Kyushu University [Kouta Funakoshi (Assistant Professor) Kyushu University Hospital, Center for Clinical and Translational Research(CCTR)]

Kouta Funakoshi

Last modified date：2022.07.05

Assistant Professor / Center for Clinical and Translational Research(CCTR)
Kyushu University Hospital

1 Research Interests

2 Academic Activities

2.1 Papers

3 Membership in Academic Society

4 Awards

Academic Degree

Country of degree conferring institution (Overseas)

Field of Specialization

Cardiology, Regulatory Science, Epidemiology, Biostatistics, Medical Informatics

Total Priod of education and research career in the foreign country

00years00months

Research

Research Interests

creating a feedback Mechanism Of performance measUreS with an aim to improve QUality of care in Elderly diabetic patients: A naTional collAboration of core hospitals for clInical research to create Real world Evidence (MOUSQUETAIRE)
keyword : diabetes, core hospitals for clinical research, real world data, real world evidence
2018.10～2022.07.
Trial design of pivotal trial of medical devices
keyword : trial design, medical device
2017.10～2024.07.

Academic Activities

Papers

Show All Papers >>

Kouta Funakoshi, Kazuya Hosokawa, Takuya Kishi, Tomomi Ide, Kenji Sunagawa, Striking Volume Intolerance Is Induced by Mimicking Arterial Baroreflex Failure in Normal Left Ventricular Function, JOURNAL OF CARDIAC FAILURE, 10.1016/j.cardfail.2013.11.007, 20, 1, 53-59, 2014.01, Background: Patients with heart failure and preserved ejection fraction (HFpEF) are supersensitive to volume overload, and a striking increase in left atrial pressure (LAP) often occurs transiently and is rapidly resolved by intravascular volume reduction. The arterial baroreflex is a powerful regulator of intravascular stressed blood volume. We examined whether arterial baroreflex failure (FAIL) mimicked by constant carotid sinus pressure (CSP) causes a striking increase in LAP and systemic arterial pressure (AP) by volume loading in rats with normal left ventricular (LV) function.

Methods and results: In anesthetized Sprague-Dawley rats, we isolated bilateral carotid sinuses and controlled CSP by a servo-controlled piston pump. We mimicked the normal arterial baroreflex by matching CSP to instantaneous AP and FAIL by maintaining CSP at a constant value regardless of AP. We infused dextran stepwise (infused volume [Vi]) until LAP reached 15 mm Hg and obtained the LAP-Vi relationship. We estimated the critical Vi as the Vi at which LAP reached 20 mm Hg. In FAIL, critical Vi decreased markedly from 19.4 ± 1.6 mL/kg to 15.6 ± 1.6 mL/kg (P < .01), whereas AP at the critical Vi increased (194 ± 6 mm Hg vs 163 ± 6 mm Hg; P < .01). We demonstrated that an artificial arterial baroreflex system we recently developed could fully restore the physiologic volume intolerance in the absence of native arterial baroreflex.

Conclusions: Arterial baroreflex failure induces striking volume intolerance in the absence of LV dysfunction and may play an important role in the pathogenesis of acute heart failure, especially in states of HFpEF..

Membership in Academic Society

Japanese Association for Medical Informatics
The Japanese Circulation Society
The Japanese Society of Internal Medicine
Japanese Society of Echocardiography
The Biometric Society of Japan
Society for Regulatory Science of Medical Products

Awards

Utilization of risk matrix for safety evaluation of medical devices

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