TY - JOUR
T1 - Blood Pressure Responses to Endovascular Stimulation
T2 - A Potential Therapy for Autonomic Disorders With Vasodilatation
AU - Naksuk, Niyada
AU - Killu, Ammar M.
AU - Yogeswaran, Vidhushei
AU - Desimone, Christopher V.
AU - Suddendorf, Scott H.
AU - Ladewig, Dorothy J.
AU - Powers, Joanne M.
AU - Weber, Sarah
AU - Madhavan, Malini
AU - Cha, Yong Mei
AU - Kapa, Suraj
AU - Asirvatham, Samuel J.
N1 - Publisher Copyright:
© 2016 Wiley Periodicals, Inc.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2016/9/1
Y1 - 2016/9/1
N2 - Background: We have previously shown that sympathetic ganglia stimulation via the renal vein rapidly increases blood pressure. This study further investigated the optimal target sites and effective energy levels for stimulation of the renal vasculatures and nearby sympathetic ganglia for rapid increase in blood pressure. Methods: The pre-study protocol for endovascular stimulations included 2 minutes of stimulation (1–150 V and 10 pulses per second) and at least 2 minutes of rest during poststimulation. If blood pressure and/or heart rate were changed during the stimulation, time to return to baseline was allowed prior to the next stimulation. Results: In 11 acute canine studies, we performed 85 renal artery, 30 renal vein, and 8 hepatic vasculature stimulations. The mean arterial pressure (MAP) rapidly increased during stimulation of renal artery (95 ± 18 mmHg vs. 103 ± 15 mmHg; P < 0.0001), renal vein (90 ± 16 mmHg vs. 102 ± 20 mmHg; P = 0.001), and hepatic vasculatures (74 ± 8 mmHg vs. 82 ± 11 mmHg; P = 0.04). Predictors of a significant increase in MAP were energy >10 V focused on the left renal artery, bilateral renal arteries, and bilateral renal veins (especially the mid segment). Overall, heart rate was unchanged, but muscle fasciculation was observed in 22.0% with an output >10 V (range 15–150 V). Analysis after excluding the stimulations that resulted in fasciculation yielded similar results to the main findings. Conclusions: Stimulation of intra-abdominal vasculatures promptly increased the MAP and thus may be a potential treatment option for hypotension in autonomic disorders. Predictors of optimal stimulation include energy delivery and the site of stimulation (for the renal vasculatures), which informs the design of subsequent research.
AB - Background: We have previously shown that sympathetic ganglia stimulation via the renal vein rapidly increases blood pressure. This study further investigated the optimal target sites and effective energy levels for stimulation of the renal vasculatures and nearby sympathetic ganglia for rapid increase in blood pressure. Methods: The pre-study protocol for endovascular stimulations included 2 minutes of stimulation (1–150 V and 10 pulses per second) and at least 2 minutes of rest during poststimulation. If blood pressure and/or heart rate were changed during the stimulation, time to return to baseline was allowed prior to the next stimulation. Results: In 11 acute canine studies, we performed 85 renal artery, 30 renal vein, and 8 hepatic vasculature stimulations. The mean arterial pressure (MAP) rapidly increased during stimulation of renal artery (95 ± 18 mmHg vs. 103 ± 15 mmHg; P < 0.0001), renal vein (90 ± 16 mmHg vs. 102 ± 20 mmHg; P = 0.001), and hepatic vasculatures (74 ± 8 mmHg vs. 82 ± 11 mmHg; P = 0.04). Predictors of a significant increase in MAP were energy >10 V focused on the left renal artery, bilateral renal arteries, and bilateral renal veins (especially the mid segment). Overall, heart rate was unchanged, but muscle fasciculation was observed in 22.0% with an output >10 V (range 15–150 V). Analysis after excluding the stimulations that resulted in fasciculation yielded similar results to the main findings. Conclusions: Stimulation of intra-abdominal vasculatures promptly increased the MAP and thus may be a potential treatment option for hypotension in autonomic disorders. Predictors of optimal stimulation include energy delivery and the site of stimulation (for the renal vasculatures), which informs the design of subsequent research.
KW - autonomic disorder
KW - blood pressure
KW - ganglia stimulation
KW - neurocardiogenic syncope
KW - reflex syncope
KW - renal nerve stimulation
KW - sympathetic stimulation
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U2 - 10.1111/jce.13018
DO - 10.1111/jce.13018
M3 - Article
C2 - 27234884
AN - SCOPUS:84985919192
SN - 1045-3873
VL - 27
SP - 1078
EP - 1085
JO - Journal of cardiovascular electrophysiology
JF - Journal of cardiovascular electrophysiology
IS - 9
ER -