Acute lower urinary tract dysfunction (LUTD) following traumatic brain injury (TBI) in rats

Benjamin J. Moody, Caleb Liberman, Peter Zvara, Phillip P. Smith, Kalev Freeman, Katarina Zvarova*

*Kontaktforfatter for dette arbejde

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Aims The aim of this study was to assess experimental traumatic brain injury (TBI)-induced lower urinary tract dysfunction (LUTD) by monitoring systemic and urodynamic parameters using an implantable telemetry system. Methods A single lateral fluid percussion TBI (FP-TBI; 3.4 atm) was administered to 10 female rats. Pressure micro-catheters were implanted in the abdominal aorta and bladder dome for simultaneous data recording. Hemodynamic and urodynamic variables recorded 24hr before and 24hr after injury were analyzed and compared. Results TBI in the acute phase resulted in LUTD affecting bladder emptying, characterized by failure of voiding reflex, high capacity bladder, increased voided volume, prolonged intermicturition intervals, and loss of compliance. The dominant symptom was urinary retention (100%) and incontinence (60%). The effects followed a pattern of initial loss of bladder function followed by either altered recovery of reflex micturition or a period of incontinence. With a moderate injury symptoms were temporary in 90% of animals and permanent in 10% of animals. Injury produced only transient hypertension (≤1hr) with a maximum systolic pressure of 172.64±14.53mmHg (70% of animals). Conclusions The results demonstrate that experimental FP-TBI causes temporary bladder dysfunction that in more severe cases becomes permanent. Telemetry recordings revealed a sequence of events following injury that establishes moderate TBI as a risk factor for neurogenic bladder disorder. Results also suggest a correlation between lateral FP-TBI and incontinence.

OriginalsprogEngelsk
TidsskriftNeurourology and Urodynamics
Vol/bind33
Udgave nummer7
Sider (fra-til)1159-1164
ISSN0733-2467
DOI
StatusUdgivet - 1. jan. 2014
Udgivet eksterntJa

Fingeraftryk

Urinary Tract
Urodynamics
Wounds and Injuries
Percussion
Urinary Retention
Urination
Compliance
Catheters

Citer dette

Moody, Benjamin J. ; Liberman, Caleb ; Zvara, Peter ; Smith, Phillip P. ; Freeman, Kalev ; Zvarova, Katarina. / Acute lower urinary tract dysfunction (LUTD) following traumatic brain injury (TBI) in rats. I: Neurourology and Urodynamics. 2014 ; Bind 33, Nr. 7. s. 1159-1164.
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abstract = "Aims The aim of this study was to assess experimental traumatic brain injury (TBI)-induced lower urinary tract dysfunction (LUTD) by monitoring systemic and urodynamic parameters using an implantable telemetry system. Methods A single lateral fluid percussion TBI (FP-TBI; 3.4 atm) was administered to 10 female rats. Pressure micro-catheters were implanted in the abdominal aorta and bladder dome for simultaneous data recording. Hemodynamic and urodynamic variables recorded 24hr before and 24hr after injury were analyzed and compared. Results TBI in the acute phase resulted in LUTD affecting bladder emptying, characterized by failure of voiding reflex, high capacity bladder, increased voided volume, prolonged intermicturition intervals, and loss of compliance. The dominant symptom was urinary retention (100{\%}) and incontinence (60{\%}). The effects followed a pattern of initial loss of bladder function followed by either altered recovery of reflex micturition or a period of incontinence. With a moderate injury symptoms were temporary in 90{\%} of animals and permanent in 10{\%} of animals. Injury produced only transient hypertension (≤1hr) with a maximum systolic pressure of 172.64±14.53mmHg (70{\%} of animals). Conclusions The results demonstrate that experimental FP-TBI causes temporary bladder dysfunction that in more severe cases becomes permanent. Telemetry recordings revealed a sequence of events following injury that establishes moderate TBI as a risk factor for neurogenic bladder disorder. Results also suggest a correlation between lateral FP-TBI and incontinence.",
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Acute lower urinary tract dysfunction (LUTD) following traumatic brain injury (TBI) in rats. / Moody, Benjamin J.; Liberman, Caleb; Zvara, Peter; Smith, Phillip P.; Freeman, Kalev; Zvarova, Katarina.

I: Neurourology and Urodynamics, Bind 33, Nr. 7, 01.01.2014, s. 1159-1164.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Acute lower urinary tract dysfunction (LUTD) following traumatic brain injury (TBI) in rats

AU - Moody, Benjamin J.

AU - Liberman, Caleb

AU - Zvara, Peter

AU - Smith, Phillip P.

AU - Freeman, Kalev

AU - Zvarova, Katarina

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Aims The aim of this study was to assess experimental traumatic brain injury (TBI)-induced lower urinary tract dysfunction (LUTD) by monitoring systemic and urodynamic parameters using an implantable telemetry system. Methods A single lateral fluid percussion TBI (FP-TBI; 3.4 atm) was administered to 10 female rats. Pressure micro-catheters were implanted in the abdominal aorta and bladder dome for simultaneous data recording. Hemodynamic and urodynamic variables recorded 24hr before and 24hr after injury were analyzed and compared. Results TBI in the acute phase resulted in LUTD affecting bladder emptying, characterized by failure of voiding reflex, high capacity bladder, increased voided volume, prolonged intermicturition intervals, and loss of compliance. The dominant symptom was urinary retention (100%) and incontinence (60%). The effects followed a pattern of initial loss of bladder function followed by either altered recovery of reflex micturition or a period of incontinence. With a moderate injury symptoms were temporary in 90% of animals and permanent in 10% of animals. Injury produced only transient hypertension (≤1hr) with a maximum systolic pressure of 172.64±14.53mmHg (70% of animals). Conclusions The results demonstrate that experimental FP-TBI causes temporary bladder dysfunction that in more severe cases becomes permanent. Telemetry recordings revealed a sequence of events following injury that establishes moderate TBI as a risk factor for neurogenic bladder disorder. Results also suggest a correlation between lateral FP-TBI and incontinence.

AB - Aims The aim of this study was to assess experimental traumatic brain injury (TBI)-induced lower urinary tract dysfunction (LUTD) by monitoring systemic and urodynamic parameters using an implantable telemetry system. Methods A single lateral fluid percussion TBI (FP-TBI; 3.4 atm) was administered to 10 female rats. Pressure micro-catheters were implanted in the abdominal aorta and bladder dome for simultaneous data recording. Hemodynamic and urodynamic variables recorded 24hr before and 24hr after injury were analyzed and compared. Results TBI in the acute phase resulted in LUTD affecting bladder emptying, characterized by failure of voiding reflex, high capacity bladder, increased voided volume, prolonged intermicturition intervals, and loss of compliance. The dominant symptom was urinary retention (100%) and incontinence (60%). The effects followed a pattern of initial loss of bladder function followed by either altered recovery of reflex micturition or a period of incontinence. With a moderate injury symptoms were temporary in 90% of animals and permanent in 10% of animals. Injury produced only transient hypertension (≤1hr) with a maximum systolic pressure of 172.64±14.53mmHg (70% of animals). Conclusions The results demonstrate that experimental FP-TBI causes temporary bladder dysfunction that in more severe cases becomes permanent. Telemetry recordings revealed a sequence of events following injury that establishes moderate TBI as a risk factor for neurogenic bladder disorder. Results also suggest a correlation between lateral FP-TBI and incontinence.

KW - bladder dysfunction

KW - cystometry

KW - fluid percussion injury

KW - telemetry

KW - traumatic brain injury

U2 - 10.1002/nau.22470

DO - 10.1002/nau.22470

M3 - Journal article

VL - 33

SP - 1159

EP - 1164

JO - Neurourology and Urodynamics

JF - Neurourology and Urodynamics

SN - 0733-2467

IS - 7

ER -