title: Bionic baroreceptor corrects postural hypotension in rats with impaired baroreceptor.
abstract: BACKGROUND
  Impairment of the arterial baroreflex causes orthostatic hypotension. Arterial baroreceptor sensitivity degrades with age. Thus, an impaired baroreceptor plays a pivotal role in orthostatic hypotension in most elderly patients. There is no effective treatment for orthostatic hypotension. The aims of this investigation were to develop a bionic baroreceptor (BBR) and to verify whether it corrects postural hypotension.
  
  
  RESULTS
  The BBR consists of a pressure sensor, a regulator, and a neurostimulator. In 35 Sprague-Dawley rats, we vascularly and neurally isolated the baroreceptor regions and attached electrodes to the aortic depressor nerve for stimulation. To mimic impaired baroreceptors, we maintained intracarotid sinus pressure at 60 mm Hg during activation of the BBR. Native baroreflex was reproduced by matching intracarotid sinus pressure to the instantaneous pulsatile aortic pressure. The encoding rule for translating intracarotid sinus pressure into stimulation of the aortic depressor nerve was identified by a white noise technique and applied to the regulator. The open-loop arterial pressure response to intracarotid sinus pressure (n=7) and upright tilt-induced changes in arterial pressure (n=7) were compared between native baroreceptor and BBR conditions. The intracarotid sinus pressure-arterial pressure relationships were comparable. Compared with the absence of baroreflex, the BBR corrected tilt-induced hypotension as effectively as under native baroreceptor conditions (native, -39±5 mm Hg; BBR, -41±5 mm Hg; absence, -63±5 mm Hg; P<0.05).
  
  
  CONCLUSIONS
  The BBR restores the pressure buffering function. Although this research demonstrated feasibility of the BBR, further research is needed to verify its long-term effect and safety in larger animal models and humans.
authors.affiliation: Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Fukuoka, 812-8582, Japan. hosokawa.ka621@gmail.com
authors.forename: Kazuya
authors.initials: K
authors.lastname: Hosokawa
authors.forename: Tomomi
authors.initials: T
authors.lastname: Ide
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Tobushi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Sakamoto
authors.forename: Ken
authors.initials: K
authors.lastname: Onitsuka
authors.forename: Takafumi
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Takeo
authors.initials: T
authors.lastname: Fujino
authors.forename: Keita
authors.initials: K
authors.lastname: Saku
authors.forename: Kenji
authors.initials: K
authors.lastname: Sunagawa
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001342:Autonomic Nervous System Diseases / Q000503:physiopathology / Q000628:therapy; D001701:Bionics / Q000379:methods* / Q000592:standards; D001794:Blood Pressure / Q000502:physiology; D002346:Carotid Sinus / Q000502:physiology; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy / Q000379:methods* / Q000592:standards; D007024:Hypotension, Orthostatic / Q000503:physiopathology* / Q000628:therapy*; D008955:Models, Cardiovascular; D011187:Posture / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015203:Reproducibility of Results