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The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats

Pulmonary artery impedance (PAZ) that measures the pulsatile properties of the vasculature provides diagnostic and prognostic information in patients with pulmonary vascular diseases. While downstream pressure [i.e., left atrial (LA) pressure] should be considered when calculating static properties...

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Autores principales: Fukumitsu, Masafumi, Kawada, Toru, Shimizu, Shuji, Sugimachi, Masaru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6295444/
https://www.ncbi.nlm.nih.gov/pubmed/30556341
http://dx.doi.org/10.14814/phy2.13946
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author Fukumitsu, Masafumi
Kawada, Toru
Shimizu, Shuji
Sugimachi, Masaru
author_facet Fukumitsu, Masafumi
Kawada, Toru
Shimizu, Shuji
Sugimachi, Masaru
author_sort Fukumitsu, Masafumi
collection PubMed
description Pulmonary artery impedance (PAZ) that measures the pulsatile properties of the vasculature provides diagnostic and prognostic information in patients with pulmonary vascular diseases. While downstream pressure [i.e., left atrial (LA) pressure] should be considered when calculating static properties of pulmonary vasculature, PAZ is commonly estimated without taking into account the pulsatile component of LA pressure. We examined whether PAZ can be estimated with reasonable accuracy without using LA pressure. Pulmonary artery (PA) flow, PA pressure, and LA pressure were measured under irregular pacing in eight normal Sprague‐Dawley rats. PAZ was estimated by analyzing a one‐input, one‐output system (I1O1 analysis) that does not include LA pressure, and a two‐input, one‐output system (I2O1 analysis) that includes LA pressure. Using a tube and 3‐element Windkessel model, PAZ was parameterized as peripheral resistance (R(P)), arterial compliance (C(P)), characteristic impedance (Z(C)), and transmission time to the reflection site (T(D)). These parameters were not significantly different between the I1O1 and I2O1 analyses (R(P): 0.286 ± 0.040 vs. 0.274 ± 0.038 mmHg·min/mL, C(P): 0.352 ± 0.049 vs. 0.343 ± 0.041 mL/mmHg, Z(C): 0.115 ± 0.005 vs. 0.117 ± 0.005 mmHg·min/mL, T(D): 13.2 ± 1.8 vs. 12.9 ± 1.7 msec). In conclusion, the I1O1 analysis that does not use LA pressure estimates PAZ with reasonable accuracy compared with the I2O1 analysis that uses LA pressure in normal rats. Our finding that the pulsatile component of LA pressure contributes little to PAZ estimation may justify the clinical use of the I1O1 analysis.
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spelling pubmed-62954442018-12-19 The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats Fukumitsu, Masafumi Kawada, Toru Shimizu, Shuji Sugimachi, Masaru Physiol Rep Original Research Pulmonary artery impedance (PAZ) that measures the pulsatile properties of the vasculature provides diagnostic and prognostic information in patients with pulmonary vascular diseases. While downstream pressure [i.e., left atrial (LA) pressure] should be considered when calculating static properties of pulmonary vasculature, PAZ is commonly estimated without taking into account the pulsatile component of LA pressure. We examined whether PAZ can be estimated with reasonable accuracy without using LA pressure. Pulmonary artery (PA) flow, PA pressure, and LA pressure were measured under irregular pacing in eight normal Sprague‐Dawley rats. PAZ was estimated by analyzing a one‐input, one‐output system (I1O1 analysis) that does not include LA pressure, and a two‐input, one‐output system (I2O1 analysis) that includes LA pressure. Using a tube and 3‐element Windkessel model, PAZ was parameterized as peripheral resistance (R(P)), arterial compliance (C(P)), characteristic impedance (Z(C)), and transmission time to the reflection site (T(D)). These parameters were not significantly different between the I1O1 and I2O1 analyses (R(P): 0.286 ± 0.040 vs. 0.274 ± 0.038 mmHg·min/mL, C(P): 0.352 ± 0.049 vs. 0.343 ± 0.041 mL/mmHg, Z(C): 0.115 ± 0.005 vs. 0.117 ± 0.005 mmHg·min/mL, T(D): 13.2 ± 1.8 vs. 12.9 ± 1.7 msec). In conclusion, the I1O1 analysis that does not use LA pressure estimates PAZ with reasonable accuracy compared with the I2O1 analysis that uses LA pressure in normal rats. Our finding that the pulsatile component of LA pressure contributes little to PAZ estimation may justify the clinical use of the I1O1 analysis. John Wiley and Sons Inc. 2018-12-16 /pmc/articles/PMC6295444/ /pubmed/30556341 http://dx.doi.org/10.14814/phy2.13946 Text en © 2018 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 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
Fukumitsu, Masafumi
Kawada, Toru
Shimizu, Shuji
Sugimachi, Masaru
The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title_full The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title_fullStr The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title_full_unstemmed The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title_short The pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
title_sort pulsatile component of left atrial pressure has little effect on pulmonary artery impedance estimation in normal rats
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6295444/
https://www.ncbi.nlm.nih.gov/pubmed/30556341
http://dx.doi.org/10.14814/phy2.13946
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