[Early removal of the urethral catheter after transurethral plasma kinetic resection of the prostate in the treatment of BPH].

OBJECTIVE: To investigate the feasibility and effect of early removal of the urethral catheter after transurethral plasma kinetic resection of the prostate (PKRP) in the treatment of benign prostatic hyperplasia (BPH). METHODS: We equally randomized 128 BPH patients treated by PKRP to an experimental group and a control group, urethral catheters removed at 1 -2 days for the former and at 5 -7 days for the latter. We compared the relevant indexes and clinical effects between the two groups. RESULTS: The baseline data were not significantly different between the two groups. Compared with the controls, the experimental group showed a significantly shorter postoperative hospital stay ([6.8 +/- 1.9] d vs [3.7 +/- 1.5] d, P < 0.05) and lower infection rate (25.0% vs 10.9%, P < 0.05). All the patients were followed up for 3 -6 months postoperatively. At 3 months after surgery, both the experimental and the control groups showed remarkable improvement in the International Prostatic Symptoms Scores (4. 9 +/- 2. 2 vs 5. 3 +/- 2. 3), maximum urine flow rate ([21.5+/- 5.6 ] ml/s vs [19.1 +/-4.9 ] ml/s) , and residual urine ( [ 16.8+/- 10.3 ] ml vs [18.9 +/- 12.3 ] ml), but with no significant differences between the two (P > 0.05) , and no significant differences were observed in postoperative complications (P >0.05). CONCLUSION: Early removal of the urethral catheter after PKRP, with its advantages of shorter postoperative hospital stay, lower infection rate, and no influence on the long-term effect, deserves to be recommended as a routine method in the treatment of BPH.

[Transurethral bipolar plasmakinetic enucleation and resection versus transurethral bipolar plasmakinetic resection of the prostate for BPH: a randomized controlled trial on the incidence of postoperative urinary incontinence].

OBJECTIVE: To compare the incidence rates of postoperative urinary incontinence between transurethral bipolar plasmakinetic enucleation and resection of the prostate (PKERP) and transurethral bipolar plasmakinetic resection of the prostate (PKRP), and provide evidence for the clinical application of PKERP. METHODS: Totally, 180 BPH patients were equally and randomly assigned to undergo PKERP and PKRP, respectively. We measured the urinary incontinence of the patients by pad test at 24 hours after extubation and every week after surgery for 4 weeks. Meanwhile, we recorded and compared the PSA level, prostate volume, Qmax, residual urine, IPSS, QOL, and the results of pad test between the two groups before and after surgery. RESULTS: The incidence rates of urinary incontinence in the PKERP and PKRP groups were 35.56% and 18.89% (P < 0.01) at 24 hours after extubation, 20.00% and 7.78% at 1 week after surgery (P < 0.05), and 3.33% and 2.22% at 2 weeks. There was no significant difference in the severity of urinary incontinence between the two groups at any time point (P > 0.05). No permanent urinary incontinence was observed in either group. CONCLUSION: Compared with PKRP, PKERP has a higher incidence rate of short-term urinary incontinence in the treatment of BPH, but not that of genuine incontinence, with similar severity and recovery time.

The role of Toll-like receptor (TLR) 2 and 9 in renal ischemia and reperfusion injury.

OBJECTIVE: To determine the involvement of Toll-like receptor (TLR) 2, TLR9, and TLR2+9 in renal ischemia/reperfusion (I/R) injury. METHODS: Mice with gene knock-out of TLR2, TLR9, and TLR2+9 underwent renal I/R injury. Tubular damage, expression of proinflammatory cytokines and chemokines, and kidney dysfunction were evaluated on different days after reperfusion. RESULTS: Mice deficient in TLR2, but not TLR9, were protected from renal I/R injury with less tubular damage, decreased cytokine production, and lower serum creatinine and urea levels than wild-type mice. TLR2+9 double-deficiency did not have an additional effect on tissue injury compared with TLR2 deficiency alone. CONCLUSION: These results suggest that activation of TLR2 signaling contributes to the pathogenesis of renal I/R injury, whereas TLR9 may be redundant for the development of this injury.

[Effects of penile vasoactive mediators on the development of erectile dysfunction].

Penile corpus cavernosum can be seen as a special kind of vascular structure. The cause of erectile dysfunction (ED) is often related to the changes of penile vasoactive mediators which modulate the functional conditions of penile erectile tissues. The penile vasoactive mediators including angiotensin and kinins, prostaglandins, endothelins, endothelium-derived hyperpolarizing factors (EDHF), NOS and NO, RhoA/Rho-kinases, etc., may play an important role in the development of ED. Further researches on these mediators can furnish some theoretical evidence for the clinical treatment of ED.

[Effects of angiotensin II on male rats with diabetic erectile dysfunction].

OBJECTIVE: To investigate the changes of angiotensin II (Ang II) and its receptors in male rats with diabetic erectile dysfunction (DED) so as to study its effects. METHODS: Out of 40 male SD rats, 30 were taken at random for diabetic models. After 8 weeks, the rats with erectile dysfunction were selected from these models. All the rats were divided into 3 groups: control ( n = 10), diabetes mellitus( DM, n = 9) and DED (n = 8). For each rat, the Ang II levels in the blood and homogenate prepared from part of the isolated penile tissues were determined respectively, and the Ang II receptors of the rest of the penile tissues were analyzed through immunohistochemical (IHC) assay. RESULTS: Compared with the control group, Ang II levels in the blood and penile tissues in the DM group, and that in the blood of the DED group were very high and the differences were statistically significant (P < 0.05). Ang II in the penile tissues of the DED increased sharply (P < 0.01). The receptors of Ang II changed contrariwise to the level of Ang ll. CONCLUSION: Ang II may play an important role in the pathogenesis of DED, and the Ang II antagonist or inhibitor of the angiotensin-converting enzyme (ACEI) may become a therapeutic method for DED in the future.