Bladder-outlet obstruction leads to detrusor smooth-muscle hypertrophy/hyperplasia. Despite this overall increase in muscle mass, smooth-muscle contractility decreases and bladder emptying is impaired. The goal of this study was to determine whether smooth-muscle myosin heavy-chain (MHC) alterations occur in conjunction with partial obstruction of the rabbit bladder. Total MHC and MHC-isoform protein concentrations were determined by quantitative gel electrophoresis in rabbit bladders partially obstructed for 1-4 weeks. MHC gene expression was assessed by Northern and nuclease protection assays. Two MHC isoforms (SM1/SM2) were identified in the normal rabbit bladder. After 2 weeks of obstruction the ratio of SM1/SM2 changed from 0.4:0.6 to 0.5:0.5 (P < 0.01). As compared with sham-operated values, the level of MHC mRNA decreased significantly as of 1 day after obstruction. Quantitation of MHC-isoform mRNA levels revealed a nearly 3-fold increase in the SM1/SM2 ratio. In this animal model of bladder-outlet obstruction, early changes in MHC isoforms as well as an overall decrease of MHC mRNA expression were demonstrated, suggesting that obstruction induces significant alterations in myofilament gene expression.
Until recently, treatment options for patients with cystine calculi were not favorable. Using holmium:yttrium-aluminum-garnet (YAG) lasers to fragment cystine calculi, however, may provide a minimally invasive and cost-effective alternative to current treatments. This article describes cystine calculi and the diagnostic methods and current medical and surgical interventions used to treat patients and discusses the differences between flash lamp pulsed dye lasers and holmium:YAG lasers. Preoperative, intraoperative, and postoperative considerations for laser ureterolithotripsy of cystine calculi also are discussed.
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