METHODS: We performed a prospective cohort study with patients diagnosed with benign prostatic hyperplasia (BPH) and undergoing HoLEP. The surgeries were performed by a high skilled surgeon in the method. The occurrence of dysuria was actively evaluated using a Likert scale, where scores from 0 to 3 were classified as mild dysuria and scores from 4 to 10 as moderate to severe dysuria. Patients were assessed weekly. For the analysis of risk factors, we selected 6 categorical clinical variables and 14 continuous clinical variables. For the analysis of categorical variables, we used Fisher's exact and Chisquare tests. For analysis of continuous variables, we used Student's and Mann-Whitney's t tests. The homogeneity of the samples was evaluated using the Levene test. For statistical significance we considered a p<0.05.RESULTS: To date, 23 patients have reached a sufficient follow-up period for the study. The prevalence of moderate to severe dysuria was 66.7% in the first week and 33.3% in the fourth week (Figure 1). In the first week, no variable was relevant in the occurrence of dysuria. At week four, the mean age among patients with moderate to severe dysuria was statistically lower (62.5 vs 68.4 years; p[0.02), and the prevalence of moderate to severe dysuria was statistically higher among patients with a history of preoperative prostate biopsy (66.7% vs 14.3%, p[0.037). Symptom score, prostatic volume, energy density used, surgical time, use of Moses technology, among others, were not related to the intensity of dysuria (Table 1).CONCLUSIONS: When actively and early evaluated, the prevalence of moderate to severe dysuria is significant in the first weeks after HoLEP. Younger patients and cases with a history of prostate biopsy have higher rates of dysuria in the fourth postoperative week.
Very little is known about the physiological role of nicotinic receptors in canine bladders, although functional nicotinic receptors have been reported in bladders of many species. Utilizing in vitro methods, we evaluated nicotinic receptors mediating bladder function in dogs: Control (9 female and 11 male normal controls, 5 sham-operated), Decentralized (9 females, decentralized 6-21 mo), and obturator-to-pelvic nerve transfer reinnervated (ObNT-Reinn; 9 females; decentralized 9-13 mo, then reinnervated with 8-12 mo recovery). Muscle strips were collected, mucosa-denuded and mounted in muscle baths before incubation with neurotransmitter antagonists and contractions to the nicotinic receptor agonist epibatidine was determined. Strip response to epibatidine, expressed as percent potassium chloride, were similar (approximately 35% in Controls, 30% in Decentralized, and 24% in ObNT-Reinn). Differentially, epibatidine responses in Decentralized and ObNT-Reinn bladder strips were lower than Controls after tetrodotoxin (a sodium channel blocker that inhibits axonal action potentials). Yet, in all groups, epibatidine-induced strip contractions were similarly inhibited by mecamylamine and hexamethonium (ganglionic nicotinic receptor antagonists), SR 16584 (α3β4 neuronal nicotinic receptor antagonist), atracurium and tubocurarine (neuromuscular nicotinic receptor antagonists), and atropine (muscarinic receptor antagonist), indicating that nicotinic receptors (particularly α3β4 subtypes), neuromuscular and muscarinic receptors play roles in bladder contractility. In Control bladder strips, since tetrodotoxin did not inhibit epibatidine contractions, nicotinic receptors are likely located on nerve terminals. The tetrodotoxin inhibition of epibatidine-induced contractions in Decentralized and ObNT-Reinn suggests a relocation of nicotinic receptors from nerve terminals to more distant axonal sites, perhaps as a compensatory mechanism to recover bladder function.
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