BLOOD FLOW, PRESSURE AND COMPLIANCE IN THEMALE HUMAN BLADDER

RICHARD T. KERSHEN, KAZEM M. AZADZOI AND MIKE B. SIROKYFrom the Departments of Urology and Pathology, Boston University School of Medicine and Department of Urology, Boston Veterans

Affairs Health Care, Boston, Massachusetts

ABSTRACT

Purpose: The regulation of human bladder blood flow during filling is poorly understood. Wecharacterized changes in bladder blood flow with filling and examined the relationship of bladdercompliance and blood flow.

Materials and Methods: A total of 17 awake male patients underwent saline cystometryfollowed by cystoscopy while under local anesthesia, during which a laser Doppler flow probe wasplaced into the posterior bladder wall detrusor. Systemic blood pressure, bladder blood flow andintravesical pressure were measured with the bladder empty and filled to 25%, 50%, 75% and100% of awake maximum cystometric capacity as well as immediately after bladder drainage.

Results: Mean bladder blood flow was lowest in the empty bladder and increased with bladderfilling. A mean peak flow plus or minus standard error of 7.6 � 1.1 ml. per minute per 100 gm.tissue was observed at volumes greater than 75% but less than 100% of maximum cystometriccapacity. At 100% maximum cystometric capacity mean intravesical pressure increased by 73%from 25.2 to 43.5 cm. water and bladder blood flow decreased by 36%. Rapid bladder drainage wasassociated with a rebound in mean bladder blood flow to approximately 1.6 times baseline.Bladder compliance calculated for the whole filling curve positively correlated with bladder bloodflow (p � 0.025), that is low compliance was associated with low blood flow.

Conclusions: Human bladder blood flow tends to increase with increasing volume and pressure,and depends largely on local regulation. At capacity bladder blood flow is significantly decreased.Immediately after bladder drainage there is a rebound in blood flow, allowing reperfusion tooccur. Decreased bladder blood flow and decreased bladder wall compliance correlated strongly,suggesting that ischemia may lead to structural changes in the bladder wall.

KEY WORDS: bladder, blood pressure, reperfusion, physiology, urination

The increased prevalence of lower urinary tract symptomsin elderly men and women is well documented.1–4 Lowerurinary tract symptoms in men have traditionally been as-cribed to bladder outlet obstruction due to prostate enlarge-ment. However, recent studies show that in approximately athird to more than half of symptomatic male patients there isno urodynamic evidence of obstruction.4–7 These studies alsoshow that on validated symptom indexes women have scoressimilar to those of their male counterparts.4–6 On urody-namic examination women have age associated bladder dys-function comparable to men.4–6 These observations suggestthat bladder outlet obstruction alone does not adequatelyexplain the pathophysiology of the aging lower urinary tract.

In a recent review we summarized supporting evidence forthe role of pelvic arterial insufficiency in erectile and detru-sor dysfunction.8 There is increasing clinical9, 10 as well asexperimental11, 12 evidence that supports a strong associationof atherosclerosis with erectile dysfunction in men.13 Simi-larly experimental studies revealed that chronic bladderischemia is associated with marked changes in detrusor com-pliance14 and contractility.15 Detrusor instability and loss ofcompliance were also observed in the aging human detrusor.6

To determine whether ischemia has any role in detrusordysfunction it is necessary to establish normative data onchanges in bladder blood flow in response to filling. The fewstudies in humans that have been published provide contra-dictory results, most likely due to different measurementtechniques (mucosa versus detrusor muscle) and different

states of bladder fullness (distended versus empty). As aresult, reliable data on the normal response of the bladdercirculation to filling does not exist. We characterized thechanges in male bladder blood flow and microcirculatoryresistance with increasing bladder distension and deter-mined whether bladder wall compliance correlates with bloodflow.

MATERIALS AND METHODS

A total of 17 men 44 to 86 years old (mean age 69) under-going cystoscopy as part of evaluation for lower urinary tractsymptoms (12), hematuria (2) or followup screening for blad-der cancer (3) were asked to participate in our study. Theysigned an institutional review board approved consent form.All patients undergoing surveillance cystoscopy for bladdercancer had no evidence of tumor.

Determination of maximum cystometric capacity. After ure-thral catheterization with a 16Fr Foley catheter each patientunderwent water cystometry using body temperature salineat a filling rate of 50 ml. per minute to determine awakemaximum cystometric capacity, defined as the volume atwhich detrusor contraction occurred or further filling couldnot be tolerated.

Technique of blood flow measurement. A 19Fr rigid cysto-scope with 30-degree lens was placed under direct vision intothe bladder of each awake patient under local anesthesia.The bladder was visually surveyed, followed by the place-ment of a specially designed sharp-tipped endoscopic laserDoppler blood flow probe (1 mm. in diameter) at 1 site intothe detrusor muscle of the posterior bladder wall. The prin-

Accepted for publication February 22, 2002.Supported by National Institutes of Health Grant RO1AG/

DK17165 and a grant from the Veterans Affairs Central Office.

0022-5347/02/1681-0121/0THE JOURNAL OF UROLOGY® Vol. 168, 121–125, July 2002Copyright © 2002 by AMERICAN UROLOGICAL ASSOCIATION, INC.® Printed in U.S.A.

121

ciples and technique of laser Doppler flowmetry have beendescribed previously.14, 15 The bladder was then completelyemptied and maintained at rest for 5 minutes. The analogoutput of the laser Doppler flowmeter (0 to 10 V.) was con-nected to a 2-channel strip chart recorder. The time constantwas set at 3 seconds to dampen the response. The outflowport of the cystoscope was connected by vinyl tubing to apressure transducer for intravesical pressure measurement.To obtain simultaneous pressure and blood flow meas-urements the pressure transducer was connected to the samechart recorder as the laser Doppler flowmeter. All channelswere calibrated before each case.

Estimation of systemic blood pressure. A blood pressurecuff placed on the left arm of each patient was connected toan automatic inflator and used to record systolic and diastolicblood pressure at the time of each bladder blood flow meas-urement.

Blood flow measurement protocol. Initial blood flow meas-urements were obtained with the bladder completely empty(0% maximum cystometric capacity). Each bladder was thencycled through a sequence that consisted of filling the blad-der slowly by hand with normal saline warmed to body tem-perature to a volume of 25%, 50%, 75% and 100% of awakemaximum cystometric capacity. The bladder was then com-pletely drained (fig. 1). Simultaneous measurements of sys-temic blood pressure in mm. Hg, bladder blood flow in ml. perminute per 100 gm. tissue and intravesical pressure in cm.water were obtained at each degree of bladder filling andimmediately after drainage. Measurements at each degree offilling were obtained after a 2-minute equilibration period.Blood flow was measured for approximately 3 minutes todecrease the influence of movement artifacts.

Calculation of bladder microcirculation resistance (Rmi-cro). To normalize blood flow for varying systemic blood pres-sure we calculated the mean microcirculatory resistance ateach volume using the formula, Rmicro � (diastolic BP in mm.Hg � 1/3 pulse pressure)/bladder blood flow in ml. per minuteper 100 gm. tissue, where BP represents blood pressure andpulse pressure � systolic BP-diastolic BP.

Determination of bladder compliance. Bladder compliance

in each patient for the whole course of the filling curve wascalculated from the infused volume and intravesical pressure(Pves) using the formula, compliance � infused volume at100% Cmax/(Pves at 100% Cmax � Pves at 0% Cmax), whereCmax represents maximum cystometric capacity.

Statistical analysis. All statistical comparisons were doneusing commercially available software. Average bladderblood flow was compared with calculated bladder complianceusing the correlation coefficient. Changes in bladder volume,intravesical pressure and bladder blood flow were analyzedby analysis of variance. Significance was considered at p�0.05.

RESULTS

Effect of filling on intravesical pressure. Intravesical pres-sure increased gradually during filling up to 75% of capacity.As bladder filling increased from 75% to 100% maximumcystometric capacity, a 73% increase in mean intravesicalpressure was observed from 25.2 � 4.7 to 43.5 � 7.3 cm.water. Bladder emptying resulted in a decrease in intraves-ical pressure to pre-filling levels (10.7 � 2.3 cm. water) (fig.2).

Effect of filling on bladder blood flow. In the empty bladdermean blood flow was lowest at 4.2 � 1.0 ml. per minute per100 gm. tissue (see table). With filling mean blood flow in-creased (fig. 1). A mean peak flow of 7.6 � 1.1 ml. per minuteper 100 gm. tissue was observed at volumes greater than 75%but less than 100% of maximum cystometric capacity. As100% maximum cystometric capacity was approached, intra-vesical pressure significantly increased, as mentioned. It wasaccompanied by a 36% decrease in mean bladder blood flowfrom 7.6 � 1.1 to 4.9 � 0.7 ml. per minute per 100 gm. tissue(see table and fig. 2). With bladder emptying there was arebound increase in bladder blood flow that remained ele-vated for approximately 5 minutes at 6.9 � 1.1 ml. perminute per 100 gm. or about 1.6 times that in the emptystate.

Relationship of intravesical pressure and blood flow. Therewas a complex nonlinear relationship of intravesical pressure

FIG. 1. Re-drawn bladder blood flow and intravesical pressure record during stepwise filling shows rebound in flow after bladderdrainage.

BLOOD FLOW, PRESSURE AND COMPLIANCE IN MALE BLADDER122

and bladder blood flow. Bladder blood flow tended to increaseduring the early stages of filling and decrease during thelater stages. Peak blood flow was associated with an intra-vesical pressure of about 23 cm. water (fig. 3).

Relationship of bladder wall compliance and blood flow.Bladder compliance calculated for the whole course of fillingcorrelated significantly with baseline blood flow, changes inblood flow observed during filling up to 75% maximum cys-tometric capacity and blood flow at maximum cystometriccapacity (p � 0.04, 0.02 and 0.03, respectively). Patients withdecreased bladder compliance had lower mean empty bladder

blood flow, smaller increases in flow with filling and de-creased perfusion at maximal capacity.

DISCUSSION

Various conditions are associated with decreased bladderblood flow, including aging,16 outflow obstruction,17 meno-pause18 and interstitial cystitis.19, 20 Recent studies suggestthat decreased vesical blood flow is associated with impor-tant functional and structural abnormalities of the bladder.Azadzoi et al noted that chronic bladder ischemia in a rabbit

FIG. 2. Bladder blood flow and intravesical pressure versus bladder volume in 17 patients

Data obtained during bladder filling

Bladder Filling (% max.cystometric capacity)

Mean Bladder Pressure� SEM (cm. water)

Mean Bladder Vol.� SEM (ml.)

Mean Bladder BloodFlow � SEM (ml./

min./100 gm.)

Mean MicrocirculatoryResistance � SEM (mm.

Hg/ml./min./100 gm.)

0, Empty 9.4 � 1.7 0 4.2 � 1.0 35.6 � 4.625 16.4 � 3.4 99.3 � 14.0 6.4 � 1.0 22.0 � 3.550 20.6 � 4.0 198.5 � 28.0 7.5 � 1.2 19.1 � 3.175 25.2 � 4.7 306.7 � 45.5 7.6 � 1.1 17.7 � 3.1100 43.5 � 7.3 450 � 64.4 4.9 � .74 30.4 � 4.8

0, Drained 10.7 � 2.3 0 6.9 � 1.1 22.3 � 4.6

FIG. 3. Relationship of intravesical pressure and bladder blood flow in 17 patients

BLOOD FLOW, PRESSURE AND COMPLIANCE IN MALE BLADDER 123

model resulted in decreased compliance,14 unstable contrac-tions and impaired contractility.15 On the cellular level therewas increased expression of transforming growth factor-�1with resultant collagen deposition, smooth muscle atrophyand fibrosis.14, 15 In vivo bladders with severe chronic isch-emia have impaired contractility.15, 21

Some of these findings in animal models of ischemia aresimilar to those in the aging bladder. In aged rats increasedcollagen was reported in the detrusor muscle22, 23 and anincreased incidence of detrusor instability was noted.24 Inhumans the prevalence of lower urinary tract symptoms in-creases with age and that condition develops with similarfrequency in men and women.1–4 The aging bladder seems tobe characterized by a progressive decrease in the ratio ofsmooth muscle-to-connective tissue in the 2 sexes indepen-dent of bladder outlet obstruction.25, 26

Studies in humans suggest age related impairment of de-trusor function. For example, Ameda et al observed in agroup of elderly men without outlet obstruction who com-plained of lower urinary tract symptoms that the prevalenceof detrusor instability with impaired contractility increasedwith age.7 Homma et al reported an age related decrease inbladder capacity, detrusor contractility and flow rate inasymptomatic men and women.27

The development of the laser Doppler flowmeter has en-abled real-time dynamic estimation of blood flow and it wasfirst applied to the bladder microcirculation in a caninemodel by Siroky et al.28, 29 In a later study Azadzoi et al notedthat canine bladder blood flow decreased with filling as in-travesical pressure increased.30 Using laser Doppler flow-metry in a conscious pig model Greenland and Brading ob-served that bladder blood flow decreased only with lowcompliance filling, suggesting that high intravesical pressureis the principal determinant of bladder blood flow.31

The first studies of human bladder blood flow using laserDoppler flowmetry were reported in 1993 by Irwin andGalloway.19 In anesthetized patients they estimated bloodflow at the mucosal level at an intravesical volume of 100 ccand at maximum capacity. Batista et al first reported laserDoppler flow measurements in human detrusor muscle.32

When comparing blood flow in the detrusor muscle in theempty state and after filling with normal saline, they notedthat bladder distention to 300 cc resulted in a significantdecrease in mean bladder blood flow.

Our results show that there is a complex biphasic relation-ship among bladder volume, intravesical pressure and micro-circulatory resistance in the bladder. During the filling phasebladder blood flow increases approximately 1.8 times that ofthe empty bladder. As intravesical volume approaches 100%of maximum cystometric capacity, intravesical pressure in-creases more rapidly and bladder blood flow is significantlydecreased to about 1.2 times that of the empty bladder.Because of the increase in blood flow associated with filling,it remains above the blood flow in the empty state despiteincreased intravesical pressure. Immediately after bladderdrainage a rebound increase in flow occurs, raising blood flowto about 1.6 times that of the empty bladder.

To explain these observations an anatomical and a neuro-physiological hypothesis may be put forward. Miodonski andLitwin studied vascular corrosion casts of the human bladderwith scanning electron microscopy and observed that in theempty/collapsed state the bladder microvasculature is ex-tremely tortuous and tightly coiled.33 In this conformationthe vessels would have high resistance, correlating with lowblood flow. With filling and expansion the bladder microvas-culature undergoes topographical rearrangement withstraightening and stretching of the vessels. This scenariowould result in decreased resistance and increased blood flowdespite a likely increase in bladder wall tension. As thebladder approaches maximum cystometric capacity and in-travesical pressure increases, the microvasculature within

the thinning bladder wall is likely compressed, resulting in adecrease in bladder blood flow. However, ultrasound of bloodvessels in human bladder fail to show significant change inthe resistive index in the full and empty states.34

A neural hypothesis is suggested by evidence that thebladder can regulate its circulation (autoregulation).Hohlbrugger et al used color Doppler to visualize arterioles inthe bladder wall of normal human volunteers.35 They notedthat filling the bladder with normal saline from 50 cc tomaximum cystometric capacity significantly increased peaksystolic velocity. Since there was no change in the resistiveindex during filling, they presumed that there was an in-crease in perfused blood volume rather than a decrease inmean microcirculatory resistance. Interestingly they ob-served an increase in flow of about 1.9-fold, almost identicalto our results. Filling the bladder with KCl rather thannormal saline induced a 66% increase in baseline blood flowat 50 cc volume. From this observation they proposed thatlocal reflexes subserved by C-fiber afferents in the bladdermucosa or submucosa are involved in regulating bladderblood flow.

The reperfusion phenomenon that we observed after drainingthe distended bladder was described by others.31 A possibleexplanation for this phenomenon may be the accumulation oflocal vasodilatory substances, such as prostaglandins or vaso-active intestinal peptide, in response to increased metabolicdemand on the detrusor from distention at high pressure. Thesesubstances have been implicated as mediators of local vesicalvasodilatation.36

To our knowledge we report the first study to demonstratea correlation of compliance with blood flow in the male hu-man bladder. Our results confirm those of Greenland andBrading, who noted in a conscious pig model that low com-pliance filling was associated with a decrease in observedbladder blood flow.31 The question remains whether ischemialeads to loss of compliance, whether low compliance leads toischemia or whether each possibility is true. In our rabbitmodel chronic vesical ischemia resulted in increased expres-sion of locally produced transforming growth factor-�1, lead-ing to collagen deposition, fibrosis and noncompliance.14

Thus, animal studies seem to support the idea that ischemiaalone can lead to decreased bladder compliance. Interestinglywe observed that poorly compliant bladders had the lowestmean blood flow not only when distended, but also whenempty. This finding suggests that decreased blood flow evenwithout high intravesical pressure is associated with a loss ofcompliance and supports the idea that ischemia induces blad-der fibrosis.

Other findings also suggest that by increasing intravesicalpressure decreased bladder compliance reduces bladderblood flow. We observed that poor compliance was associatedwith decreased perfusion during filling to capacity. Poor ves-ical compliance was also associated with smaller increases inflow during filling and with a greater decrease in blood flowat maximum cystometric capacity.

CONCLUSIONS

We report that in awake human males progressive bladderdistention results in an increase in bladder blood flow untilthe bladder approaches maximum cystometric capacity. Theblood flow increases to about 1.8 times baseline flow. Atcapacity we observed a decrease in bladder blood flow toabout 1.2 times baseline flow. After emptying the bladderthere is a rebound in blood flow to about 1.6 times baselinethat lasts approximately 5 minutes. We noted a statisticallysignificant correlation of bladder blood flow with compliance.Further investigations are needed to determine whetherthere is any correlation among symptoms, detrusor functionand bladder blood flow.

BLOOD FLOW, PRESSURE AND COMPLIANCE IN MALE BLADDER124

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