Lower urinary tract function in spinal cord-injured rats: midthoracic contusion versus transection

Abstract

Objectives: To compare changes in lower urinary tract (LUT) function with modifications in pathways that regulate LUT function using two different animal models (incomplete and complete) of spinal cord injury (SCI). Methods: Female Sprague-Dawley rats were used. SCI was made at Th8/9 by a contusion injury (contusion, n ¼ 9) or a complete transection (transection, n ¼ 9). Unoperated rats were used as normal controls (normal, n ¼ 6). LUT function was evaluated by micturition behavior in metabolic cages for 24 h and cystometry in awake animals. Immunocytochemical staining at the L6 spinal cord, spinal areas associated with LUT, was performed to identify descending modulatory fibers and dorsal root afferents that project to the L6 spinal cord. Results: Volume/micturition in metabolic cages gradually increased in both contusion and transection groups compared with normals, and operated groups did not differ from each other. Urodynamic parameters from cystometry were significantly different in contusion and transection groups compared with normals, but again there was no significant difference between contusion and transection groups. Immunocytochemical analyses at the L6 spinal cord showed no serotonergic or noradrenergic fibers in transection group, but some descending fibers remained in contusion group, indicating sparing. Small dorsal root afferents were denser in both contusion and transection groups than in normals, indicating sprouting. Conclusions: Although differences were not found in LUT function in operated animals, supraspinal and dorsal root projections to the L6 spinal cord responded differently to contusion and transection. This suggests that the benefits of pharmacologic treatments may be different in two lesion models. Spinal Cord (2014) 52, 658-661; doi:10.1038/sc.2014.114; published online 15 July 2014 INTRODUCTION Spinal cord injury (SCI) is classified clinically into complete injuries,where function below the level of a injury is lost, and incomplete injuries where some sensory and/or motor function is retained. Nevertheless, it is known that some descending pathways are spared in many cases of clinically complete injuries. 1 Lower urinary tract (LUT) dysfunction in SCI results from damage to descending modulatory pathways and increased sensory input through sprouting of primary afferent pathways. A contusion injury that we use destroys the dorsal spinal cord in the thoracic region, including the dorsal columns, the corticospinal tract and the dorsolateral (DL) funiculus, damages the dorsal horn (DH) and impinges on the intermediolateral column. 2-4 Thus, the ventral funiculi and the ventral portions of the lateral funiculi, which contain descending modulatory pathways, were partially spared in contusion injuries, but not in transection injuries.Serotonergic axons project to the DL nucleus in the spinal cord, which has been implicated in the central control of the bladder and the urethra and recovery of bladder-external urethral sphincter coordination in SCI rats. 5,6 Brainstem-spinal noradrenerg...

Small-sample performance and underlying assumptions of a bootstrap-based inference method for a general analysis of covariance model with possibly heteroskedastic and nonnormal errors

“…After SCI, the bladder is known to turn into a pathological state, as indicated by alterations in cystometric variables, such as the voided volume and detrusor pressure. 38 We would like to emphasize that these pathological changes in human urinary bladder function are among the most serious consequences of SCI, being associated with a substantially decreased quality of life and a high risk of mortality. 39,40 Therefore, the main goal of any pharmacological treatment in SCI is to improve cystometric characteristics towards the pre-SCI level.…”

Spinal Transection Alters External Urethral Sphincter Activity during Spontaneous Voiding in Freely Moving Rats

“…In the present study, the number of voids per day decreased and void size increased after transection at either level, which was consistent with other reports of urinary function after spinal injury. 31,32 The decrease in the number of daily voids could reflect any number of causes, including increased capacity due to bladder enlargement after SCI, enhanced urine retention due to an elevated threshold for voiding, and the inability to release urine due to EUS occlusion of the urethra during attempted voiding (i.e., DSD during non-voiding…”

Correlating spinal cord injuries with neurogenic bladder pathophysiology

“…A similar study including cSCI and tSCI models found that, while micturition pressure, non‐voiding contractions, bladder capacity and post‐void residual urine volumes differed from controls, there was no significant difference between the cSCI and tSCI groups. CGRP was significantly elevated in the dorsal horn in the SCI groups compared with the control group, but was not different between the SCI groups.…”