PL 22. Highlight in OAB
Podium Lecture

PL 22. Highlight in OAB

Bo Song

Department of Urology, Southwest Hospital, Third Military Medical University

OAB is considered to be one kind of abnormalities in bladder function. However, neural reflex might take potential and important part in OAB initiation. The organs neighbored with the bladder, such as the prostate, the rectum, the female reproductive system and the pelvic floor muscles, might influence the bladder excitation through the nerve-nerve interaction. As we know, the patients with prostatitis always suffer the voiding dysfunction, probably via an autonomic nerve reflex. Simultaneously, inflammation in chronic cervicitis can also bring excitation variation in bladder function. Among these mechanisms, the psychological, neurogenical and/or myogenical factors are thought to be involved.

I. Pelvic nerves and LUTS

(I) Prostatitis and voiding dysfunctions

Posterior urethral infections were traditionally considered to be the main cause for voiding dysfunction. Our results revealed that the block in the peri-prostate nerves can reduce the reaction of the bladder function to the prostatitis, which hints that a "visceral reflex" between the prostate and the bladder. Further study with PI/Bb double-labeled fluorescence confirmed this result.

(II) Chronic cervicitis and bladder functions

Our studies in animal model revealed that the gynecological infection electrically diffused, with neural factors involved. Nerve tract technique revealed that the bladder and the cervix uteri were innervated by the same neuron, which hinted an "axonaxon reflex" between the bladder and the uteri.

(III) Rectum and voiding

OAB often combined with constipation. Besides the psychological influence, Is there any other mechanism involved? Studies on animals revealed that the constipation can cause voiding dysfunctions, including the reduce of bladder volume, increase of the detrusor pressure, and occurrence of the detrusor instability.

II. Neurogeni/ myogenic factors in bladder instability

The traditional hypothesis to explain the detrusor instability is the supersensitivity of autonomic nerves. How about other studies?

(I) Detrusor spontaneous excitation

Detrusor owes the capability to contract independent to M and β cholinergic receptors, which was also confirmed in the studies on VIP and purine receptors.

(II) Stretch load and detrusor excitation

Stretch load can induce the bladder excitation. Over-tension and permanent stretch load can cause uncontrollable bladder excitation, which seems to be independent to the innervation.

(III) Whole-bladder study

The whole-bladder can contract in vitro. There seems to be no distinguish in this kind of whole-bladder contraction between the neurogenic and obstructive instability.

III. Psychological behaviors and bladder excitation

Sympathetic skin reflex (SSR) was found to be high concord with the bladder sensory function. SSR might be a good and objective parameter for indicating the bladder sensory for normal, oversensitive, hyposensitive, and OAB patients.

IV. Bladder pacemaking and pacemaker

Pacemaking current, higher excitation and unobstructed transmission are the basic conditions for pacemaking. Bladder interstitial of Cajal cell behaves as the pacemaking cell in some kind of degree. Studies showed:

(I) It owes the simultaneous physiological characteristics, and positive for c-kit dye.

(II) Bladder ICC contains the capabilities of spontaneous and post-stretch excitation. iii) Excitation can transmit from ICC to the detrusor myocytes by fluorescence recovery after phtobleaching (FRAP) studies.

(III) Bladder ICC changed in detrusor instatilities.

(V) c-kit blocker, Glivec can reduce the bladder constriction.

DOI: 10.3978/j.issn.2223-4683.2012.s237

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