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Effect of T3 Spinal Contusion Injury on Upper Urinary Tract Function
Jason H Gumbel1, Charles H Hubscher1,2
1Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, Kentucky, USA.
Neurotrauma Reports
|May 13, 2022
Summary
Spinal cord injury (SCI) at the T3 level causes excessive urination (polyuria) by disrupting autonomic regulation. This study shows higher-level SCI damages descending pathways, leading to salt and water balance issues.
Area of Science:
- Neuroscience
- Physiology
- Urology
Background:
- Spinal cord injury (SCI) disrupts autonomic regulation, affecting bodily systems.
- Excessive urine production (polyuria) post-SCI is understudied.
- Previous research used lower spinal lesions (T8-T10), impacting both supraspinal and local kidney-regulating pathways.
Purpose of the Study:
- To investigate polyuria following a higher-level T3 spinal cord contusion injury.
- To identify the source of SCI-induced polyuria by isolating the impact of supraspinal pathway damage.
Main Methods:
- Adult male rats received T3 contusion or sham surgery.
- Metabolic cages were used for 24-hour urine collection and volume measurement.
- Urine and serum biomarkers, including atrial natriuretic peptide and arginine vasopressin (AVP), were analyzed.
- AVP-labeled cells in the suprachiasmatic nucleus were quantified.
Main Results:
- T3-injured rats showed significantly increased urine void volume from 1 to 6 weeks post-injury compared to shams.
- Urine atrial natriuretic peptide levels increased, while serum arginine vasopressin (AVP) levels decreased post-SCI.
- A significant reduction in AVP-labeled cells was observed in the suprachiasmatic nucleus of T3-injured rats.
Conclusions:
- SCI at the T3 level induces chronic polyuria, confirming the role of descending supraspinal pathways.
- Disruption of these pathways impairs homeostatic control of salt and water balance.
- The findings link higher-level SCI to polyuria and altered AVP regulation, potentially contributing to nocturia.
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