scholarly journals Acute High-glucose Exposure Potentiates The Response To Capsaicin-induced Trpv1 Activation In Group Iv Muscle Afferents.

2021 ◽  
Vol 53 (8S) ◽  
pp. 89-89
Author(s):  
Rie Ishizawa ◽  
Norio Hotta ◽  
Han Kyul Kim ◽  
Gary A. Iwamoto ◽  
Jere H. Mitchell ◽  
...  
2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e48 ◽  
Author(s):  
Maddison Turner ◽  
Larissa Reid ◽  
Mercedes Munkonda ◽  
Dylan Burger

2006 ◽  
Vol 290 (3) ◽  
pp. H1214-H1219 ◽  
Author(s):  
Angela E. Kindig ◽  
Shawn G. Hayes ◽  
Ramy L. Hanna ◽  
Marc P. Kaufman

Injection into the arterial supply of skeletal muscle of pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS), a P2 receptor antagonist, has been shown previously to attenuate the reflex pressor responses to both static contraction and to tendon stretch. In decerebrated cats, we tested the hypothesis that PPADS attenuated the responses of groups III and IV muscle afferents to static contraction as well as to tendon stretch. We found that injection of PPADS (10 mg/kg) into the popliteal artery attenuated the responses of both group III ( n = 16 cats) and group IV afferents ( n = 14 cats) to static contraction. Specifically, static contraction before PPADS injection increased the discharge rate of the group III afferents from 0.1 ± 0.05 to 1.6 ± 0.5 impulses/s, whereas contraction after PPADS injection increased the discharge of the group III afferents from 0.2 ± 0.1 to only 1.0 ± 0.5 impulses/s ( P < 0.05). Likewise, static contraction before PPADS injection increased the discharge rate of the group IV afferents from 0.3 ± 0.1 to 1.0 ± 0.3 impulses/s, whereas contraction after PPADS injection increased the discharge of the group IV afferents from 0.2 ± 0.1 to only 0.3 ± 0.1 impulses/s ( P < 0.05). In addition, PPADS significantly attenuated the responses of group III afferents to tendon stretch but had no effect on the responses of group IV afferents. Our findings suggest that both groups III and IV afferents are responsible for evoking the purinergic component of the exercise pressor reflex, whereas only group III afferents are responsible for evoking the purinergic component of the muscle mechanoreflex that is evoked by tendon stretch.


2018 ◽  
Vol 472 ◽  
pp. 57-67 ◽  
Author(s):  
Elin Hall ◽  
Marloes Dekker Nitert ◽  
Petr Volkov ◽  
Siri Malmgren ◽  
Hindrik Mulder ◽  
...  

2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Sofia Pavlou ◽  
Jaime Lindsay ◽  
Rebecca Ingram ◽  
Heping Xu ◽  
Mei Chen

2015 ◽  
Vol 14 (1) ◽  
Author(s):  
Valeria De Nigris ◽  
Gemma Pujadas ◽  
Lucia La Sala ◽  
Roberto Testa ◽  
Stefano Genovese ◽  
...  

PROTEOMICS ◽  
2010 ◽  
Vol 10 (1) ◽  
pp. 59-71 ◽  
Author(s):  
Yohann Couté ◽  
Yannick Brunner ◽  
Domitille Schvartz ◽  
Céline Hernandez ◽  
Alexandre Masselot ◽  
...  

2017 ◽  
Vol 37 (4) ◽  
pp. 407-413 ◽  
Author(s):  
Melissa Nataatmadja ◽  
Yeoungjee Cho ◽  
Elaine M. Pascoe ◽  
Darsy Darssan ◽  
Carmel M. Hawley ◽  
...  

BackgroundGlucose is the primary osmotic medium used in most peritoneal dialysis (PD) solutions, and exposure to glucose has been shown to exert detrimental effects both locally, at the peritoneal membrane, and systemically. Moreover, high dialysate glucose exposure may predispose patients to an increased risk of peritonitis, perhaps as a result of impaired host defences, vascular disease, and damage to the peritoneal membrane.MethodsIn this post-hoc analysis of a multicenter, multinational, open-label randomized controlled trial of neutral pH, low-glucose degradation product (GDP) versus conventional PD solutions ( balANZ trial), the relationship between peritonitis rates of low (< 123.1 g/day) versus high (≥ 123.1 g/day) dialysate glucose exposure was evaluated in 177 incident PD patients over a 2-year study period.ResultsPeritonitis rates were 0.44 episodes per patient-year in the low-glucose exposure group and 0.31 episodes per patient-year in the high-glucose exposure group, (incidence rate ratio [IRR] 0.69, p = 0.09). There was no significant association between dialysate glucose exposure and peritonitis-free survival on univariable analysis (high glucose exposure hazard ratio [HR] 0.66, 95% confidence interval [CI] 0.40 –1.08) or on multivariable analysis (adjusted HR 0.64, 95% CI 0.39 – 1.05). Moreover, there was no relationship between peritoneal glucose exposure and type of organism causing peritonitis. Physician-rated severity of first peritonitis episodes was similar between groups, as was rate and duration of hospital admission.ConclusionsOverall, this study did not identify an association between peritoneal dialysate glucose exposure and peritonitis occurrence, severity, hospitalization, or outcomes. A further large-scale, prospective, randomized controlled trial evaluating patient-level outcomes is merited.


2016 ◽  
Vol 36 (5) ◽  
pp. 533-539 ◽  
Author(s):  
Anouk T.N. van Diepen ◽  
Sadie van Esch ◽  
Dirk G. Struijk ◽  
Raymond T. Krediet

Background and objective Little or no clinical evidence is available on the association between glucose exposure and peritoneal host defense in peritoneal dialysis (PD) patients. The objective of the present study was to quantify the exposure to glucose during the first year on PD and investigate the association with subsequent peritonitis. Methods We analyzed prospectively collected demographic and peritonitis data from incident adult PD patients between 1990 and 2010. For the present study, we conducted a review of both in- and outpatient medical records of all patients to obtain their day-to-day dialysis schemes during the first year on PD. From these data, the average exposure to glucose was quantified. The exposure was stratified into low- and high-glucose groups based on the median, analyzed per standard deviation and in quartiles. Cox proportional hazard models were used to calculate crude and adjusted hazard ratios (HRs) and 95% confidence intervals for the association between glucose exposure and peritonitis. Adjustments were made for age, sex, primary kidney disease, diabetes mellitus, Davies comorbidity score and the treatment period. Results In total, 230 patients were included in the study of whom 151 (66%) experienced a first peritonitis episode. The median follow-up time was 2.6 years (interquartile range [IQR]: 1.9 – 3.8) in the low-glucose group and 3.1 (IQR: 2.1 – 4.2) in the high-glucose group. After adjustment for confounding factors, no association between high glucose exposure and the risk of peritonitis was found (HR: 0.81; 0.55 – 1.17). No association was present when glucose exposure was analyzed per standard deviation (SD) (HR: 0.98; 0.79 – 1.21) or patient quartiles were applied. No association was identified between glucose exposure and severe peritonitis, Staphylococcus aureus peritonitis, or a peritonitis episode that lasted more than 14 days. Conclusions Exposure to glucose is not associated with an increased risk of peritonitis. The equilibrium between glycemic harm to peritoneal host defense and detrimental effects of glucose on invading microorganisms may determine the susceptibility to peritoneal infection.


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