Cardiac output is improved in rats with myocardial infarction by enhancement of respiratory sinus arrhythmia

Abstract

Respiratory sinus arrhythmia (RSA) is the physiological modulation of heart rate during respiration. Whilst its physiological function is debated, recent mathematical modelling predicts that RSA saves cardiac energy. Heart failure is associated with a loss of RSA. We aimed to test whether RSA would improve cardiac function in rats 3 days after left ascending coronary artery ligation (post‐MI). Cardiac dysfunction was indicated by infarct size (43±7% of left ventricle) and prolonged systole duration accompanied by reduced peak aortic flow compared to SHAM rats. We built and used a novel central pattern generator (CPG) that, utilizing real‐time diaphragm electromyogram input, generated RSA via respiratory phase‐locked stimulus output to the right cervical vagus nerve. In post‐MI rats, RSA enhancement caused a 12±3% increase in stroke volume, irrespective of the RSA amplitude. Tonic VNS at matched average heart rate increased stroke volume to a similar degree (8±1%, P =0.25 compared to RSA) (n = 7). Despite the increase in stroke volume, myocardial lactate concentrations were unchanged after 45 min of RSA (29±7bpm) or tonic VNS treatment (P = 0.35, One‐way ANOVA). Using a novel CPG device we have demonstrated that, in an acute setting, RSA increases stroke volume in post‐MI rats.British Heart Foundation and Fundação de Amparo à Pesquisa do Estado de São Paulo