Electrical Diuretics: Dorsal Root Ganglion Stimulation to Increase Diuresis

Background: Stimulation of diuresis is an essential component of heart failure treatment to reduce fl uid overload. Over time, increasing doses of loop diuretics are required to achieve adequate urine output, and approximately 30% to 45% of patients develop diuretic resistance. We investigated the feasibility of affecting renal afferent sensory nerves by dorsal root ganglion neurostimulation as an alternative to medication to increase diuresis. Materials and Methods: Acute volume overload with an elevated and stable pulmonary capillary wedge pressure (PCWP) was induced by infusion of isotonic fl uid in swine (N = 7). In each experiment, diuresis and blood electrolyte levels were measured during cycles of up to two hours (baseline, stimulation, poststimulation) through bladder catheterization. Efficacy was tested using bilateral dorsal root ganglion (bDRG) stimulation at the T11 and/or T12 vertebral levels. Results: An elevated, stable PCWP (15 +/- 4 mm Hg, N = 7) was obtained after uploading. Under these conditions, average diuresis increased 20% to 205% compared with no stimulation. Side effects such as motor stimulation were mitigated by decreasing current or terminated spontaneously without intervention. There was no negative effect on acute kidney function because blood electrolyte concentrations remained stable. When stimulation was deactivated, urine output decreased significantly but did not return to baseline levels, suggesting a carry-over effect of up to two hours. Conclusions: Electrical stimulation (bDRG) at T11 and/or T12 increased diuresis in an acute volume overload model. Side effects caused by unintended (motor) stimulation could be eliminated by reducing the electrical current while sustaining increased diuresis.