Electrophysiological effects on renal ischemia/reperfusion-induced cardiac hypertrophy

摘要

Acute kidney injury has been previously shown to develop cardiac hypertrophy (CH) also by catecholamines release. This study aims to investigate the influence of sympathetic nervous system (SNS) on the CH-induced by ischemic renal (I/R) injury. Methods: Mice (C57Bl/6) were divided in 4 groups: Sham, I/R, Sham atenolol (ATE) and I/R ATE. Morphometric conditions were evaluated and ECG collection was performed using in-house custom written system (hardware and platform). Heart Rate, R-R interval, R-peak amplitude, QT interval and QTc (Mitchell's QT-correction) were manually inspected and calculated by LabChart (V8.1.5, AD Instruments). Results: CH was induced by I/R after 12d when compared to sham (p<;0.05). ATE prevented CH, (p<;0.05). I/R induced an increase on QT interval I/R vs Sham, p<;0.05). I/R had 30% of R-peak reduction (vs. Sham) whereas in the treated group it increased 3% (I/R ATE vs Sham ATE). R-peak also had increase 8% at the I/R group (vs. I/R ATE). Sham's R-R interval (78,8 ± 1,6 ms) and QTc (158,1± 15,6 ms) had not differences when compared respectively with the other groups. Conclusion: I/R developed CH with morphology and electrophysiology changes.