Abstract
Neurocardiogenic syncope is a common disorder resulting from a transient increase in vagal tone and central sympathetic withdrawal leading to varying degrees of vasodilation and bradycardia. Hence an effective treatment should address both the bradycardia and vasodilation. We hypothesized that, stimulation of the renal sympathetic nerves using high frequency stimulation in the renal vein will increase blood pressure through an increase in sympathetic output and therefore may be of use in treating neurocardiogenic syncope. Renal nerve stimulation was performed under Isoflurane anesthesia in 5 dogs and 1 baboon using a 4 mm quadripolar catheter in unilateral renal vein using a Grass stimulator (square wave, 120 V, 900 pps, 30–200 s). A consistent increase in arterial systolic BP [mean (SD) pre- vs peak-stimulation 103 (± 27) vs. 122 (± 41) mmHg] and diastolic BP [69 (± 19) vs. 82 (± 31) mmHg] was noted during stimulation. Median interquartile change in systolic BP was 11 (5–22) mmHg and 6 (− 2–16) mmHg in diastolic BP. To conclude, renal nerve stimulation through the renal vein increased BP. Potential applications include treatment of vasodilatory component of neurocardiogenic syncope and confirmation of successful renal nerve ablation for the treatment of hypertension.
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Introduction
Neurocardiogenic syncope is a common disorder with a prevalence of 22% in the USA . Recurrent syncope can occur in 30% and result in significant injuries and lifestyle limitations . Neurocardiogenic syncope results from transient autonomic dysfunction. This results in vagal-induced cardio-inhibition causing a slowing of heart rate and vasodilation due to withdrawal of sympathetic tone . Current treatment strategies, including the use of cardiac pacemakers, have not been uniformly effective in preventing recurrent syncope . This is due to the lack of device capability to acutely raise blood pressure when needed independent of heart rate changes . There is a pressing need for more effective treatment strategies that address both pathophysiologic mechanisms; both on the heart and on the vasculature. Renal vessels are richly innervated by afferent and efferent renal sympathetic nerves which, when stimulated, raise blood pressure through vasoconstriction and are therefore a potential target for treatment of neurocardiogenic syncope.
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Methods and results
In order to assess the efficacy of renal sympathetic nerve stimulation to increase systemic blood pressure, we performed studies of renal nerve stimulation in 5 dogs and 1 baboon using a 4-mm quadripolar catheter in the renal vein ( Fig. 1 ) with a Grass stimulator (square wave, 120 V, 900 pps, 30–200 s, Grass Technologies).
We noted an acute and sustained increase in blood pressure (BP) after stimulation of the renal vein. Consistent increase in arterial systolic BP [mean (SD) pre- vs peak-stimulation 103 (± 27) vs. 122 (± 41) mmHg] ( Fig. 2 ) and diastolic BP [69 (± 19) vs. 82 (± 31) mmHg] was noted during stimulation. Median interquartile change in systolic BP was 11 (5–22) mmHg and 6 (− 2–16) mmHg in diastolic BP ( Fig. 3 ). Blood pressure returned to baseline within 1 min of cessation of stimulation. Direct current ablation in the renal artery (5000 mA, flow 60 ml/h, 120 s, 2 applications) in one dog abolished the blood pressure response.
