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Impact of lipopolysaccharide-induced acute inflammation on baroreflex-controlled sympathetic arterial pressure regulation.
PLoS One. 2018; 13(1):e0190830.Plos

Abstract

BACKGROUND

Lipopolysaccharide (LPS) induces acute inflammation, activates sympathetic nerve activity (SNA) and alters hemodynamics. Since the arterial baroreflex is a negative feedback system to stabilize arterial pressure (AP), examining the arterial baroreflex function is a prerequisite to understanding complex hemodynamics under LPS challenge. We investigated the impact of LPS-induced acute inflammation on SNA and AP regulation by performing baroreflex open-loop analysis.

METHODS

Ten anesthetized Sprague-Dawley rats were used. Acute inflammation was induced by an intravenous injection of LPS (60 μg/kg). We isolated the carotid sinuses from the systemic circulation and controlled carotid sinus pressure (CSP) by a servo-controlled piston pump. We matched CSP to AP to establish the baroreflex closed-loop condition, whereas we decoupled CSP from AP to establish the baroreflex open-loop condition and changed CSP stepwise to evaluate the baroreflex open-loop function. We recorded splanchnic SNA and hemodynamic parameters under baroreflex open- and closed-loop conditions at baseline and at 60 and 120 min after LPS injection.

RESULTS

In the baroreflex closed-loop condition, SNA continued to increase after LPS injection, reaching three-fold the baseline value at 120 min (baseline: 94.7 ± 3.6 vs. 120 min: 283.9 ± 31.9 a.u.). In contrast, AP increased initially (until 75 min), then declined to the baseline level. In the baroreflex open-loop condition, LPS reset the neural arc (CSP-SNA relationship) upward to higher SNA, while shifted the peripheral arc (SNA-AP relationship) downward at 120 min after the injection. As a result, the operating point determined by the intersection between function curves of neural arc and peripheral arc showed marked sympatho-excitation without substantial changes in AP.

CONCLUSIONS

LPS-induced acute inflammation markedly increased SNA via resetting of the baroreflex neural arc, and suppressed the peripheral arc. The balance between the augmented neural arc and suppressed peripheral arc determines SNA and hemodynamics in LPS-induced acute inflammation.

Authors+Show Affiliations

Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.Department of Advanced Risk Stratification for Cardiovascular Diseases, Center for Disruptive Cardiovascular Medicine, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, Osaka, Japan.Department of Advanced Risk Stratification for Cardiovascular Diseases, Center for Disruptive Cardiovascular Medicine, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.Department of Therapeutic Regulation of Cardiovascular Homeostasis, Center for Disruptive Cardiovascular Medicine, Kyushu University, Fukuoka, Japan.Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29329321

Citation

Tohyama, Takeshi, et al. "Impact of Lipopolysaccharide-induced Acute Inflammation On Baroreflex-controlled Sympathetic Arterial Pressure Regulation." PloS One, vol. 13, no. 1, 2018, pp. e0190830.
Tohyama T, Saku K, Kawada T, et al. Impact of lipopolysaccharide-induced acute inflammation on baroreflex-controlled sympathetic arterial pressure regulation. PLoS ONE. 2018;13(1):e0190830.
Tohyama, T., Saku, K., Kawada, T., Kishi, T., Yoshida, K., Nishikawa, T., Mannoji, H., Kamada, K., Sunagawa, K., & Tsutsui, H. (2018). Impact of lipopolysaccharide-induced acute inflammation on baroreflex-controlled sympathetic arterial pressure regulation. PloS One, 13(1), e0190830. https://doi.org/10.1371/journal.pone.0190830
Tohyama T, et al. Impact of Lipopolysaccharide-induced Acute Inflammation On Baroreflex-controlled Sympathetic Arterial Pressure Regulation. PLoS ONE. 2018;13(1):e0190830. PubMed PMID: 29329321.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Impact of lipopolysaccharide-induced acute inflammation on baroreflex-controlled sympathetic arterial pressure regulation. AU - Tohyama,Takeshi, AU - Saku,Keita, AU - Kawada,Toru, AU - Kishi,Takuya, AU - Yoshida,Keimei, AU - Nishikawa,Takuya, AU - Mannoji,Hiroshi, AU - Kamada,Kazuhiro, AU - Sunagawa,Kenji, AU - Tsutsui,Hiroyuki, Y1 - 2018/01/12/ PY - 2017/09/13/received PY - 2017/12/20/accepted PY - 2018/1/13/entrez PY - 2018/1/13/pubmed PY - 2018/2/16/medline SP - e0190830 EP - e0190830 JF - PloS one JO - PLoS ONE VL - 13 IS - 1 N2 - BACKGROUND: Lipopolysaccharide (LPS) induces acute inflammation, activates sympathetic nerve activity (SNA) and alters hemodynamics. Since the arterial baroreflex is a negative feedback system to stabilize arterial pressure (AP), examining the arterial baroreflex function is a prerequisite to understanding complex hemodynamics under LPS challenge. We investigated the impact of LPS-induced acute inflammation on SNA and AP regulation by performing baroreflex open-loop analysis. METHODS: Ten anesthetized Sprague-Dawley rats were used. Acute inflammation was induced by an intravenous injection of LPS (60 μg/kg). We isolated the carotid sinuses from the systemic circulation and controlled carotid sinus pressure (CSP) by a servo-controlled piston pump. We matched CSP to AP to establish the baroreflex closed-loop condition, whereas we decoupled CSP from AP to establish the baroreflex open-loop condition and changed CSP stepwise to evaluate the baroreflex open-loop function. We recorded splanchnic SNA and hemodynamic parameters under baroreflex open- and closed-loop conditions at baseline and at 60 and 120 min after LPS injection. RESULTS: In the baroreflex closed-loop condition, SNA continued to increase after LPS injection, reaching three-fold the baseline value at 120 min (baseline: 94.7 ± 3.6 vs. 120 min: 283.9 ± 31.9 a.u.). In contrast, AP increased initially (until 75 min), then declined to the baseline level. In the baroreflex open-loop condition, LPS reset the neural arc (CSP-SNA relationship) upward to higher SNA, while shifted the peripheral arc (SNA-AP relationship) downward at 120 min after the injection. As a result, the operating point determined by the intersection between function curves of neural arc and peripheral arc showed marked sympatho-excitation without substantial changes in AP. CONCLUSIONS: LPS-induced acute inflammation markedly increased SNA via resetting of the baroreflex neural arc, and suppressed the peripheral arc. The balance between the augmented neural arc and suppressed peripheral arc determines SNA and hemodynamics in LPS-induced acute inflammation. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/29329321/Impact_of_lipopolysaccharide_induced_acute_inflammation_on_baroreflex_controlled_sympathetic_arterial_pressure_regulation_ L2 - http://dx.plos.org/10.1371/journal.pone.0190830 DB - PRIME DP - Unbound Medicine ER -