (medians within interquartile ranges) were compared by the Mann-Whitney U-test. The location of the geometric center was significantly more distal in vehicle-treated than in sildenafil-treated rats at 20, 30, and 40 min after test meal instillation (3.3 (3.0-3.6) vs 2.9 (2.7-3.1); 3.8 (3.4-4.0) vs 2.9 (2.5-3.1), and 4.3 (3.9-4.5) vs 3.4 (3.2-3.7), respectively; P < 0.05). MAP was unchanged in vehicletreated rats but decreased by 25% (P < 0.05) within 10 min after sildenafil injection. In conclusion, besides transiently decreasing MAP, sildenafil delays the intestinal transit of a liquid test meal in awake rats. Sildenafil citrate belongs to a class of compounds called phosphodiesterase (PDE) inhibitors. PDEs constitute a family of enzymes that hydrolyze cyclic nucleotides (cyclic adenosine monophosphate and cyclic guanosine monophosphate, cGMP) and play a critical role in the modulation of the second messenger pathway (1). Sildenafil citrate is a selective PDE type 5 inhibitor widely used due to its therapeutic efficacy in human erectile dysfunction and pulmonary hypertension. It effectively blocks the PDE 5-mediated hydrolysis of cGMP inside vascular smooth muscle cells, relaxing the arterioles that supply the corpus cavernosum (2) and the lung parenchyma (3).Sildenafil increases the gastric resistance to injury by non-steroidal anti-inflammatory drugs (4), decreases the distal esophageal peristalsis (5), and inhibits the gastric emptying of test meals both in humans and rats (6,7), and decreases the contractility of isolated duodenal strips (8).Since the gastrointestinal transit rate results from a complex interplay between gastric tonus, distal stomach phasic activity and resistance and propulsion offered by the small intestine (9), we measured the effect of sildenafil on the small bowel intestinal transit of a liquid test meal in awake rats.
Penile prosthesis implant is the definitive treatment for refractory erectile dysfunction. Fracture of malleable prosthesis is rarely described due to its low incidence. We describe a case of multiple, bilateral fracture of a malleable penile implant, ten years after implantation. After the diagnosis, a review surgery was performed and the implants were replaced. No corporal rupture or urethral lesion was observed. Review of the literature shows few articles reporting penile implant fractures, and to our knowledge no other article has described multiple, bilateral fractures of a penile prosthesis.
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