Dynamic and pharmacologic urethral pressure profile (UPP) studies were performed on 68 individuals to investigate the neurogenic control of and its contribution to the activity of the sphincteric urethra.
Control profile at rest and with stepwise increase of bladder volume were obtained. Drugs administered were sympathomimetics [noradrenaline (α-stimulant), proterenol (β-stimulant)], sympatholytics [regitine (α-blocker), applobal (β-blocker)], parasympathomimetic [besacholine] and parasympatholytic [buscopan]. Maximum urethral pressure and total urethral length which is the summation of functional urethral length and distal urethral segment were defined as UPmax and UL=fUL+DUS. FUL is the length from the internal urethral orifice to the point where leakage occurred with a fall in UPmax.
Results.
1) Normal individuals: Normal females demonstrated a stable profile with UPmax [adults (13) 46.5±7.6mmHg, children (8) 41.5±15mmHg] situated at midurethra. Relative predominance of DUS in the adults, 40% vs 25%, was an interesting difference between the two groups. In normal males (5) Upmax was 46.0±11.1mmHg and fUL was 3.6±0.6cm. α-block, independent of its cardiovascular effect, lowered the profile most, followed by spinal anesthesia and anticholinergic medication. The profile was increased on bladder distention with or without drugs, none becoming incontinent.
2) Stress incontinent patients (2) failed to increased profile on bladder distention. α-block aggravated this trend further with urinary leakage even on supine position. A patient with stress urge incontinence demonstrated an unstable profile similar to that of uninhibited bladder.
3) In the prostatectomized patients (15) with open prostatic cavity, profile (UPmax 32.7±6.9mmHg, fUL 1.35±0.37cm) was obtained only distal to the cavity where “passive” continence zone and rhabdosphincter exist. Again α-block affected this most. Some experienced incontinence following α-block albeit none before. Pudendal block affected in lesser degree and disturbed only rarely the “active” continence. Other drugs had no effect nor did spinal anesthesia on T 10 level. Successive administration of pudendal block, α-block and buscopan failed to abolish the sphincteric tonicity which is enough to sustain continence.
4) a) Patients with uninhibited bladder (8) showed unstable urethra with bladder distention. This was further augmented by besacholine and was ameriolated by buscopan, while α-block had no effect nor did the others. Synchronization of this unstable activity with uninhibited contraction and urethrovesical regurgitation was confirmed. b) In myelodysplasia (5), in whom dysplasia of the sphincteric neuromuscularity is expected, profile was generally low compared to the normal. Sphincteric incompetency was unquestionable, which was further exaggerated with α-block. When besacholie was given after α-block, profile remained low while detrusor supersensitivity was noted in the bladder. c) In patients (5) with iatrogenic autonomous neurogenic bladder as a result of radical intrapelvic procedures, both denervating factors and structural aberration from the loss of the posterior support were considered to account for the spincteric incompetency. Among them those with intact pudendal innervation responded normally to bladder distention with increase in profile and continence.
5) Lumbar sympathectomy (2) had no effect on UPP.
Sphincteric urethra was surmised as a complexly integrated detrusor-trigono-rhabdomuscular tube with triple parasympathetic-sympathetic-somatic innervation. Intactness of this neuromuscularity with inherent tonicity is essential for the sound sphincteric activity. A functionally normal urethra was defined as one which could withstand various dynamic and pharmacologic stresses. Evidence was presented for the predominant rol
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