Letter-to-the-Editor RE: Lai HH, Boone TB, Thompson TC, Smith CP, Somogyi GT: Using Caveolin-1 Knockout Mouse to Study Impaired Detrusor Contractility and Disrupted Muscarinic Activity in the Aging Bladder
Letter-to-the-Editor RE: Lai HH, Boone TB, Thompson TC, Smith CP, Somogyi GT: Using Caveolin-1 Knockout Mouse to Study Impaired Detrusor Contractility and Disrupted Muscarinic Activity in the Aging Bladder
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发表时间:
2008
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影响因子:
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通讯作者:
George A Kuchel
中科院分区:
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作者:
George A Kuchel
In an important recent study, Lai et al .6 examined the impact of a caveolin-1 gene deletion on the amplitude of muscle contractility mediated by nerve stimulation and carbachol in detrusor muscle strips obtained from 3 and 12 months old male mice. Detrusor underactivity (DU) which has been defined as a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span1 is a remarkably common problem among frail older adults who suffer from incontinence or other voiding difficulties12. The precise prevalence of DU among community-dwelling elderly remains unknown. Nevertheless, elevated post-void residuals are common in older individuals of both genders, while urodynamically documented DU in the absence of bladder outlet obstruction has been demonstrated in 59% of incontinent nursing home residents10. The clinical management of elderly individuals with DHIC (detrusor hyperactivity with impaired contractility) remains particularly unsatisfactory because antispasmodic anticholinergic medications may worsen retention, whereas bethanechol does not improve bladder emptying resulting from DU 12 . The "dense band" pattern with caveolar depletion has been described as being the ultrastructural pattern associated with normative bladder aging4, lack of estrogen15, diabetes11 and injury3. Many key signaling molecules including muscarinic and purinergic receptors are known to cluster in caveolae14. Moreover, the authors have previously demonstrated a decreased ability of cholinergic agonists