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Microvascular Injury in Ketamine-Induced Bladder Dysfunction.

Chih-Chieh Lin1,2,3, Alex Tong-Long Lin2,3, An-Hang Yang1,4,5

  • 1Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.

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|August 17, 2016
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Summary
This summary is machine-generated.

Ketamine-induced cystitis involves bladder microvascular injury and endothelial cell changes, leading to bladder dysfunction. This study investigated these mechanisms in patients with a history of ketamine use.

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Area of Science:

  • Urology
  • Pathology
  • Cell Biology

Background:

  • Ketamine-induced cystitis (KC) pathogenesis is not fully understood.
  • Microvascular injury is a potential contributing factor to KC.

Purpose of the Study:

  • To investigate bladder microvascular injury and endothelial cell alterations in KC.
  • To explore the role of N-methyl-d-aspartate receptor subunit 1 (NMDAR1) and mesenchymal transition in KC.

Main Methods:

  • Prospective study of 36 KC patients and 9 controls.
  • Utilized questionnaires (ICSI, ICPI), urodynamic studies, and radiological exams.
  • Performed double-immunofluorescence staining, electron microscopy (EM), and proximity ligation assay (PLA) on bladder tissues.

Main Results:

  • KC patients exhibited significantly higher ICSI and ICPI scores and reduced bladder capacity.
  • EM revealed significant basement membrane duplication in KC bladder microvessels.
  • PLA showed significant co-expression of CD31 and FSP-1, indicating mesenchymal transition in endothelial cells.

Conclusions:

  • Bladder microvascular injury, including basement membrane duplication, is implicated in KC.
  • Endothelial cells in KC patients undergo mesenchymal phenotypic alteration.
  • These microvascular and cellular changes may contribute to KC-induced bladder dysfunction.