Streptozotocin-induced diabetes mellitus or the consumption of 5 % sucrose in place of drinking water cause an increase in rat urinary bladder capacity and mass. Length-tension curves were generated using bladder body strips isolated from control, diabetic, or sucrose-drinking rats to determine whether the length-tension relationship was altered by the bladder hypertrophy associated with diabetic and nondiabetic diuresis. In addition, we compared the data using three different methods of expression: (1) absolute grams tension developed; (2) grams tension/100 mg tissue, and (3) grams tension/mm². The cross-sectional area of strips from diabetic rats was increased compared to the other two groups. The length-passive tension curves for all three groups increased with increasing tissue length to a plateau. No optimal resting length for generation of active tension was found. Strips from diabetic and sucrose-drinking rats reached the plateau at a slightly larger passive tension than did strips from control rats. In addition, strips from diabetic and sucrose-drinking rats generally developed a greater active tension than did strips from control rats depending on the method of data presentation used. The data suggest that the complex nonlinear arrangement of smooth muscle fibers in the bladder wall results in the unusual length-tension curves generated by urinary bladder strips (as compared to skeletal or vascular smooth muscle). This relationship would be of benefit in the urinary bladders of early-stage diabetic patients before neuropathy development, where the stretching of the bladder wall would allow accommodation without any compromise of bladder function. The data indicate that comparisons of bladder strip function from control and diabetic rats should be done at passive tensions of ≥2 g to ensure that maximal active tension is generated.

No abstract

The effects of acute overstretching on detrusor function are unclear. Based on a new method to catheterize male rat bladder through the whole urethra, three groups (control, shamoperated, and acute bladder overdistension) of male rats were utilized in the present experiment. The contraction generated by in vitro bladders immediately post-overdistension in response to 2 Hz and 32 Hz stimulation significantly decreased at 0.75 ml and 1.5 ml intravesical volumes respectively; however, by 1 day post-overdistension the contractile responses increased toward normal. By three days the ability of the bladder to generate pressure completely returned to normal, and the average bladder weight for this group was increased. Similarly, the ability to empty was reduced at 0.75 ml and 1.5 ml immediately following overdistension and recovered fully after 3 days. The ability of the sham-operated bladders to empty at high intravesical volume was slightly reduced immediately following overdistension, and this was the only pathophysiological change observed in this group. Acute bladder overdistension did not alter intravesical capacity. It is clear that acute overdistension induced reversible changes in basic bladder function. o 1992 Wiley-Liss, Inc.

No abstract

No abstract