BACKGROUND. To date, the mechanisms of small stone elimination by lithokinetic therapy (LCT) have not been elucidated.   THE AIM of this investigation was to estimate the activity of receptors controlling the contraction and relaxation of smooth muscle cells (SMC) against the background of α1A-adrenoreceptor blockade during LCT in patients with small stones localization in the middle third of ureter.   PATIENTS AND METHODS. The study was prospective and included 40 patients in whom standard LCT was done for localization of small concrements (≤6 mm) in the middle third of ureter. The functional activity of receptors modulating ureteric peristalsis was analyzed in vitro using platelet suspension. The agonists used were ATP, ADP, adenosine, epinephrine, angiotensin-2 (Sigma-Aldrich Chemie GmbH, Germany) at EC50 concentrations causing aggregation at 50 % in healthy subjects. Platelet aggregation was assessed by turbidimetric method on ChronoLog analyzer (USA).   RESULTS. No differences in the rate of small concrements elimination from the middle third of ureter was found in presence and absence of α1A-adrenoreceptor blocker in LCT. Before LCT, α2-adrenoreceptor hyperresponsiveness, normoreponsiveness of purine P2X1- and P2Y-receptors, adenosine A2-receptor and angiotensin AT1-receptor were found. After 9 days of LCT with verified elimination of concrements, an increase in P2X1-receptor and AT1-receptor activity (p < 0.001) was found regardless of the administration of α1A-adrenoceptor blocker. P2Y-receptor hyperresponsiveness was seen in the presence and normoreponsiveness in the absence of α1A-adrenoreceptor blocker in LCT.   CONCLUSION. At the lithokinetic therapy irrespective of α1A-adrenoreceptor blocker prescription, compensatory mechanisms, aimed at enhancement of contractile activity and preservation of smooth muscle cell relaxation take part in the traffics of small concrements from the middle third of ureter.

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BACKGROUND: Improving the efficiency and reducing the frequency of complications of surgical treatment of urolithiasis is an actual problem in urology. AIM: To establish the molecular mechanisms that modulate the hemostasis and development of acute pyelonephritis after percutaneous contact ureteral lithotripsy. MATERIALS AND METHODS: The study included 21 patients with urolithiasis and concretions in the upper third of the ureter in whom, after standard lithokinetic therapy for 7 days, according to imaging control data, the calculus did not move from the pyelo-ureteral zone to the middle third of the ureter. All patients underwent contact ureteral lithotripsy. After the operation, nonsteroidal anti-inflammatory drugs and antibiotics were used for 2 days. The severity of hematuria and leukocyturia was assessed 24, 48, and 72 h after contact ureteral lithotripsy. Functional activity receptors were analyzed in vitro on a platelet suspension. Platelet aggregation was assessed by the turbidimetric method using a ChronoLog analyzer (USA). RESULTS: At 24, 48, and 72 h after contact ureteral lithotripsy, a significant decrease was found in the severity of microhematuria (p 0.001). The leukocyturia level decreased over 48 h (p 0.05) and increased 72 h after surgery (p 0.001). The above dynamics of complications after hours indicates that two pathological processes simultaneously develop in the ureteral mucosa: induction of thrombogenesis and modulation of an acute inflammatory reaction. Аfter 24 h of NSAID discontinuation (3 days after contact ureteral lithotripsy), normoreactivity of the 2-adrenergic receptors, GPVI receptors, AT1 receptors, PAF receptors, P2X1 receptors, and A2A receptors was found, as well as hyporeactivity of purine P2Y receptors and 2-adrenergic receptors. The correlation between the severity of hematuria and the activity of GPVI receptors for collagen, 2-adrenergic receptors for adrenaline, and AT1 receptors for angiotensin-2 (p 0.05) makes it possible to specify the possible interaction of platelet receptors that maintain hemostasis during inhibition of the COXTxA2 axis. Maintaining the severity of pyelonephritis after contact ureteral lithotripsy is associated with the interaction of the PAF receptors, purine ionotropic P2X1 receptors, and 2-adrenergic receptors on blood cells. CONCLUSIONS: The analysis of targets receptors on platelets and leukocytes after contact ureteral lithotripsy in the upper third of the ureter with ineffective lithokinetic therapyallows us to outline ways to improve conservative therapy to limit the development of postoperative complications.

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