A T Lin1, K K Chen, C H Yang, L S Chang. 1. Division of Urology, Department of Surgery, Taipei Veterans General Hospital and the Department of Urology, National Yang-Ming University School of Medicine, Taipei, Taiwan.
Abstract
OBJECTIVES: To investigate the existence and functional significance of the enhanced lipid peroxidation in bladder overdistension injury and to explore the effect of mannitol, a free radical scavenger. METHODS: Overdistension of rabbit bladders was induced and maintained for 3 hours by infusing normal saline into the bladder while keeping the intravesical pressure at 30 cm H(2)O. The bladders were then emptied and decompressed. Intravenous 20% mannitol was initiated 5 minutes before decompressing the overdistension. Detrusor tissue was obtained from the following groups: control, at the end of the overdistension period, and 30 minutes, 2 hours, and 7 days after decompressing the bladder. The tissue level of adenosine triphosphate (ATP) and phosphocreatine (PCr) and the lipid peroxidation product malondialdehyde (MDA) was assayed. Detrusor contractility was assessed by the response of the detrusor strips to KCl and bethanechol. RESULTS: Decompressing the overdistended bladder led to a period of enhanced lipid peroxidation with an increase of MDA content from 225 to 384 pmol/mg protein 30 minutes after the decompression. Two hours later, the MDA content had recovered to the normal level. Mannitol abolished this period of enhanced lipid peroxidation. Overdistension impaired detrusor contractility and reduced the content of PCr (from 24.1 to 10.8 nmol/mg protein) and ATP (from 9.6 to 4.6 nmol/mg protein). Both detrusor contractility and the content of PCr and ATP further decreased 30 minutes after the decompression (PCr 5.4 nmol/mg, ATP 2.8 nmol/mg). They had recovered, but not fully, 7 days later. Mannitol prevented the further decrease in detrusor contractility and in the content of PCr and ATP during the initial decompression period (30 minutes after the decompression). In addition, the mannitol-treated group had quicker recovery in PCr and ATP levels, which returned to normal 7 days later. CONCLUSIONS: Decompressing an overdistended bladder leads to enhanced lipid peroxidation, which is associated with an additionally decreased energetic metabolism and a more impaired contractile function. Mannitol effectively prevents enhanced lipid peroxidation and facilitates functional recovery. These results show that reactive oxygen species play a significant role in bladder overdistension injury.
OBJECTIVES: To investigate the existence and functional significance of the enhanced lipid peroxidation in bladder overdistension injury and to explore the effect of mannitol, a free radical scavenger. METHODS: Overdistension of rabbit bladders was induced and maintained for 3 hours by infusing normal saline into the bladder while keeping the intravesical pressure at 30 cm H(2)O. The bladders were then emptied and decompressed. Intravenous 20% mannitol was initiated 5 minutes before decompressing the overdistension. Detrusor tissue was obtained from the following groups: control, at the end of the overdistension period, and 30 minutes, 2 hours, and 7 days after decompressing the bladder. The tissue level of adenosine triphosphate (ATP) and phosphocreatine (PCr) and the lipid peroxidation product malondialdehyde (MDA) was assayed. Detrusor contractility was assessed by the response of the detrusor strips to KCl and bethanechol. RESULTS: Decompressing the overdistended bladder led to a period of enhanced lipid peroxidation with an increase of MDA content from 225 to 384 pmol/mg protein 30 minutes after the decompression. Two hours later, the MDA content had recovered to the normal level. Mannitol abolished this period of enhanced lipid peroxidation. Overdistension impaired detrusor contractility and reduced the content of PCr (from 24.1 to 10.8 nmol/mg protein) and ATP (from 9.6 to 4.6 nmol/mg protein). Both detrusor contractility and the content of PCr and ATP further decreased 30 minutes after the decompression (PCr 5.4 nmol/mg, ATP 2.8 nmol/mg). They had recovered, but not fully, 7 days later. Mannitol prevented the further decrease in detrusor contractility and in the content of PCr and ATP during the initial decompression period (30 minutes after the decompression). In addition, the mannitol-treated group had quicker recovery in PCr and ATP levels, which returned to normal 7 days later. CONCLUSIONS: Decompressing an overdistended bladder leads to enhanced lipid peroxidation, which is associated with an additionally decreased energetic metabolism and a more impaired contractile function. Mannitol effectively prevents enhanced lipid peroxidation and facilitates functional recovery. These results show that reactive oxygen species play a significant role in bladder overdistension injury.