STRUCTURAL BASIS OF GERIATRIC VOIDING DYSFUNCTION .3. DETRUSOR OVERACTIVITY
STRUCTURAL BASIS OF GERIATRIC VOIDING DYSFUNCTION .3. DETRUSOR OVERACTIVITY
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DOI：
10.1016/s0022-5347(17)35868-8
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发表时间：
1993-11-01
影响因子：
6.6
通讯作者：
RESNICK, NM
中科院分区：
文献类型：
--
作者：
ELBADAWI, A;YALLA, SV;RESNICK, NM
在没有出口梗阻的情况下，逼尿肌过度活动在老年人中很常见。现有的关于过度活动逼尿肌结构的研究很少，一般只涉及其神经支配。我们进行了一项前瞻性研究，以检查肌细胞的超微结构，膀胱和神经的逼尿肌活检从35名老年受试者，以确定结构相关的各种尿动力学定义的排尿功能障碍的形式。在15例逼尿肌活检中，盲法确定了一种独特的连接障碍结构模式。这些模式匹配12名女性和3名男性，年龄66至96岁（平均年龄79岁），通过前瞻性尿动力学评价将他们独立地分为逼尿肌过度活动组。除1例患者外，所有患者均出现尿失禁和/或其他症状，无糖尿病或明显神经功能缺损。连接障碍模式的特点是适度增宽的细胞间隙，缺乏中间肌细胞连接，丰富的独特的突起连接和超紧密的细胞邻接，并没有扩大肥大细胞的特征。8例标本中有重叠的广泛的肌细胞和轴突变性，这与逼尿肌收缩力受损的患者亚组相匹配。其余7例无退变的标本与收缩力正常的患者相匹配。Projunctions交界处和基台提出作为一个可能的表现与自然衰老相关的肌肉细胞去分化的过程，以及介体过度活跃逼尿肌的电耦合的肌肉细胞，代替他们的正常机械耦合削减显着减少中间细胞连接。在此基础上，提出了一个双向肌源性机制，以解释不自主收缩，但允许神经触发的单一排尿收缩过度活跃的逼尿肌。叠加变性被认为是逼尿肌收缩力受损的结构基础。
Detrusor overactivity in the absence of outlet obstruction is common in the elderly. The few available studies on structure of the overactive detrusor generally have dealt only with its innervation. We conducted a prospective study to examine the ultrastructure of muscle cells, interstitium and nerves of the detrusor in biopsies from 35 elderly subjects to identify structural correlates of various urodynamically defined forms of voiding dysfunction. A distinctive dysjunction structural pattern was identified blindly in 15 detrusor biopsies. These patterns matched 12 women and 3 men 66 to 96 years old (mean age 79 years) who were segregated independently as a detrusor overactivity group by prospective urodynamic evaluation. All but 1 patient had incontinence and/or other symptoms, and none had diabetes or a significant neurological deficit. The dysjunction pattern was characterized by moderately widened intercellular spaces, scarce intermediate muscle cell junctions, abundant distinctive protrusion junctions and ultra-close cell abutments, and absence of profiles characteristic of enlarged hypertrophic cells. There was superimposed widepsread degeneration of muscle cells and axons in 8 specimens, which matched the subgroup of patients with impaired detrusor contractility. The remaining 7 specimens with no degeneration matched the patients with normal contractility. Protrusion junctions and abutments are proposed as a possible manifestation of a process of muscle cell de-differentiation associated with natural aging, as well as the mediator in overactive detrusor of electrical coupling of muscle cells, in lieu of their normal mechanical coupling curtailed by marked reduction of intermediate cell junctions. On this basis, a bipartite myogenic mechanism is proposed to account for the involuntary contractions yet allow neurally triggered unitary voiding contractions in the overactive detrusor. Superimposed degeneration is proposed as the structural basis of impaired detrusor contractility, when also present.