Diabetes slows the recovery from urinary incontinence due to simulated childbirth in female rats

This study was done to test the hypothesis that simulated vaginal birth by vaginal distension (VD) causes more severe urinary incontinence and slower recovery in diabetic rats. After measuring baseline leak point pressure (LPP) in 16 diabetes mellitus (DM) and 16 age- and weight-matched control (Ct) female Sprague-Dawley rats, these animals underwent either VD or sham VD (sham). Four and ten days after the procedures, LPP and conscious cystometry were assessed. Tissues were then harvested and examined by light microscopy. LPP at baseline was equal among all four groups. Four days after VD, LPP in both VD groups dropped to significantly lower levels than in sham rats ( P < 0.001). Moreover, LPP in the DM+VD group was significantly lower than in the Ct+VD group. At 10 days, LPP in the Ct+VD group had recovered to its baseline value, whereas the LPP in the DM+VD group remained significantly reduced. DM rats had larger bladder capacity and longer voiding intervals than Ct rats. Histological findings included more severe damage to the external sphincter striated musculature of the urethra in DM+VD group compared with Ct+VD. In conclusion, these findings suggest that DM causes increased severity and delayed functional recovery from the effects of simulated childbirth.

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Rat Mesenchymal Stem Cell Secretome Promotes Elastogenesis and Facilitates Recovery from Simulated Childbirth Injury

Cell Transplantation ◽

10.3727/096368913x670921 ◽

2014 ◽

Vol 23 (11) ◽

pp. 1395-1406 ◽

Cited By ~ 41

Author(s):

Charuspong Dissaranan ◽

Michelle A. Cruz ◽

Matthew J. Kiedrowski ◽

Brian M. Balog ◽

Bradley C. Gill ◽

...

Keyword(s):

Female Rats ◽

Urethral Sphincter ◽

Leak Point Pressure ◽

External Urethral Sphincter ◽

Paracrine Factors ◽

Pelvic Organs ◽

Point Pressure ◽

Urethral Smooth Muscle ◽

And Function ◽

Vaginal Distension

Vaginal delivery is a risk factor for stress urinary incontinence (SUI). Mesenchymal stem cells (MSCs) home to injured organs and can facilitate repair. The goal of this study was to determine if MSCs home to pelvic organs after simulated childbirth injury and facilitate recovery from SUI via paracrine factors. Three experiments were performed. Eighteen female rats received vaginal distension (VD) or sham VD and labeled intravenous (IV) MSCs to investigate if MSCs home to the pelvic organs. Whole-organ imaging and immunofluorescence were performed 1 week later. Thirty-four female rats received VD and IV MSCs, VD and IV saline, or sham VD and IV saline to investigate if MSCs accelerate recovery of continence. Twenty-nine female rats received VD and periurethral concentrated conditioned media (CCM), VD and periurethral control media, or sham VD and periurethral control media to investigate if factors secreted by MSCs accelerate recovery from VD. Urethral histology and function were assessed 1 week later. Significantly more MSCs were observed in the urethra, vagina, and spleen after VD compared to sham VD. Continence as measured by leak point pressure (LPP) was significantly reduced after VD in rats treated with saline or control media compared to sham VD but not in those given MSCs or CCM. External urethral sphincter (EUS) function as measured by electromyography (EMG) was not improved with MSCs or CCM. Rats treated with MSCs or CCM demonstrated an increase in elastin fibers near the EUS and urethral smooth muscle more similar to that of sham-injured animals than rats treated with saline or control media. MSCs homed to the urethra and vagina and facilitated recovery of continence most likely via secretion of paracrine factors. Both MSCs and CCM have promise as novel noninvasive therapies for SUI.

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Daily bilateral pudendal nerve electrical stimulation improves recovery from stress urinary incontinence

Interface Focus ◽

10.1098/rsfs.2019.0020 ◽

2019 ◽

Vol 9 (4) ◽

pp. 20190020 ◽

Cited By ~ 2

Author(s):

Kangli Deng ◽

Brian M. Balog ◽

Dan Li Lin ◽

Brett Hanzlicek ◽

Qi-Xiang Song ◽

...

Keyword(s):

Urinary Incontinence ◽

Electrical Stimulation ◽

Stress Urinary Incontinence ◽

Pudendal Nerve ◽

Sprague Dawley ◽

External Urethral Sphincter ◽

Bdnf Expression ◽

Nerve Crush ◽

Sprague Dawley Rats ◽

Point Pressure

Stress urinary incontinence (SUI) in women is strongly associated with childbirth which injures the pudendal nerve (PN) and the external urethral sphincter (EUS) during delivery. Electrical stimulation (ES) can increase brain-derived neurotrophic factor (BDNF) expression in injured neurons, activate Schwann cells and promote neuroregeneration after nerve injury. The aim of this study was to determine if more frequent ES would increase recovery from SUI in a rat model. Forty female Sprague–Dawley rats underwent either sham injury or pudendal nerve crush (PNC) and vaginal distention (VD) to establish SUI. Immediately after injury, electrodes were implanted at the pudendal nerve bilaterally. Each injured animal underwent sham ES, twice per week ES (2/week), or daily ES of 1 h duration for two weeks. Urethral and nerve function were assessed with leak point pressure (LPP), EUS electromyography and pudendal nerve sensory branch potential (PNSBP) recordings two weeks after injury. LPP was significantly increased after daily ES compared to 2/week ES. EUS neuromuscular junction innervation was decreased after injury with sham ES, but improved after 2/week or daily ES. This study demonstrates that daily bilateral ES to the pudendal nerve can accelerate recovery from SUI. Daily ES improved urethral function more than 2/week ES.

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CLINICAL SCORE PREDICTIVE OF THE ABDOMINAL LEAK POINT PRESSURE (ALPP) <60 CM H2O IN WOMEN WITH STRESS URINARY INCONTINENCE.

10.26226/morressier.59b63e42d462b802923897e3 ◽

2017 ◽

Author(s):

Leandro Arribillaga

Keyword(s):

Urinary Incontinence ◽

Stress Urinary Incontinence ◽

Clinical Score ◽

Leak Point Pressure ◽

Point Pressure

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Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.4.1828 ◽

2001 ◽

Vol 91 (4) ◽

pp. 1828-1835 ◽

Cited By ~ 60

Author(s):

Nicole Stupka ◽

Peter M. Tiidus

Keyword(s):

Muscle Damage ◽

Ischemia Reperfusion Injury ◽

Serum Insulin ◽

Ischemia Reperfusion ◽

Neutrophil Infiltration ◽

Female Rats ◽

Protective Effects ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

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Comparison of leak point pressure methods in an animal model of stress urinary incontinence

International Urogynecology Journal ◽

10.1007/s00192-004-1263-4 ◽

2005 ◽

Vol 16 (5) ◽

pp. 359-363 ◽

Cited By ~ 58

Author(s):

Deirdre A. Conway ◽

Izumi Kamo ◽

Naoki Yoshimura ◽

Michael B. Chancellor ◽

Tracy W. Cannon

Keyword(s):

Animal Model ◽

Urinary Incontinence ◽

Stress Urinary Incontinence ◽

Leak Point Pressure ◽

Point Pressure

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Electroacupuncture at Zusanli Rescues the Enteric Neuronal Loss in the Stomach of Diabetic Rats

Journal of Evidence-Based Complementary & Alternative Medicine ◽

10.1177/2156587212455646 ◽

2012 ◽

Vol 18 (1) ◽

pp. 5-14 ◽

Cited By ~ 2

Author(s):

Min Hu ◽

Fan Du ◽

Shi Liu

Keyword(s):

High Frequency ◽

Low Frequency ◽

Neuronal Loss ◽

Diabetic Rats ◽

Enteric Neurons ◽

Control Group ◽

Sprague Dawley ◽

Long Duration ◽

Sprague Dawley Rats ◽

Zusanli Acupoint

The purpose of this study was to investigate the effects of electroacupuncture at Zusanli acupoint on the enteric neuropathy in diabetic rats. Sprague–Dawley rats were divided into different groups depending on the total electroacupuncture span and frequency. The expression of nitric oxide synthase (nNOS), choline acetyltransferase (CHAT), protein gene product 9.5 (PGP9.5), and doublecortin was significantly decreased in the diabetic group compared with the control group. Long-term electroacupuncture at Zusanli with either high frequency or low frequency could increase the expression levels of nNOS, CHAT, PGP9.5, and doublecortin, and the increase was greater in the high-frequency group. But no obvious changes were seen in the short-term electroacupuncture groups. These results suggest that electroacupuncture at Zusanli can restore the deficiency of enteric neurons in diabetes partly but a comparative long duration of stimuli (6 weeks) is required. The increase of doublecortin may be involved in this positive process.

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KELULUT HONEY SUPPLEMENTATION PREVENTS SPERM AND TESTICULAR OXIDATIVE DAMAGE IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

Jurnal Teknologi ◽

10.11113/jt.v79.9674 ◽

2017 ◽

Vol 79 (3) ◽

Cited By ~ 3

Author(s):

Siti Balkis Budin ◽

Fatin Farhana Jubaidi ◽

Siti Nur Farahana Mohd Noor Azam ◽

Nur Liyana Mohamed Yusof ◽

Izatus Shima Taib ◽

...

Keyword(s):

Oxidative Damage ◽

Sperm Quality ◽

Diabetic Control ◽

Diabetic Rats ◽

Sprague Dawley ◽

Control Groups ◽

Sod Activity ◽

Male Adult ◽

Pathological Conditions ◽

Sprague Dawley Rats

Previous studies found that Kelulut Honey produced by Trigona spp. bees is able to prevent oxidative damage in various pathological conditions. Thus, the present study aimed to determine whether Kelulut Honey could prevent the sperm and testicular damage in streptozotocin-induced diabetic rats. Male Adult male Sprague-Dawley rats were divided into four groups: Non-Diabetic (NDM), Non-Diabetic with Kelulut Honey supplementation (NDMKH), Diabetic without supplementation (DM) and Diabetic with Kelulut Honey supplementation (DMKH). Kelulut honey was given at the dose of 2.0 g/kg weight daily via gavage for 28 consecutive days. Results showed that sperm quality produced by diabetic rats supplemented with Kelulut honey significantly improved compared to the diabetic control groups (p<0.05). SOD activity and GSH level increased significantly (p<0.05) whereas PC and MDA levels significantly decreased in sperm and testis of DMKH rats when compared to DM rats (p<0.05). Histological observation showed obvious increase in spermatozoa in the lumen of epididymis and increased spermatogenic cells density in the testis of DMKH group. In conclusion, Kelulut Honey has a potential in preventing the damage of sperm and testis in diabetic rats.

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Ameliorating effects of cloperastine on dysfunction of the urinary bladder caused by cerebral infarction in conscious rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y09-078 ◽

2009 ◽

Vol 87 (11) ◽

pp. 893-899 ◽

Cited By ~ 5

Author(s):

Gen Yamamoto ◽

Fumio Soeda ◽

Tetsuya Shirasaki ◽

Kazuo Takahama

Keyword(s):

Urinary Bladder ◽

Cerebral Infarction ◽

Flow Rate ◽

Bladder Capacity ◽

Left Middle Cerebral Artery ◽

Sprague Dawley ◽

Urinary Bladder Dysfunction ◽

Sprague Dawley Rats ◽

Urethral Resistance ◽

Effective Doses

We investigated the effects of the centrally acting antitussives dextromethorphan and cloperastine on urinary bladder dysfunction 24 h after cerebral infarction in rats using the cystometry technique. First, cystometrography was performed in conscious male Sprague–Dawley rats. Cerebral infarction was then induced by occlusion of the left middle cerebral artery. Twenty-four hours after cerebral infarction, the effect of each drug on micturition disorder was estimated for 5 parameters: bladder capacity, maximum voiding pressure, micturition latency, flow rate, and urethral resistance. Cerebral infarction markedly reduced bladder capacity, micturition latency, and flow rate and increased urethral resistance. After cerebral infarction, intravenous dosing of saline had no effect on these parameters. Dextromethorphan (20 mg/kg) and cloperastine (2.5 and 5.0 mg/kg) at antitussive effective doses significantly increased bladder capacity and micturition latency. Unlike dextromethorphan, cloperastine ameliorated decreases in flow rate and increases in urethral resistance caused by cerebral infarction. These results suggest that cloperastine may have therapeutic value for the treatment of disorders of the micturition reflex associated with cerebral infarction, and that the drug may become a base compound from which to develop more active drugs for such disorders.

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Infarct size is increased in female post-MI rats treated with rapamycin

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y09-031 ◽

2009 ◽

Vol 87 (6) ◽

pp. 460-470 ◽

Cited By ~ 6

Author(s):

Claude Lajoie ◽

Viviane El-Helou ◽

Cindy Proulx ◽

Robert Clément ◽

Hugues Gosselin ◽

...

Keyword(s):

Left Ventricle ◽

Female Rats ◽

Coronary Artery Ligation ◽

Female Rat ◽

Sprague Dawley ◽

Ischemic Insult ◽

Fibrotic Response ◽

Artery Ligation ◽

Sprague Dawley Rats ◽

Scar Healing

Rapamycin represents a recognized drug-based therapeutic approach to treat cardiovascular disease. However, at least in the female heart, rapamycin may suppress the recruitment of putative signalling events conferring cardioprotection. The present study tested the hypothesis that rapamycin-sensitive signalling events contributed to the cardioprotective phenotype of the female rat heart after an ischemic insult. Rapamycin (1.5 mg/kg) was administered to adult female Sprague–Dawley rats 24 h after complete coronary artery ligation and continued for 6 days. Rapamycin abrogated p70S6K phosphorylation in the left ventricle of sham rats and the noninfarcted left ventricle (NILV) of 1-week postmyocardial-infarcted (MI) rats. Scar weight (MI 0.028 ± 0.006, MI+rapamycin 0.064 ± 0.004 g) and surface area (MI 0.37 ± 0.08, MI+rapamycin 0.74 ± 0.03 cm2) were significantly larger in rapamycin-treated post-MI rats. In the NILV of post-MI female rats, rapamycin inhibited the upregulation of eNOS. Furthermore, the increased expression of collagen and TGF-β3 mRNAs in the NILV were attenuated in rapamycin-treated post-MI rats, whereas scar healing was unaffected. The present study has demonstrated that rapamycin-sensitive signalling events were implicated in scar formation and reactive fibrosis. Rapamycin-mediated suppression of eNOS and TGF-β3 mRNA in post-MI female rats may have directly contributed to the larger infarct and attenuation of the reactive fibrotic response, respectively.

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