Abstract
The objective of this study was to investigate the effects and mechanism of Transcutaneous Electrical Nerve Stimulation (TENS) on the diabetic cytopathy (DCP) in the diabetic bladder. A total of 45 rats were randomly divided into diabetes mellitus (DM)/TENS group (n = 15), DM group (n = 15) and control group (n = 15). The rats in the DM/TENS and TENS groups were electronically stimulated (stimulating parameters: intensity-31 V, frequency-31 Hz, and duration of stimulation of 15 min) for three weeks. Bladder histology, urodynamics and contractile responses to field stimulation and carbachol were determined. The expression of calcitonin gene-related peptide (CGRP) was analyzed by RT-PCR and Western blotting. The results showed that contractile responses of the DM rats were ameliorated after 3 weeks of TENS. Furthermore, TENS significantly increased bladder wet weight, volume threshold for micturition and reduced PVR, V% and cAMP content of the bladder. The mRNA and protein levels of CGRP in dorsal root ganglion (DRG) in the DM/TENS group were higher than those in the DM group. TENS also significantly up-regulated the cAMP content in the bladder body and base compared with diabetic rats. We conclude that TENS can significantly improve the urine contractility and ameliorate the feeling of bladder fullness in DM rats possibly via up-regulation of cAMP and CGRP in DRG.
Highlights
As a urinary complication of diabetes, diabetic cytopathy (DCP) is manifested as neurogenic bladder and urethral dysfunction with an incidence of about 50% in diabetic patients [1]
The rats in the experimental group were further divided into diabetes mellitus (DM)/Transcutaneous Electrical Nerve Stimulation (TENS) group (n = 15) in which the DM rats were treated with Transcutaneous ENS and DM group (n = 15) in which TENS was not applied
DCP is a common complication of diabetes with an incidence of 40%–100% in diabetic patients
Summary
As a urinary complication of diabetes, diabetic cytopathy (DCP) is manifested as neurogenic bladder and urethral dysfunction with an incidence of about 50% in diabetic patients [1]. The exact pathogenesis of DCP is still not clear. Besides myogenic dysfunction of detrusor, lesions of the peripheral nerve of the urinary bladder play a vital role in the pathogenic mechanisms. There are no effective treatments for DCP. Cystostomy has been widely applied in clinical treatment, but it can only improve the clinical symptoms and considerably affect the quality of life [2]. Prevention of the DCP development in early stage is critical for the comprehensive treatment and improvement of the life quality in patients with diabetes. Studies on the safe and effective treatments for DCP are greatly needed
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