Basic study on velocity-flow urodynamics using Doppler sonography: Simultaneous detection of cavitation and Doppler signals in an artificial urethral model

BACKGROUND: We have developed velocity-flow urodynamics using Doppler sonography based on the hypothesis that microbubbles formed in the urethra are responsible for Doppler signals. In order to confirm this hypothesis derived from Bernoulli's principle, we investigated the simultaneous detection of cavitation noise and Doppler signals in an experimental system. METHODS: An experimental circuit was built in which a stenosis was created using a glass or silicon tube with tap water used as the sample fluid. Doppler signals, pressure before and after the stenosis, flow rate, flow velocity and cavitation noise were measured. Direct detection of cavitation with a high-speed charged-coupled device (CCD) camera was conducted in the glass tube. The relationship between cross-sectional area and flow velocity in terms of the detection of Doppler signals was analyzed in the silicon tube study. RESULTS: In the glass tube study, a high-speed CCD camera clearly detected masses of microbubbles associated with cavitation. The range of flow rates creating cavitation completely corresponded with those producing Doppler signals detected by ultrasonography. A similar correlation was observed in the silicon tube study, which showed that a low flow velocity of 41.5 cm/sec through a stenosis with a cross-sectional area of 20 mm(2) created Doppler signals at a flow rate of 8.3 mL/sec. CONCLUSION: The results of the present study confirmed that microbubbles created in flowing urine are responsible for Doppler signals. Measurement of velocity-flow urodynamics has great potential to become a non-invasive and reliable alternative to conventional pressure- flow urodynamic studies.     

Quantitative variations in polymorphic types of human red cell esterase D

Human red cell esterase D was analysed quantitatively in Japanese samples. Among the three esterase D phenotypes there was a significant difference in catalytic activity, with an approximate ratio of 7:5:3 for EsD 1, EsD 2-1 and EsD 2. With a few inter-type individuals, the distribution of their activity values was plotted in a tri-modal curve. These results suggest that the esterase D system in human red cells is qualitatively and even quantitatively controlled by genes.     

Alternations in atrial natriuretic peptide release after DC cardioversion of non-valvular chronic atrial fibrillation

The response of atrial natriuretic peptide (ANP) release tohaemodynamic influences after cardioversion of atrial fibrillationhas not been fully examined. We measured plasma concentrationsof ANP and assessed haemodynamic changes 60–120 min afterDC cardioversion in 22 patients with non-valvular chronic atrialfibrillation. Passive leg elevation to enhance volume expansionwas performed 60 min after DC cardioversion. Sinus rhythm wasrestored in 18 of the 22 patients (successful DC cardioversiongroup). The control group consisted of seven patients with non-valvularchronic atrial fibrillation who did not undergo DC cardioversion(atrial fibrillation control group). In the successful DC cardioversiongroup, the mean pulmonary artery wedge pressure decreased significantly15 min after cardioversion (P<0.05) and then remained unchanged.Plasma concentrations of ANP also decreased significantly 15min after cardioversion (P<0.05). Furthermore, there wasan additional significant decrease in ANP levels for up to 60min after cardioversion (P<0.05 from 15 min). Passive legelevation for 15 min led to an increase in the mean pulmonaryartery wedge pressure (P<0.01) and right atrial pressure(P<0.05), but did not result in increased plasma concentrationsof ANP (47.1 ± 27.6 vs 43.9 ± 34.4 pg. ml^–1,mean ± SD, P=ns). In the atrial fibrillation controlgroup, passive leg elevation increased the mean pulmonary arterywedge pressure (P<0.01), the mean right atrial pressure (P<0.05)and plasma concentrations of ANP (139.9 ± 85.8 vs 1681±108.2, P<0.05). In summary, after successful DC cardioversionof non-valvular chronic atrial fibrillation, plasma concentrationsof ANP decreased in conjunction with decreased mean pulmonaryartery wedge pressure. The response of ANP release to volumeexpansion, however, appears to be dysregulated in this patientpopulation.