Histopathological alterations of the vas deferens in rats exposed to polypropylene mesh.

OBJECTIVE: To assess the histological and physiological effects of polypropylene mesh for inguinal herniorraphy, as it can cause lesions in the vas deferens in 0.3-2.0%, leading to infertility, and induces an inflammatory process and adjacent fibrosis, strengthening the posterior inguinal wall. MATERIALS AND METHODS: In all, 40 male albino rats (3 months old) had bilateral vas deferens dissection followed by mesh implantation on one side; the contralateral side was used as the control. The rats were killed 90 (group 1) and 120 (group 2) days later, and the vas deferens, epididymides and testicles assessed histopathologically. RESULTS: There was a foreign-body reaction after mesh implantation, but not in the controls. The mean lumen dilatation in regions proximal to the mesh in groups 1 and 2 was 0.468 and 0.371 mm(2), respectively, and all the sections had spermatozoids. The mean dilatation in control groups 1 and 2 was 0.239 and 0.170 mm(2), respectively, with spermatozoids present in 58% and 75%, respectively (significant, P < 0.05). In group 1 the wall thickness of mesh-implanted segments reduced to 0.177 mm, and in segments proximal to the mesh to 0.099 mm; the control segment was 0.298 mm (P < 0.05). In group 2 the mean thickness of mesh-implanted and proximal segments was 0.134 and 0.224 mm, respectively, while in the control it was 0.284 mm (not significant). There was loss of mucosal folding in all segments proximal to the mesh but not in the control. The epididymides and testicles were unchanged. CONCLUSION: Polypropylene mesh induces a foreign-body reaction, with histological changes in the vas deferens that cause functional obstruction, with dilatation and spermatozoid repression.

In vivo and in vitro effect of imipramine and fluoxetine on Na+,K+-ATPase activity in synaptic plasma membranes from the cerebral cortex of rats.

The effects of in vivo chronic treatment and in vitro addition of imipramine, a tricyclic antidepressant, or fluoxetine, a selective serotonin reuptake inhibitor, on the cortical membrane-bound Na+,K+-ATPase activity were studied. Adult Wistar rats received daily intraperitoneal injections of 10 mg/kg of imipramine or fluoxetine for 14 days. Twelve hours after the last injection rats were decapitated and synaptic plasma membranes (SPM) from cerebral cortex were prepared to determine Na+,K+-ATPase activity. There was a significant decrease (10%) in enzyme activity after imipramine but fluoxetine treatment caused a significant increase (27%) in Na+,K+-ATPase activity compared to control (P<0.05, ANOVA; N = 7 for each group). When assayed in vitro, the addition of both drugs to SPM of naive rats caused a dose-dependent decrease in enzyme activity, with the maximal inhibition (60-80%) occurring at 0.5 mM. We suggest that a) imipramine might decrease Na+,K+-ATPase activity by altering membrane fluidity, as previously proposed, and b) stimulation of this enzyme might contribute to the therapeutic efficacy of fluoxetine, since brain Na+,K+-ATPase activity is decreased in bipolar patients.

In vivo and in vitro effect of imipramine and fluoxetine on Na+, K+-ATPase activity in synaptic plasma membranes from the cerebral cortex of rats

The effects of in vivo chronic treatment and in vitro addition of imipramine, a tricyclic antidepressant, or fluoxetine, a selective serotonin reuptake inhibitor, on the cortical membrane-bound Na+,K+-ATPase activity were studied. Adult Wistar rats received daily intraperitoneal injections of 10 mg/kg of imipramine or fluoxetine for 14 days. Twelve hours after the last injection rats were decapitated and synaptic plasma membranes (SPM) from cerebral cortex were prepared to determine Na+,K+-ATPase activity. There was a significant decrease (10 percent) in enzyme activity after imipramine but fluoxetine treatment caused a significant increase (27 percent) in Na+,K+-ATPase activity compared to control (P<0.05, ANOVA; N = 7 for each group). When assayed in vitro, the addition of both drugs to SPM of naive rats caused a dose-dependent decrease in enzyme activity, with the maximal inhibition (60-80 percent) occurring at 0.5 mM. We suggest that a) imipramine might decrease Na+,K+-ATPase activity by altering membrane fluidity, as previously proposed, and b) stimulation of this enzyme might contribute to the therapeutic efficacy of fluoxetine, since brain Na+,K+-ATPase activity is decreased in bipolar patients