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[Detrusor ischemia. linical effects].

B A Berdichevsky1, V B Berdichevsky1

  • 1Department of Oncology with a course of urology of FGBOU VO Tyumen State Medical University of the Ministry of Healthcare of the Russian Federation, Tyumen, Russia.

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|December 7, 2019
PubMed
Summary
This summary is machine-generated.

Overactive bladder may stem from neurogenic, myogenic, or urothelial factors. A new theory suggests detrusor ischemic disease, caused by impaired blood flow during bladder overactivity or high urine volume, contributes to overactive bladder development.

Keywords:
clinical effectsdetrusor ischemiahypoactive bladderoveractive bladder

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Area of Science:

  • Urology
  • Physiology
  • Pathology

Background:

  • Overactive bladder (OAB) is a condition with significant clinical impact.
  • Current understanding of OAB pathophysiology includes neurogenic, myogenic, and urothelial theories supported by evidence.

Purpose of the Study:

  • To review existing theories on overactive bladder development.
  • To propose a novel theory regarding the role of ischemia in OAB.

Main Methods:

  • Literature analysis of experimental and clinical evidence for OAB theories.
  • Synthesis of findings to propose a new pathogenetic mechanism.

Main Results:

  • Established evidence supports neurogenic, myogenic, and urothelial theories of OAB.
  • A novel hypothesis, detrusor ischemic disease, is proposed.

Conclusions:

  • Detrusor ischemic disease may arise from impaired blood flow during bladder overactivity.
  • This ischemia could result from vessel compression due to incomplete relaxation or high urine volume in hypoactive bladder.