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Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure

Fluid retention is the main reason for the high hospitalization rate among patients with chronic heart failure (CHF). Given the lack of knowledge about fluid intake regulation and its consequences in patients with CHF, current guidelines do not provide clear direction for fluid management. Using a r...

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Autores principales: Zheng, Can, Li, Meihua, Kawada, Toru, Inagaki, Masashi, Uemura, Kazunori, Sugimachi, Masaru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5688786/
https://www.ncbi.nlm.nih.gov/pubmed/29122962
http://dx.doi.org/10.14814/phy2.13497
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author Zheng, Can
Li, Meihua
Kawada, Toru
Inagaki, Masashi
Uemura, Kazunori
Sugimachi, Masaru
author_facet Zheng, Can
Li, Meihua
Kawada, Toru
Inagaki, Masashi
Uemura, Kazunori
Sugimachi, Masaru
author_sort Zheng, Can
collection PubMed
description Fluid retention is the main reason for the high hospitalization rate among patients with chronic heart failure (CHF). Given the lack of knowledge about fluid intake regulation and its consequences in patients with CHF, current guidelines do not provide clear direction for fluid management. Using a rat model of CHF, we investigated altering drinking behaviors and explored fluid management strategies. CHF was induced by ligating the left anterior descending coronary arteries in 8‐week‐old, male, Sprague‐Dawley rats. A custom‐designed drop counting and feedback control system was used to record and modulate drinking behaviors. During the first month after an induced myocardial infarction (MI), we observed that the spontaneous per drinking volume (PDV) was significantly increased in animals with prolonged intervals between drinking episodes. In addition, there was a significant inverse correlation between the early PDV and the post‐MI lifespan (r = −0.907; P < 0.001). Moreover, modulating the drinking behavior of rats with CHF to involve frequent drinking of small PDVs significantly enhanced hemodynamics and prevented cardiac remodeling, with a significant improvement in the 180‐day survival rate, compared with animals allowed to drink freely (50% vs. 36%; P < 0.01). The results of dynamic PDV changes, after MI, suggest that an impaired thirst mechanism is associated with the sensing and regulating of fluid balance in rats with CHF. These results suggest that increasing the drinking frequency, with small PDVs, may be beneficial to preventing progression of cardiac dysfunction in CHF.
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spelling pubmed-56887862017-11-24 Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure Zheng, Can Li, Meihua Kawada, Toru Inagaki, Masashi Uemura, Kazunori Sugimachi, Masaru Physiol Rep Original Research Fluid retention is the main reason for the high hospitalization rate among patients with chronic heart failure (CHF). Given the lack of knowledge about fluid intake regulation and its consequences in patients with CHF, current guidelines do not provide clear direction for fluid management. Using a rat model of CHF, we investigated altering drinking behaviors and explored fluid management strategies. CHF was induced by ligating the left anterior descending coronary arteries in 8‐week‐old, male, Sprague‐Dawley rats. A custom‐designed drop counting and feedback control system was used to record and modulate drinking behaviors. During the first month after an induced myocardial infarction (MI), we observed that the spontaneous per drinking volume (PDV) was significantly increased in animals with prolonged intervals between drinking episodes. In addition, there was a significant inverse correlation between the early PDV and the post‐MI lifespan (r = −0.907; P < 0.001). Moreover, modulating the drinking behavior of rats with CHF to involve frequent drinking of small PDVs significantly enhanced hemodynamics and prevented cardiac remodeling, with a significant improvement in the 180‐day survival rate, compared with animals allowed to drink freely (50% vs. 36%; P < 0.01). The results of dynamic PDV changes, after MI, suggest that an impaired thirst mechanism is associated with the sensing and regulating of fluid balance in rats with CHF. These results suggest that increasing the drinking frequency, with small PDVs, may be beneficial to preventing progression of cardiac dysfunction in CHF. John Wiley and Sons Inc. 2017-11-09 /pmc/articles/PMC5688786/ /pubmed/29122962 http://dx.doi.org/10.14814/phy2.13497 Text en © 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Zheng, Can
Li, Meihua
Kawada, Toru
Inagaki, Masashi
Uemura, Kazunori
Sugimachi, Masaru
Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title_full Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title_fullStr Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title_full_unstemmed Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title_short Frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
title_sort frequent drinking of small volumes improves cardiac function and survival in rats with chronic heart failure
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5688786/
https://www.ncbi.nlm.nih.gov/pubmed/29122962
http://dx.doi.org/10.14814/phy2.13497
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