Tıp Fakültesi / Faculty of Medicine
Permanent URI for this collectionhttps://hdl.handle.net/11727/1403
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Item Catheterized Uroflowmetry as a Noninvasive Test for Detrusor Acontractility(2014) Egilmez, Tulga; Goren, Mehmet Resit; https://orcid.org/0000-0001-5644-5672; https://orcid.org/0000-0002-2001-1386; 24642885; AAK-9166-2021; Y-6143-2019Objective: To evaluate the efficacy of uroflowmetry performed through an indwelling catheter on the differential diagnosis of detrusor acontractility. Patients and Methods: 50 men aged between 51 and 85 years (mean 66 years) presenting to the outpatient urology department with indwelling catheters due to urinary retention were included in the study. In the supine position, 300 ml of saline was instilled into the bladder and the catheter was blocked; with the patient standing by the flowmeter, the catheter was opened, allowing the patient to void through the catheter. The evaluation continued with a cystometry and pressure-flow study (PFS). The patients were separated into two groups according to the results of the PFS-group 1 with positive detrusor pressure and group 2 with negative detrusor pressure (detrusor acontractility)-and the catheterized uroflow and PFS data were compared. Results: Statistical significance was seen between detrusor acontractility and peak flow rate (Q(max)) on catheterized uroflow when Q(max) <10 ml/s was taken as a threshold value (p = 0). Conclusion: A quick, noninvasive and inexpensive means of assessing lower urinary tract function would improve the management of men needing PFS. This study reveals that catheterized uroflow is a very easy and useful test if the question is whether the bladder is acontractile or not. (C) 2014 S. Karger AG, BaselItem Effects of Sacral Neuromodulation on Isolated Urinary Bladder Function in a Rat Model of Spinal Cord Injury(2015) Kumsar, Sukru; Keskin, Ulya; Akay, Alaaddin; Bilgilisoy, Ugur Taylan; Erdem, S. Remzi; Peskircioglu, C. Levent; Ozkardes, Hakan; 0000-0002-7277-449X; 24917133; AAH-1052-2020IntroductionSacral neuromodulation has been considered as an effective treatment option for various types of chronic voiding dysfunction, but the mechanism of action has not been well understood. The aim of this study was to evaluate the effect of chronic sacral neuromodulation on isolated bladder functions in a rat model of spinal cord injury. Materials and MethodsFemale Sprague-Dawley rats (250-300g; N = 20) were assigned to four groups as follows: 1) control group (N = 6); 2) spinal cord transection group (SCT; N = 5); 3) spinal cord transection + sacral neuromodulation group (SCT + SNM; N = 5); 4) sham (spinal cord transection + electrode wire implantation without sacral neuromodulation; N = 4). The rats in the SCT, SCT + SNM, and sham groups were anesthetized with ketamine (60mg/kg, i.p.) and xylazine (7mg/kg, i.p.). The spinal cord was completely transected at T8-T9 level in SCT and SCT + SNM groups. Electrode wires were implanted into S3 dorsal foramina in both sham and SNM groups, but only the SNM group was subjected to electrical stimulation for four hours a day for three weeks. Twenty-one days later, the rats were sacrificed via anesthetic overdose, and isolated longitudinal bladder strip preparations were placed in organ baths for the investigation of their isometric responses to pharmacological agents. ResultsIn isometric contraction experiments, SCT was found to increase the contraction responses of the bladder strips to muscarinic stimulation, and SNM could not prevent this increase. In isometric relaxation experiments, SCT caused a decrease in -adrenergic relaxation responses, and SNM augmented the bladder's -adrenergic relaxation responses. Nitric oxide did not affect the relaxation responses. ConclusionIn our rat model of SCT, SNM seemed to alter adrenergic receptor function in the urinary bladder. Further studies are required to clarify the mechanism of these alterations at the level of bladder receptors following sacral neuromodulation.