Vagal nerve stimulation preserves right ventricular function in a rat model of right ventricular pressure overload

Vagal nerve stimulation (VNS) ameliorates pulmonary vascular remodeling and improves survival in a rat model of pulmonary hypertension (PH). However, the direct impact of VNS on right ventricular (RV) function, which is the key predictor of PH patients, remains unknown. We evaluated the effect of VNS among the three groups: pulmonary artery banding (PAB) with sham stimulation (SS), PAB with VNS, and control (no PAB). We stimulated the right cervical vagal nerve with an implantable pulse generator, initiated VNS 2 weeks after PAB, and stimulated for 2 weeks. Compared to SS, VNS increased cardiac index (VNS: 130 +/- 10 vs. SS: 93 +/- 7 ml/min/kg; p < 0.05) and end-systolic elastance assessed by RV pressure-volume analysis (VNS: 1.1 +/- 0.1 vs. SS: 0.7 +/- 0.1 mmHg/mu l; p < 0.01), but decreased RV end-diastolic pressure (VNS: 4.5 +/- 0.7 vs. SS: 7.7 +/- 1.0 mmHg; p < 0.05). Furthermore, VNS significantly attenuated RV fibrosis and CD68-positive cell migration. In PAB rats, VNS improved RV function, and attenuated fibrosis, and migration of inflammatory cells. These results provide a rationale for VNS therapy as a novel approach for RV dysfunction in PH patients.