Modulation of urethral alpha-sympathetic by parasympathetic before and following bethanechol chloride injection

INTRODUCTION AND OBJECTIVES: Chagas' disease causes specific parasympathetic denervation and in its digestive clinic form promotes also functional alterations in bladder. Thus, the aim was to investigate the existence of balance between sympathetic and parasympathetic systems in lower urinary tract, as occurs in other organs. We verified the urethral closing pressure before and following parasympathetic stimulus. PATIENTS AND METHODS: For that, the urethral closure pressure was studied before and after the injection of 5 mg of bethanechol chloride subcutaneously in 28 voluntary female patients, divided into 4 groups. The constitution of theses groups was: A) normal control = 6 patients; B) Chagas' disease with positive serology only = 5 patients; C) Chagas' disease with cardiac disease = 6 patients, and D) Chagas' disease with digestive disease and vesical hyporeflexia = 11 patients. Urethral profilometry was performed through perfusion urethral catheter with a 6.5 ml/minute flow and a traction rate of 5 mm/minute. RESULTS: Means and standard deviations for urethral closure pressure before bethanechol chloride were respectively: group A = 67.3 ± 7.1; group B = 69.2 ± 7.4; group C = 95.8 ± 5.1; group D = 82.1 ± 8.4. After bethanechol chloride they were: group A = 66.0 ± 6.6; group B = 77.0 ± 7.6; group C = 98.3 ± 8.8; group D = 45.9 ± 6.2. The Kruskal Wallis statistical test did not show statistically significance difference between groups A, B, C. However, it was statistically significant between groups C and D with p = 0.003. Wilcoxon test showed p = 0.001, only for values in group D before and following bethanechol chloride. CONCLUSIONS: Chagas' disease in its intestinal form seems to alter urethral function as well. Parasympathetic stimulation decreased urethral pressure, indicating potential modulation by the parasympathetic system over the sympathetic system

Change in muscarinic modulation of transmitter release in the rat urinary bladder after spinal cord injury.

Muscarinic facilitation of 14C-ACh release from post-ganglionic parasympathetic nerve terminals was studied in bladder strips prepared from spinal intact (SI) and spinal cord transected (SCT) rats. The spinal cord was transected at the lower thoracic spinal segments 3 weeks prior to the experiments. Using non-facilitatory stimulation (2 Hz) the release of ACh in spinal intact rats did not change in the presence of a non-specific muscarinic antagonist, atropine (100 nM), an M(1) specific antagonist (pirenzepine, 50 nM) or an M(1)-M(3) specific antagonist (4-DAMP, 5 nM). However, during a facilitatory stimulation paradigm (10 Hz or 40 Hz, 100 shocks) atropine and pirenzepine, but not 4-DAMP inhibited the release of ACh in bladders from spinal intact rats, indicating an M(1) receptor-mediated facilitation. In spinal cord transected rats, 2 Hz stimulation-induced release was significantly inhibited by atropine or 4-DAMP but not by pirenzepine indicating that a pre-junctional facilitatory mechanism mediated via M(3) muscarinic receptors could be induced by a non-facilitatory stimulation paradigm after spinal injury. In bladders of spinal cord transected rats, 10 Hz stimulation-evoked release of ACh was also inhibited by atropine and 4-DAMP (5 nM) but not by pirenzepine (50 nM). These results indicate that pre-junctional muscarinic receptors at cholinergic nerve endings in the bladder change after chronic spinal cord injury. It appears that low affinity M(1) muscarinic receptors are replaced by high affinity M(3) receptors. This change in modulation of ACh release may partly explain the bladder hyperactivity after chronic spinal cord injury.

Modulation of urethral alpha-sympathetic by parasympathetic before and following bethanechol chloride injection.

INTRODUCTION AND OBJECTIVES: Chagas' disease causes specific parasympathetic denervation and in its digestive clinic form promotes also functional alterations in bladder. Thus, the aim was to investigate the existence of balance between sympathetic and parasympathetic systems in lower urinary tract, as occurs in other organs. We verified the urethral closing pressure before and following parasympathetic stimulus. PATIENTS AND METHODS: For that, the urethral closure pressure was studied before and after the injection of 5 mg of bethanechol chloride subcutaneously in 28 voluntary female patients, divided into 4 groups. The constitution of theses groups was: A) normal control = 6 patients; B) Chagas' disease with positive serology only = 5 patients; C) Chagas' disease with cardiac disease = 6 patients, and D) Chagas' disease with digestive disease and vesical hyporeflexia = 11 patients. Urethral profilometry was performed through perfusion urethral catheter with a 6.5 ml/minute flow and a traction rate of 5 mm/minute. RESULTS: Means and standard deviations for urethral closure pressure before bethanechol chloride were respectively: group A = 67.3 +/- 7.1; group B = 69.2 +/- 7.4; group C = 95.8 +/- 5.1; group D = 82.1 +/- 8.4. After bethanechol chloride they were: group A = 66.0 +/- 6.6; group B = 77.0 +/- 7.6; group C = 98.3 +/- 8.8; group D = 45.9 +/- 6.2. The Kruskal Wallis statistical test did not show statistically significance difference between groups A, B, C. However, it was statistically significant between groups C and D with p = 0.003. Wilcoxon test showed p = 0.001, only for values in group D before and following bethanechol chloride. CONCLUSIONS: Chagas' disease in its intestinal form seems to alter urethral function as well. Parasympathetic stimulation decreased urethral pressure, indicating potential modulation by the parasympathetic system over the sympathetic system.

Infecçäo aguda do trato urogenital / Acute infection of the genitourinary system

Os autores fazem uma abordagem prática sobre o diagnóstico e o tratamento de pacientes com infeccao aguda do trato urogenital. Säo apresentadas as situaçöes mais comuns relacionadas à infecçäo do trato urinário baixo e do rim, assim como algumas das infecçöes sexualmente transmissíveis. Procurou-se, em cada situaçäo, comentar sobre os agentes etiológicos mais freqüentes, bem como orientar a solicitaçäo de exames subsidiários pertinentes para a confirmaçäo do diagnóstico, para a identificaçäo de complicaçäo ou de fatores predisponentes. Recomendou-se, ainda, a terapia específica mais usada para cada caso, näo só para combater os agentes infecciosos mais também os fatores predisponentes e as complicaçöes