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Fig. 1 Normal detrusor ( x 7450, 931/10). The dense band pattern of sarcolemmal alternating thick ( |
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Normal detrusor (x 7500 , 873/29). Note compact fascicles (f) of closely aligned myocytes. A normal intermediate cell junction is seen ( |
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Fig. 3 Normal detrusor (x 3900, 948/26). Again note compact fascicles (f) of closely aligned myocytes separated by abundant collagen and elastin. A pseudo-bilobed nucleus (n) is caused by cross-section at a point of nuclear invagination. There is wide variation in electron density between the darkest and lightest myocytes. Part of a degenerative cell is seen to be collapsed, electron-dense and vacuolated (*). |
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Fig. 4 Normal axon (x 51840, 873/19). Adrenergic axon enveloped by Schwann cell sheath, in the interfascicular space. These axons contain small dense core vesicles. |
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Fig. 5 Cell junctions (x 29900, 874/16). Protrusion junction (P), ultraclose abutment (U), and normal intercellular junction (*). All 3 types of intercellular junctions are found in normal subjects. |
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Fig. 6 Myohypertrophy. (X 5800) Features include, marked inter cellular
separation and cellular hypertrophy. In severe forms the muscle cells
may be large, bizarre, branched and enclosing neighbouring cells.
Excessive collagen is observed between cells. |
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Fig. 7 Degeneration in a patient with chronic retention. (X 10900) Features
include myocyte shrivelling, sarcoplasmic vacuolation, clumping of
dense bodies, disruption of endoplasmic reticulum and other organelles,
cell lysis and fragmentation. Note the markedly widened intercellular
spaces. |
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Fig. 8 Hyperelastosis. (X 24890) Deposition of elastin fibres occurs between
widely separated muscle cells. The deposition of elastin in the
interstitium is suggested as a possible structural basis for the increased bladder distensibility seen in chronic retention. |