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Artificial Baroreflex System Restores Volume Buffering Function in the Baroreflex Failure Irrespective of Left Ventricular Systolic Function
Author(s) -
Hosokawa Kazuya,
Funakoshi Kouta,
Tanaka Atsushi,
Sakamoto Takafumi,
Onitsuka Ken,
Sakamoto Kazuo,
Tobushi Tomoyuki,
Fujino Takeo,
Ide Tomomi,
Sunagawa Kenji
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.645.2
Backgrounds The arterial baroreflex stabilizes arterial pressure by mainly changing the vascular properties. We demonstrated that baroreflex impairment makes the circulatory system extremely sensitive to volume overload and predisposes to pulmonary edema irrespective of left ventricular systolic function. The aim of this study is to explore into the development of artificial baroreflex system (ABS) to restore physiological volume buffering function. Methods We vascularily isolated the baroreceptor regions in 14 Sprague‐Dawley rats. The intra‐carotid sinus pressure was controlled by a servo‐controlled pump. We attached electrodes to the aortic depressor nerves for stimulation. ABS consisted of a pressure sensor, regulator and neuro‐stimulator. We identified and implemented the transfer function (H ABS ) of regulator which dictates how ABS stimulates the depressor nerves. We infused volume stepwise and examined the left atrial pressure‐infused volume (ΔV) relationship. We quantified the critical volume (cΔV) at which left atrial pressure reaches 18 mmHg. Results Baroreflex failure decreased cΔV (20.1±3.2 vs. 16.6±4.4 ml/kg). ABS restored cΔV (21.0±3.0 ml/kg, ns. compared with native). Conclusion ABS reinstitutes the native baroreflex and would be an attractive tool in preventing pulmonary edema in heart failure irrespective of left ventricular systolic dysfunction.