Urinary bladder volumetry by means of a single retrosymphysically implantable ultrasound unit.

AIMS: Optimal voiding is a crucial issue for patients with neurogenic bladder dysfunctions to prevent long-term damage to the urinary tract. In prior studies, implantable ultrasound (US) sensors have proved an appropriate method of measuring the urinary bladder volume. Their disadvantage is that they tend to dislocate in chronic applications as they are fixed directly onto the bladder wall. In the present study, we describe an implantable US volumetry unit that does not require fixing to the bladder wall and consists of a single receiver-transmitter unit. MATERIALS AND METHODS: Six Göttinger minipigs were anesthetized in ITN; a sensor was stitched behind the symphysis into the periosteum and aligned to the bladder so that an US measurement could take place in ventro-dorsal direction. In steps of 50 ml, the bladder was filled up to 250 ml via a transurethral catheter; after each filling step the volume was measured three times and compared to the instilled volume. RESULTS: On average the measurements with implanted US differed from the actual bladder filling by 77.4% at a bladder filling of 50 ml ("error" messages were included as 0 ml), 3.8% at 100 ml, 3.8% at 150 ml, and 0.3% at 200 ml, and 3.6% at 250 ml. When the empty bladder (= 0 ml) was measured, the US sensor detected no volume in 73% of the cases. CONCLUSIONS: In our animal model, the above-described US system proved tantamount with other external US measuring units and presented a precise and low-artefact system, allowing reliable measuring of the urinary volume with good chances of preserving these positive qualities over time. We expect that clinical application of this system may help to determine the optimal voiding time and thus to avoid bladder over-extension and damage to the urinary tract over time.

Selective block of urethral sphincter contraction using a modified Brindley electrode in sacral anterior root stimulation of the dog.

AIMS: Patients with spinal cord injury often present with dysfunction of urinary bladder and urethral sphincter. One treatment option is sacral rhizotomy and sacral anterior root stimulation with the Finetech Brindley stimulator. However, a major disadvantage is the lack of selective stimulation, resulting in simultaneous contraction of sphincter and bladder followed by unphysiological micturition. This study investigated the possibility of selective bladder stimulation by using a Brindley electrode. METHODS: In 11 male anaesthetized foxhounds, a complete posterior rhizotomy was perormed. The anterior S2 roots were stimulated with different quasi-trapezoidal (QT) pulses (pulse length range, 600-1,400 microsec; stimulation current, 0.1-2.0 mA; frequency, 20 Hz) by using a tripolar Brindley electrode. Sphincter and bladder pressures were measured urodynamically. RESULTS: All 11 animals showed a maximal reduction of the highest sphincter pressure over 80%, and in 6 of 11 trials, the sphincter pressure was inhibited completely (100%). With stimulations at maximal sphincter blockade, the average achievable bladder pressure was 33.48 cm H(2)O higher than the average sphincter pressure, and in three cases, a strong micturition was observed. Selective blockade of the sphincter was possible by applying QT pulses. The bladders remained uninfluenced by this blockade and kept their excitability at any time. CONCLUSIONS: This study shows that selective bladder stimulation with little or no coactivation of the sphincter is possible. A physiological micturition can be achieved by using a tripolar Brindley electrode. Introduction of this stimulation technique into clinical practice should not face major difficulties, considering that the device is an established electrode.

Effects of acute urinary bladder overdistension on bladder response during sacral neurostimulation.

OBJECTIVE: Urinary retention and micturition disorders after overdistension are clinically well-known complications of subvesical obstruction. We attempted to evaluate whether bladder overdistension influences bladder response and whether overdistension supports detrusor decompensation. METHODS: Following lumbal laminectomy in 9 male foxhounds, the sacral anterior roots S2 and S3 were placed into a modified Brindley electrode for reproducible and controlled detrusor activation. The bladder was filled in stages of 50 ml from 0 to 700 ml, corresponding to an overdistension. At each volume, the bladder response during sacral anterior root stimulation was registered. After overdistension, the bladder was refilled stepwise from 0 to 300 ml and stimulated. RESULTS: In all dogs, the bladder response was influenced by the intravesical volume. The maximum pressure (mean 69.1 cm H(2)O) was observed at mean volume of 100 ml. During overdistension, a significant reduction in bladder response of more than 80% was seen. After overdistension, a significant reduction in intravesical pressure of 19.0% was observed. In 2 cases, reduction in bladder response was more than 50% after a single overdistension. CONCLUSIONS: We conclude that motoric bladder function is influenced during and after overdistension. A single bladder overdistension can support acute and long-lasting detrusor decompensation. In order to protect motoric bladder function, bladder overdistension must be prevented.

Smooth muscle electromyography of the urinary bladder.

To elucidate smooth muscle activity of the urinary bladder, we utilized an optimized animal model and a specially developed, computer-aided data acquisition and analysis system for bioelectrical signals. Twenty-five Wistar rats were pharmacologically paralyzed and artificially respirated. The urinary bladder was exposed by a suprapubic midabdominal incision, and both ureters were ligated to prevent physiological filling of the bladder. The bladder was initially emptied by slight manual pressure and was then filled via a transurethral catheter in 0.1-ml steps to a maximum of 0.45 ml with physiological saline. A custom-made, gold-plated needle electrode was tangentially guided by a micromanipulator to the smooth muscle of the bladder dome, and the recordings commenced. Furthermore, smooth muscle EMG recordings of the bladder were performed after pharmaco-stimulation of the detrusor with carbachol. Initial results demonstrate that, with the animal model presented here, it is possible to record reproducible and almost artifact-free smooth muscle activity from the urinary bladder. All experiments displayed a stochastic distribution of similar electrical events, increasing in appearance and amplitude with increased bladder volume and after pharmacostimulation with carbachol. Two-dimensional power spectrum analysis revealed a main signal frequency below 1 Hz.

Arterial constriction, ischemia-reperfusion, and leukocyte adherence in acute pancreatitis.

We investigated microcirculatory changes in sodium taurocholate (ST)-induced pancreatitis. Groups of rats received as tracer either fluorescein isothiocyanate-dextran or acridine orange intravenously. The microcirculation of the exposed pancreas was observed by use of a video camera attached to an epi-illumination microscope. Vessel diameters and plaques of adherent leukocytes were measured with a digital image-analyzing system. In contrast to 0.4 ml of saline, intraductal infusion of ST (4%, 0.4 ml) induced a constriction of interlobular pancreatic arteries of 79 +/- 2% (P < 0.01) within 2 min. This constriction could not be antagonized by the leukotriene antagonist CGP-35949B. The radical scavengers superoxide dismutase (SOD) and N-(2-mercaptopropionyl)glycine (MPG) prevented the arterial constriction. Constriction of pancreatic arteries was accompanied by a decrease of erythrocyte velocity in the pancreatic capillaries. Flux in the head of the pancreas measured by laser-Doppler velocimetry decreased from 300 +/- 69 to 74 +/- 23 perfusion units (P < 0.01) after 446 +/- 159 s. Subsequently an increase of perfusion values was observed indicating reperfusion phenomena. ST induced leukocyte adherence to the walls of interlobular veins forming plaques constituting 39% of the observed venular cross section within 6 min. The leukotriene antagonist, SOD, or MPG prevented leukocyte adherence. Arterial constriction followed by ischemia-reperfusion and leukocyte adherence to venular endothelium during the reperfusion period represented the sequence of microcirculatory changes in ST-induced pancreatitis. The radical scavengers SOD and MPG prevented arterial constriction and leukocyte adherence to venular endothelium, indicating the involvement of free radicals in the pathogenesis of ST-induced pancreatitis in the rat.

Microcirculatory changes in sodium taurocholate-induced pancreatitis in rats.

Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.