Changes of Rat Urinary Bladder during Acute Phase of Spinal Cord Injury

Abstract

Spinal cord injury (SCI) at Thl3 was induced in female Wistar rats, and changes in the urinary bladder were examined during the acute phase of SCI. Wet weights of the spinal bladders increased twofold over controls by 7 days after SCI. Intravesical volumes increased sixfold over control values by day 3, and then decreased 7 days after the injury. Maximal pressure within the bladder decreased in all spinal rats compared with controls. Smooth muscle cells were isolated from the urinary bladder, and their total protein and DNA content were measured by multiparametric cytofluorometry. DNA content of isolated smooth muscle cells decreased by day 3 and remained 7 days after the spinal injury. Total protein content of isolated smooth muscle cells was decreased 1 day after and increased 7 days after the spinal injury, just when spinal reflex of the bladder recovered. These findings suggest that hypertrophy of smooth muscle cells in urinary bladder is related to the activity of peripheral autonomic nerve and that smooth muscle cells already begin to hypertrophy during the spinal shock period to adjust themselves to the new state, that is, the spinal bladder.

Transplantation and repair: Combined cell implantation and chondroitinase delivery prevents deterioration of bladder function in rats with complete spinal cord injury

“…The finding that bladder size increased after the injury in the untreated group and the fact that SCI interferes with multiple aspects of lower urinary tract function is in accordance with an earlier study, in which a twofold increase in bladder size was shown 2 weeks following injury. 15 Our observations during bladder expression (during 2 weeks post lesion) indicated that bladder size increased initially in all animals during the initial weeks, however, it then decreased in the untreated animals. These findings in combination with the observed voiding efficacy in the two groups, suggests that it is not necessarily the increased bladder size that interferes with voiding and bladder dysfunction, but rather the secondary changes (that is, reduction in size).…”

Regeneration of adult rat spinal cord is promoted by the soluble KDI domain of γ1 laminin

“…Even though spinal shock (Atkinson and Atkinson, 1996) might account for the initial paralysis of animals, it was ruled out effectively by the fact that only the KDI-treated animals showed recovery during the 14-week observation period whereas the placebo group remained paralyzed. In the rat, spinal shock is known to last up to 7 days, as assessed by recovery of bladder function (Mimata et al, 1993;Shaker et al, 2003). It is thus unlikely that a spinal shock could last for 14 weeks and even less likely that it would be alleviated selectively in the KDI-treated animals.…”

Quantification of Bladder Smooth Muscle Orientation in Normal and Spinal Cord Injured Rats

“…In particular, spinal cord injuries rostral to the lumbar spine can lead to severe lower urinary tract dysfunctions including bladder outlet obstruction and detrusor instability. 3 In addition to the functional deficiency, these bladder dysfunctions are often accompanied by changes in the wall tissue morphology such as hypertrophy, 14 trabeculation, 17 and fibrosis 4 as well as by significant changes in the mechanical properties of the wall. 11,22,24 These findings suggest that there may be strong correlations between the tissue morphology, mechanical properties of the wall and the health state of the bladder.…”