Introduction Men with diabetic erectile dysfunction (ED) often have severe endothelial dysfunction and respond poorly to oral phosphodiesterase-5 inhibitors. Aim To examine whether and how freshly isolated stromal vascular fraction (SVF) promotes cavernous endothelial regeneration and restores erectile function in diabetic animals. Methods Eight-week-old C57BL/6J mice were used. Diabetes was induced by intraperitoneal injection of streptozotocin. SVF was isolated from epididymal adipose tissues of green fluorescence protein transgenic mice. At 8 weeks after the induction of diabetes, the animals were divided into six groups: controls, diabetic mice, and diabetic mice treated with a single intracavernous injection of phosphate-buffered saline (PBS) or SVF (1 × 104 cells, 1 × 105 cells, or 2 × 105 cells/20 µL, respectively). Main Outcome Measures Two weeks later, erectile function was measured by cavernous nerve stimulation. The penis was stained with antibodies to CD31, CD34, phosphohistone H3, phospho-endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor-A (VEGF-A). We also performed Western blot for phospho-eNOS and eNOS, and determined cyclic guanosine monophosphate (cGMP) concentration in the corpus cavernosum tissue. Results Significant improvement in erectile function was noted in diabetic mice treated with SVF at concentrations of 1 × 105 and 2 × 105 cells, which reached up to 82% of the control values. Local delivery of SVF significantly increased cavernous endothelial cell proliferation, eNOS phosphorylation, and cGMP expression compared with that in the untreated group and the PBS-treated diabetic group. Intracavernous injection of SVF increased cavernous VEGF-A expression and induced recruitment of CD34(+)CD31(−) progenitor cells. Some SVF underwent differentiation into cavernous endothelial cells. SVF-induced promotion of cavernous angiogenesis and erectile function was abolished in the presence of VEGF-Trap, a soluble VEGF-A neutralizing antibody. Conclusion The results support the concept of cavernous endothelial regeneration by use of SVF as a curative therapy for diabetic ED.

PurposeWe investigated bladder function, with special focus on initial functional changes, by objective report of decompensated bladder according to the percentage of residual urine volume to bladder capacity in awake, obstructed rats.Materials and MethodsThirty rats were randomly subjected to sham operations (n=10) or partial bladder outlet obstruction (BOO, n=20). Cystometric investigations were performed without anesthesia 1 or 2 weeks after BOO surgery. To reduce the influence of confounding factors in awake cystometry, we used simultaneous recordings of intravesical and intraabdominal pressures. Decompensated bladder was defined as the bladder with more than 20% of residual volume compared with bladder capacity.ResultsCompared with that in sham animals, basal pressure was elevated in both BOO groups. Threshold pressure was higher in the 2 week BOO (p<0.01) group. Compliance was decreased in the 1 week BOO group (p<0.01) and increased in the 2 week BOO group (p<0.001). Bladder capacity was not increased in the 1 week BOO group, but was increased in the 2 week BOO group (p<0.01). Decompensation was found in 62.5% of the 1 week BOO group and in 33.3% of the 2 week BOO group.ConclusionsFrom the earlier phase, the bladders exhibited serial changes in pressure and volume parameters, and decompensated bladders defined by the percentage of residual volume to bladder capacity could be seen. During the later phase, there was an increasing tendency of compensated bladders, accompanied by the bladders being enlarged and more compliant.

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