Cystometries were performed in normal rats and in rats with bladder hypertrophy due to infravesical outflow obstruction. Investigations were performed in the presence and absence of anesthesia. pentobarbital anesthesia depressed spontaneous contractile activity in the bladder and the micturition reflex, thereby making measurements of other variables, such as bladder capacity and residual volume, impossible. In conscious animals infravesical outflow obstruction led to development of increased bladder capacity, marked residual volume, and unstable detrusor contractions. The model seems to be well suited for further evaluation of the mechanisms involved in the development of detrusor instability and the responses to pharmacological treatment.

The fine structure of the muscle of the urinary bladder in female rats is similar to that of other visceral muscles, although it is arranged in bundles of variable length, cross-section and orientation, forming a meshwork. When distended, the musculature is 100-120 microns thick, with some variation and occasional discontinuity. Extended areas of cell-to-cell apposition with uniform intercellular space occur between muscle cells, whereas attachment plaques for mechanical coupling are less common than in other visceral muscles. There are no gap junctions between muscle cells. Many bundles of microfilaments and small elastic fibres run between the muscle cells. After chronic partial obstruction of the urethra, the bladder enlarges and is about 15 times heavier, but has the same shape as in controls; the growth is mainly accounted for by muscle hypertrophy. The outer surface of the hypertrophic bladder is increased 6-fold over the controls; the muscle is increased 3-fold in thickness, and is more compact. Mitoses are not found, but there is a massive increase in muscle cell size. There is a modest decrease in percentage volume of mitochondria, an increase in sarcoplasmic reticulum, and no appreciable change in the pattern of myofilaments. Gap junctions between hypertrophic muscle cells are virtually absent. Intramuscular nerve fibres and vesicle-containing varicosities appear as common in the hypertrophic muscle as in controls. There is no infiltration of the muscle by connective tissue and no significant occurrence of muscle cell death.

Hypertrophy was induced in female rat urinary bladders by partial obstruction of the urethra. After 6 weeks the bladder weight had increased almost 7-fold compared to the matched controls. At this stage the animals were anesthetized and the pelvic nerves stimulated bilaterally at different bladder volumes. Isovolumetric pressures were measured by means of a catheter inserted via the urethra. For control (C) bladders maximum active pressure (104 +/- 11 cm. H2O, n = 5) was attained with 0.10 ml. content. For volumes above this a rapid progressive decrease in active pressure was noted. For hypertrophic (H) bladders maximum active pressure (92 +/- 14 cm. H2O, n = 6) was reached at 0.50 ml. Further filling decreased active pressure only slightly. By use of the law of Laplace the volume-active pressure relations were transformed to radius-force curves. The maximum active stress was similar for C and H bladders. The radius-force relation for H bladders was shifted to the right compared to the C curve (optimum radius for active force: C: 0.4 cm., H: greater than 0.9 cm.). This shift, responsible for the decreased ability to pressure production of the H bladders at small volumes indicates a dramatic remodelling of the smooth muscle in the hypertrophic bladder wall.

Isometric and isotonic length-tension relations of longitudinal smooth muscle from rabbit urinary bladder were studied together with muscle cell length and tissue structure as revealed histologically. In vivo strip length at a bladder volume of 10 m1 is referred to as L10. The smooth muscle was relaxed by Ca2+-free solution and contracted by K+-high solution with different Ca2+-concentrations. Maximal active force, 12.5+/-0.4 N/cm2 (S.E., n =11), for wholestrips was attained at a length of 206+/-4% (S.E., n=5) of L10. Passive tension at this length was about 15% of total tension. After correction for amount of connective tissue, maximal active tension of pure muscle bundles was 19 N/cm2. Up to about 165% of L10 isometric and isotonic length-tension relations were identical; if the muscle was stretched beyond this, it failed to shorten isotonically to the same length as when contracting from a shorter starting length. This decreased shortening capacity was reversible if the muscle was shortened passively. The extent of shortening against zero load was dependent on degree of activation suggesting an internal resistance to shortening. A linear relationship was found between bladder radius and muscle cell length, indicating that no slippage occurs between the cells when the bladder is filled. Mean cell diameter in the nuclear regionat L10 was 7.2+/-0.2 mum (S.D.,n=10). Mean macimal active tension per cell was calculated to be 2.3-10(-6) N and occurred at a cell length of 655 mum.