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Aims The aim of this study was to determine the accuracy of the non-invasive condom catheter method for diagnosing B(ladder) O(utlet) O(bstruction) in patients eligible for T(rans)U(rethral) R(esection) of the P(rostate). Methods A group of 71 patients eligible for TURP on clinical grounds were invasively and non-invasively studied. On the basis of invasive pressure-flow studies they were stratified into obstructed, equivocal or unobstructed, according to the International Continence Society standard. Subsequently they were diagnosed non-invasively on the basis of a free flowrate measurement, or on the basis of the free flowrate measurement plus the isovolumetric bladder pressure measured with the condom catheter method. R(eceiver) O(perating) C(haracteristic)s were calculated. Results The A(rea) U(nder) the (RO)C for discriminating unobstructed/equivocal patients from obstructed patients was 0.68 in our population. This improved to 0.84 for the 50 patients in whom the isovolumetric bladder pressure was not underestimated by the non-invasive method. Conclusions In our population of TURP patients, the low flowrates affected the accuracy of the condom method to a degree that it did not perform better than a free flowrate measurement, which performed remarkably well. By excluding measurements in which the condom pressure underestimated the isovolumetric bladder pressure this method may contribute to a more accurate, patient friendly diagnosis of BOO in these patients. In the present study this exclusion was done by comparison with an invasive pressure measurement. A practical non-invasive test would necessitate a non-invasive exclusion criterion, which might be based on the risetime of the condom pressure. Neurourol. Urodynam. 33:408-413, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Aim To non-invasively study if compensation and decompensation occurs in the urinary bladder of healthy male volunteers in response to benign prostatic enlargement (BPE) using the condom catheter method. Methods Between 2001 and 2010, 1,020 healthy male volunteers were included in a longitudinal study based on three non-invasive urodynamic examinations during a 5-year follow-up. Inclusion criteria were an informed consent, the ability to void in a normal standing position and a minimum free flow rate of 5.4 ml/sec. Study parameters were prostate volume (PV), maximum free urinary flow rate (Qmax) and bladder contractility, quantified by the maximum isovolumetric bladder pressure, measured in the condom (Pcond.max). Volunteers also completed the International Prostate Symptom Score Form (IPSS). Results Within limitations, the included volunteers had a flat age distribution between 38 and 72 years. This made it possible to combine longitudinal analysis in a 5-year observation interval, with cross sectional analysis in a 35-year age range. Longitudinal analysis showed that with increasing age, PV increased with 1.9% per year, whereas Qmax decreased with 1.1% per year. IPSS increased with 1.1% per year when volunteers were older than 55 years. Pcond.max increased during the 5-year longitudinal follow-up, but not in the cross sectional analysis. Conclusions The difference between cross sectional and longitudinal results of the Pcond.max may have been caused by compensation of the urinary bladder resulting in a selection effect. This would imply that compensation is a relatively fast process, taking approximately 5 years. Neurourol. Urodynam. 33:78-84, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objectives: There is currently general agreement that adenosine is not involved in ischemic preconditioning (IP) in rat hearts. We hypothesized that the failure to show a role for adenosine is due to the use of brief preconditioning stimuli, and therefore investigated whether adenosine is involved when longer stimuli are employed and which receptor subtypes are involved. Methods and results: Infarct size (IS) was determined in anesthetized rats after 180 min of reperfusion (REP) following a 60-min coronary artery occlusion (CAO). IS was 69±2% (n=15) of the risk area in control rats and 45±2% (n=19; P<0.05) following IP by a single 15-min CAO. The non-selective adenosine receptor antagonist SPT, which itself had no effect on IS (74±1%), blunted the protection by IP (IS=57±2%, P<0.05) in a dose of 2×5 mg/kg i.v., and abolished the protection (IS=70±1%) at 2×25 mg/kg i.v. Following IP by three cycles of 3-min CAO and 3-min REP, IS was 24±6% (P<0.05), which was not affected by SPT in doses of 2×10 and 2×25 mg/kg i.v. The A3 antagonist MRS-1191 (3.3 mg/kg, i.p.), which itself did not affect IS (70±2%), blunted the protection by IP with a 15-min CAO (IS=54±2%, P<0.05). When 2×5 mg/kg SPT (a dose selective for A1-receptors, as it did not affect the protection by the A3 selective agonist IB-MECA, 51±3%) and MRS 1191 were combined the protection by IP was abolished (IS=67±2%). Conclusions: Involvement of adenosine in IP in rats depends critically on the duration of the stimulus. Thus, whereas adenosine was not involved when stimuli of 3-min duration were employed, activation of both A1 and A3 receptors contributed when a stimulus of 15 min was used. [ABSTRACT FROM PUBLISHER]

Objective: The aim was to investigate whether ischaemic preconditioning can be obtained by a partial coronary artery occlusion without intermittent reperfusion. Methods: In seven anaesthetised open chest pigs, the flow in the proximal left anterior descending coronary artery was reduced to 30% of baseline during 30 min before the vessel was occluded completely for 60 min (60 min total coronary occlusion, TCO). After 2 h of reperfusion, the area at risk (AR) and infarct size (IS) were determined using standard procedures. Infarct sizes were compared to those observed in control animals (n = 12), which were subjected to 60 min TCO and 2 h reperfusion, and to infarct sizes determined in animals preconditioned by 10 min TCO with either 15 min (n = 10) or 60 min (n = 5) of reperfusion before the 60 min TCO and 2 h reperfusion. In the last three groups of animals, area at risk was varied by occluding the coronary artery or its branches at different sites. Results: In the control animals infarct size was linearly related (r = 0.99, p< 0.001) to the area at risk with a positive intercept on the AR axis: IS/LVmass (×100%) = 0.88 AR/LVmass (×100%)−3.6. At comparable areas at risk, the infarct size of the animals preconditioned with a 10 min TCO was less than for the control animals. For the animals preconditioned with 10 min TCO and 15 min reperfusion, the relationship between infarct size and area at risk was again linear (r = 0.88) and also had a positive intercept on the AR axis: IS/LVmass (× 100%) = 0.68 AR/LVmass (× 100%)-4.8. All animals with the flow reduction to 30% of baseline immediately preceding the 60 min TCO had infarct sizes smaller (p < 0.05) than predicted from the regression equation for the control animals, but the infarct size limitation could not be simply related to variables such as changes in regional systolic and postsystolic segment length shortening, ATP, or ADP during the partial occlusion period. Conclusions: Myocardium can be preconditioned with a flow reduction to 30% of baseline for 30 min without intermittent reperfusion (two stage Harris model). The positive intercept on the AR axis of the IS-AR relationship warrants caution of the use of IS/AR as an index for infarct size limitation.Cardiovascular Research 1994;28:1146-1151 [ABSTRACT FROM PUBLISHER]