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10.1016/j.hrthm.2015.12.030 http://scihub22266oqcxt.onion/10.1016/j.hrthm.2015.12.030 C4801709!4801709!26711798     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Heart+Rhythm 2016 ; 13 (4): 983-91 Nephropedia Template TP {{tp|p=26711798|t=2016. Relaxin Suppresses Atrial Fibrillation in Aged Rats by reversing fibrosis and Upregulating Na+-Channels |pdf=|usr=}}{{26711798}} gab.com Text Relaxin Suppresses Atrial Fibrillation in Aged Rats by reversing fibrosis and Upregulating Na+-Channels JO: Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=26711798 #FOAvip Background: Atrial fibrillation (AF) contributes significantly to morbidity and mortality in elderly patients and has been correlated with enhanced age-dependent atrial fibrosis. Reversal of atrial fibrosis has been proposed as therapeutic strategy to suppress AF. Objective: To test the ability of relaxin to reverse aged-dependent atrial fibrosis and suppress AF. Methods: Aged F-344 rats (24-months old) were treated with subcutaneous infusion of vehicle or relaxin (0.4 mg/kg/day) for 2-weeks. Rat hearts were excised, perfused on a Langendorff apparatus and stained with voltage and Ca2+ indicator dyes. Optical mapping and programmed electrical stimulation was used to test arrhythmia vulnerability and changes in electrophysiological characteristics. Changes in protein expression and Na+-current density (INa) were measured by tissue immunofluorescence and whole-cell patch clamp technique. Results: In aged rats, sustained AF was readily induced with a premature pulse (n=7/8) and relaxin treatment suppressed sustained AF by a premature impulse or burst pacing (n=1/6) (p<0.01). Relaxin significantly increased atrial action potential conduction velocity and decreased atrial fibrosis. Relaxin-treatment increased Nav1.5 expression (n=6; 36±10%) and decreased total collagen and collagen I (n=5?6; 55?66±15%) in aged atria (p<0.05) and decreased collagen I&III and TGF-?1 mRNA (p<0.05). Voltage-clamp experiments demonstrated that relaxin-treatment (100nM for 2 days) increased atrial INa by 46±4% (n=12?13/group, p<0.02). Conclusion: Relaxin suppresses AF through an increase in atrial conduction velocity by decreasing atrial fibrosis and increasing INa. This data provides compelling evidence that relaxin may serve as an effective therapy to manage AF in geriatric patients by reversing fibrosis and modulating cardiac ionic currents. Twit Text FOAVip Relaxin Suppresses Atrial Fibrillation in Aged Rats by reversing fibrosis and Upregulating Na+-Channels ????Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=26711798 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26711798 #FOAvip English Wikipedia <ref>{{Cite pmid|26711798}}</ref> Relaxin Suppresses Atrial Fibrillation in Aged Rats by reversing fibrosis and Upregulating Na+-Channels #MMPMID26711798 Henry B; Gabris B; Li Q; Martin B; Giannini M; Parikh A; Patel D; Haney J; Schwartzman D; Shroff SG; Salama G Heart Rhythm 2016[Apr]; 13 (4): 983-91 PMID26711798show ga Background: Atrial fibrillation (AF) contributes significantly to morbidity and mortality in elderly patients and has been correlated with enhanced age-dependent atrial fibrosis. Reversal of atrial fibrosis has been proposed as therapeutic strategy to suppress AF. Objective: To test the ability of relaxin to reverse aged-dependent atrial fibrosis and suppress AF. Methods: Aged F-344 rats (24-months old) were treated with subcutaneous infusion of vehicle or relaxin (0.4 mg/kg/day) for 2-weeks. Rat hearts were excised, perfused on a Langendorff apparatus and stained with voltage and Ca2+ indicator dyes. Optical mapping and programmed electrical stimulation was used to test arrhythmia vulnerability and changes in electrophysiological characteristics. Changes in protein expression and Na+-current density (INa) were measured by tissue immunofluorescence and whole-cell patch clamp technique. Results: In aged rats, sustained AF was readily induced with a premature pulse (n=7/8) and relaxin treatment suppressed sustained AF by a premature impulse or burst pacing (n=1/6) (p<0.01). Relaxin significantly increased atrial action potential conduction velocity and decreased atrial fibrosis. Relaxin-treatment increased Nav1.5 expression (n=6; 36±10%) and decreased total collagen and collagen I (n=5?6; 55?66±15%) in aged atria (p<0.05) and decreased collagen I&III and TGF-?1 mRNA (p<0.05). Voltage-clamp experiments demonstrated that relaxin-treatment (100nM for 2 days) increased atrial INa by 46±4% (n=12?13/group, p<0.02). Conclusion: Relaxin suppresses AF through an increase in atrial conduction velocity by decreasing atrial fibrosis and increasing INa. This data provides compelling evidence that relaxin may serve as an effective therapy to manage AF in geriatric patients by reversing fibrosis and modulating cardiac ionic currents. äRelaxin Suppresses Atrial Fibrillation in Aged Rats by reversing fibro(epmc).pdf DeepDyve Pubget Overpricing