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, 29 (15), 2490-8

Persistent Polyuria in a Rat Spinal Contusion Model

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Persistent Polyuria in a Rat Spinal Contusion Model

Patricia J Ward et al. J Neurotrauma.

Abstract

Polyuria contributes to bladder overdistention, which confounds both lower and upper urinary tract management in individuals having a spinal cord injury (SCI). Bladder overdistention post-SCI is one of the most common triggers for autonomic dysreflexia, a potentially life-threatening condition. Post-SCI polyuria is thought to result from loss of vascular tone in the lower extremities, leading to edema and subsequent excess fluid, resulting in polyuria. Mild SCIs that have near complete recovery would therefore be expected to have little to no polyuria, while severe injuries resulting in flaccid limbs and lower extremity edema would be expected to exhibit severe polyuria. Since interventions that may decrease lower extremity edema are recommended to lessen the severity of polyuria, step training (which promotes vascular circulation) was evaluated as a therapy to reduce post-SCI polyuria. In the present study, polyuria was evaluated in mild, moderate, and severe contusive SCI in adult male rats. The animals were housed in metabolic cages for 24-hour periods pre- and post-SCI (to 6 weeks). Urine, feces, food, water, and body weights were collected. Other assessments included residual expressed urine volumes, locomotor scoring, in-cage activity, and lesion histology. SCI produced an immediate increase in 24-hour urine collection, as early as 3 days post-SCI. Approximately 2.6-fold increases in urine collection occurred from weeks 1-6 post-SCI for all injury severities. Even with substantial gains in locomotor and bladder function following a mild SCI, polyuria remained severe. Step training (30 min/day, 6 days/week) did not alleviate polyuria in the moderate SCI contusion group. These results indicate that (1) mild injuries retaining weight-bearing locomotion that should have mild, if any, edema/loss of vascular tone still exhibit severe polyuria, and (2) step training was unable to reduce post-SCI polyuria. Taken together, these results indicate that the current mechanistic hypothesis of post-SCI polyuria may be incomplete.

Figures

FIG. 1.
FIG. 1.
Lesion histology of the epicenter (area with the most damage), demonstrating a loss of white and gray matter with increasing severity. The 150-kD injury results in the loss of white matter without cavitation. More moderate injuries leave a small rim of white matter, such as in the ventral portions of the spinal cord, with the 210-kD injury. The addition of a 1-sec dwell time yields substantial tissue loss (epicenter area and total volume), with no visible white or gray matter at the epicenter and substantial gliosis.
FIG. 2.
FIG. 2.
Basso-Beattie-Bresnahan (BBB) locomotor scores show that although the 150-kD group was able to recover coordinated stepping, the addition of a 1-sec (1S) dwell time prevented the animals from achieving weight-bearing steps (*p<0.05 for 150 kD versus 150 kD+1S; #p<0.05 for 150 kD+1S versus 210 kD; %p<0.05 for 210 kD versus 150 kD).
FIG. 3.
FIG. 3.
Chronic urological deficits manifest as low voiding efficiency, leaving urine within the bladder. Combined with polyuria, these high residual volumes increase the risk of bladder infection, pyelonephritis, renal damage, and autonomic dysreflexia. Uninjured control value from Keirstead et al. (*p<0.05 for 150 kD+1-sec dwell time [1S] versus 150 kD; #p<0.05 for 210 kD versus 150 kD+1S).
FIG. 4.
FIG. 4.
All injury groups had significantly increased urine production from the pre-injury baseline (#p<0.01), and the 150-kD and 150-kD+1-sec groups were significantly greater than the laminectomy group at week 6 post-SCI (^p<0.01). Laminectomy controls remained the same.
FIG. 5.
FIG. 5.
Proportional representation of quiescent-phase and active-phase polyuria in a 24-h period. All injury groups significantly increased urine production at night compared to baseline. Daytime urine production was also significantly increased for the 210-kD and 150-kD+1-sec (1S) groups compared to baseline (W6, 6 weeks).
FIG. 6.
FIG. 6.
Polyuria at 6 weeks post-SCI quantified as physiological increases (in milliliters) from pre-SCI/baseline. Polyuria affected all SCI groups, and was especially notable in the active phase. Also of note is the approximately 20-mL increase in urine output for the most severely injured group (SCI, spinal cord injury).
FIG. 7.
FIG. 7.
(A) Overall water consumption. No significant changes were seen over time or between the injured and laminectomy groups after comparing daily, daytime, or night-time consumption. Therefore oral water consumption is not a significant contributing factor to SCI-induced polyuria. (B) Gastrointestinal water output. The water content of feces increased post-SCI, and therefore does not contribute to SCI-induced polyuria. Only the 210-kD injury group had significantly increased water content from the pre-injury baseline (#p<0.05). (C) Food intake was significantly increased from baseline for SCI rats, but not for laminectomy controls (#p<0.05). Therefore, they were also taking in more energy and deriving more moisture from food than uninjured animals. Digestive efficiency was not affected by SCI, and there were no significant differences between groups. SCI rats also maintained the same rate of body weight gain as uninjured animals, with no significant differences seen between the sham and SCI groups (SCI, spinal cord injury).
FIG. 8.
FIG. 8.
Activity meter data of in-cage activity following SCI, represented as both ambulatory (left) and total (right) movements. There were no statistically significant differences between injury groups, and therefore the three groups were combined as “SCI,” and compared to laminectomy only. Both quiescent-phase/lights on and active-phase/lights off are shown. No significant differences were found between the laminectomy and SCI groups. Rats naturally decrease activity with age (Jones et al.; SCI, spinal cord injury).

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