Effects of initial passage of endotoxin through the liver on the extent of acute lung injury in a rat model

Hisato Shimada, Naoki Hasegawa, Hidefumi Koh, Sadatomo Tasaka, Mie Shimizu, Wakako Yamasawa, Tomoyasu Nishimura, Kazuhisa Amakawa, Mitsutomo Kohno, Makoto Sawafuji, Kayoko Nakamura, Seitaro Fujishima, Kazuhiro Yamaguchi, Akitosi Ishizaka

研究成果: Article

15 引用 (Scopus)

抄録

We hypothesized that the extent of acute lung injury (ALI) caused by lipopolysaccharide (LPS) is modified with its initial passage through the liver. We tested this hypothesis by administering LPS, 5 mg/kg, or saline to 120 male Wistar rats via the portal vein (PV) or the inferior vena cava (IVC) over 1 h. Four experimental groups of rats were administered saline into the PV, saline into the IVC, LPS into the PV (LPS-PV group), and LPS into the IVC (LPS-IVC group), respectively. At 15 and 30 min after onset of Chromium-LPS infusion, the γ counts in the liver were higher in the LPS-PV group than that in the LPS-IVC group. The ratio of Iodine-albumin counts in lung tissue to that in plasma per unit of weight (as an assessment of pulmonary microvascular permeability) at 240 min after onset of LPS stimulation, the accumulation of polymorphonuclear cell (assessed by myeloperoxidase activity) and the concentration of tumor necrosis factor α in the lung at 60 and 240 min after onset of LPS infusion, were higher in the LPS-IVC group than in the LPS-PV group. Significant differences in several factors indicative of inflammation and in the extent of LPS-induced ALI were observed after the onset of LPS infusion, depending on whether it was delivered via the PV or the IVC. These observations suggest that the entrapping of LPS during its initial passage through the hepatic circulation may attenuate LPS-induced ALI within 4 h of initiation of LPS stimulation.

元の言語English
ページ(範囲)311-315
ページ数5
ジャーナルShock
26
発行部数3
DOI
出版物ステータスPublished - 2006 9

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Acute Lung Injury
Endotoxins
Lipopolysaccharides
Liver
Inferior Vena Cava
Portal Vein
Lung
Liver Circulation
Capillary Permeability
Chromium

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

これを引用

Effects of initial passage of endotoxin through the liver on the extent of acute lung injury in a rat model. / Shimada, Hisato; Hasegawa, Naoki; Koh, Hidefumi; Tasaka, Sadatomo; Shimizu, Mie; Yamasawa, Wakako; Nishimura, Tomoyasu; Amakawa, Kazuhisa; Kohno, Mitsutomo; Sawafuji, Makoto; Nakamura, Kayoko; Fujishima, Seitaro; Yamaguchi, Kazuhiro; Ishizaka, Akitosi.

:: Shock, 巻 26, 番号 3, 09.2006, p. 311-315.

研究成果: Article

Shimada, H, Hasegawa, N, Koh, H, Tasaka, S, Shimizu, M, Yamasawa, W, Nishimura, T, Amakawa, K, Kohno, M, Sawafuji, M, Nakamura, K, Fujishima, S, Yamaguchi, K & Ishizaka, A 2006, 'Effects of initial passage of endotoxin through the liver on the extent of acute lung injury in a rat model', Shock, 巻. 26, 番号 3, pp. 311-315. https://doi.org/10.1097/01.shk.0000224960.17274.6f
Shimada, Hisato ; Hasegawa, Naoki ; Koh, Hidefumi ; Tasaka, Sadatomo ; Shimizu, Mie ; Yamasawa, Wakako ; Nishimura, Tomoyasu ; Amakawa, Kazuhisa ; Kohno, Mitsutomo ; Sawafuji, Makoto ; Nakamura, Kayoko ; Fujishima, Seitaro ; Yamaguchi, Kazuhiro ; Ishizaka, Akitosi. / Effects of initial passage of endotoxin through the liver on the extent of acute lung injury in a rat model. :: Shock. 2006 ; 巻 26, 番号 3. pp. 311-315.
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abstract = "We hypothesized that the extent of acute lung injury (ALI) caused by lipopolysaccharide (LPS) is modified with its initial passage through the liver. We tested this hypothesis by administering LPS, 5 mg/kg, or saline to 120 male Wistar rats via the portal vein (PV) or the inferior vena cava (IVC) over 1 h. Four experimental groups of rats were administered saline into the PV, saline into the IVC, LPS into the PV (LPS-PV group), and LPS into the IVC (LPS-IVC group), respectively. At 15 and 30 min after onset of Chromium-LPS infusion, the γ counts in the liver were higher in the LPS-PV group than that in the LPS-IVC group. The ratio of Iodine-albumin counts in lung tissue to that in plasma per unit of weight (as an assessment of pulmonary microvascular permeability) at 240 min after onset of LPS stimulation, the accumulation of polymorphonuclear cell (assessed by myeloperoxidase activity) and the concentration of tumor necrosis factor α in the lung at 60 and 240 min after onset of LPS infusion, were higher in the LPS-IVC group than in the LPS-PV group. Significant differences in several factors indicative of inflammation and in the extent of LPS-induced ALI were observed after the onset of LPS infusion, depending on whether it was delivered via the PV or the IVC. These observations suggest that the entrapping of LPS during its initial passage through the hepatic circulation may attenuate LPS-induced ALI within 4 h of initiation of LPS stimulation.",
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AU - Shimada, Hisato

AU - Hasegawa, Naoki

AU - Koh, Hidefumi

AU - Tasaka, Sadatomo

AU - Shimizu, Mie

AU - Yamasawa, Wakako

AU - Nishimura, Tomoyasu

AU - Amakawa, Kazuhisa

AU - Kohno, Mitsutomo

AU - Sawafuji, Makoto

AU - Nakamura, Kayoko

AU - Fujishima, Seitaro

AU - Yamaguchi, Kazuhiro

AU - Ishizaka, Akitosi

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N2 - We hypothesized that the extent of acute lung injury (ALI) caused by lipopolysaccharide (LPS) is modified with its initial passage through the liver. We tested this hypothesis by administering LPS, 5 mg/kg, or saline to 120 male Wistar rats via the portal vein (PV) or the inferior vena cava (IVC) over 1 h. Four experimental groups of rats were administered saline into the PV, saline into the IVC, LPS into the PV (LPS-PV group), and LPS into the IVC (LPS-IVC group), respectively. At 15 and 30 min after onset of Chromium-LPS infusion, the γ counts in the liver were higher in the LPS-PV group than that in the LPS-IVC group. The ratio of Iodine-albumin counts in lung tissue to that in plasma per unit of weight (as an assessment of pulmonary microvascular permeability) at 240 min after onset of LPS stimulation, the accumulation of polymorphonuclear cell (assessed by myeloperoxidase activity) and the concentration of tumor necrosis factor α in the lung at 60 and 240 min after onset of LPS infusion, were higher in the LPS-IVC group than in the LPS-PV group. Significant differences in several factors indicative of inflammation and in the extent of LPS-induced ALI were observed after the onset of LPS infusion, depending on whether it was delivered via the PV or the IVC. These observations suggest that the entrapping of LPS during its initial passage through the hepatic circulation may attenuate LPS-induced ALI within 4 h of initiation of LPS stimulation.

AB - We hypothesized that the extent of acute lung injury (ALI) caused by lipopolysaccharide (LPS) is modified with its initial passage through the liver. We tested this hypothesis by administering LPS, 5 mg/kg, or saline to 120 male Wistar rats via the portal vein (PV) or the inferior vena cava (IVC) over 1 h. Four experimental groups of rats were administered saline into the PV, saline into the IVC, LPS into the PV (LPS-PV group), and LPS into the IVC (LPS-IVC group), respectively. At 15 and 30 min after onset of Chromium-LPS infusion, the γ counts in the liver were higher in the LPS-PV group than that in the LPS-IVC group. The ratio of Iodine-albumin counts in lung tissue to that in plasma per unit of weight (as an assessment of pulmonary microvascular permeability) at 240 min after onset of LPS stimulation, the accumulation of polymorphonuclear cell (assessed by myeloperoxidase activity) and the concentration of tumor necrosis factor α in the lung at 60 and 240 min after onset of LPS infusion, were higher in the LPS-IVC group than in the LPS-PV group. Significant differences in several factors indicative of inflammation and in the extent of LPS-induced ALI were observed after the onset of LPS infusion, depending on whether it was delivered via the PV or the IVC. These observations suggest that the entrapping of LPS during its initial passage through the hepatic circulation may attenuate LPS-induced ALI within 4 h of initiation of LPS stimulation.

KW - Acute lung injury

KW - Endotoxin

KW - Inferior vena cava

KW - Inflammatory cytokines

KW - Lipopolysaccharide

KW - Myeloperoxidase

KW - Portal vein

KW - Tumor necrosis factor

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