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Insufficient Lymph Drainage Causes Abnormal Lipid Accumulation and Vein Wall Degeneration

Identifieur interne : 008B54 ( Ncbi/Merge ); précédent : 008B53; suivant : 008B55

Insufficient Lymph Drainage Causes Abnormal Lipid Accumulation and Vein Wall Degeneration

Auteurs : Hiroki Tanaka [Japon] ; Naoto Yamamoto [Japon] ; Minoru Suzuki [Japon] ; Yuuki Mano [Japon] ; Masaki Sano [Japon] ; Nobuhiro Zaima [Japon] ; Takeshi Sasaki [Japon] ; Mitsutoshi Setou [Japon] ; Naoki Unno [Japon]

Source :

RBID : PMC:5174986

Abstract

Objective: Previously, we analyzed human varicose veins (VV) using imaging mass spectrometry (IMS) and detected the abnormal accumulation of lipid molecules in the walls of VV, possibly due to insufficient lipid drainage by the lymphatic vessels. In this study, we created an animal model of lymphatic insufficiency to investigate the effects of insufficient lymph drainage on vein walls.

Methods: In rats, the lymphatic collecting vessels surrounding the femoral vein were ligated on one side (the model tissue), which caused the local retention of lymphatic fluid in the perivascular tissue. The equivalent contralateral tissue was used as a control. A histological study of the femoral vein and the surrounding perivascular tissue was conducted. IMS was used to analyze the distribution of lipid molecules in the perivascular tissue.

Results: Fourteen days after the procedure, the lymphatic vessels in the model tissue were significantly dilated. Furthermore, IMS revealed that the composition of the lipid molecules in the perivascular regions of the model tissue had altered. Compared with the control tissue, the model tissue exhibited marked perivascular accumulation of lysophosphatidylcholine (1-acyl 16:0), phosphatidylcholine (16:0/20:4), and triglycerides (52:2). Interestingly, the walls of the femoral veins running through the model tissue were 3.4-fold thicker than those of the femoral veins running through the control tissue. The number of tumor necrosis factor α-positive adipocytes was increased in the perivascular regions of the model tissue.

Conclusion: The findings of this study indicated that the accumulation of lymphatic fluid due to insufficient lymph drainage changes the structure of vein walls, and such changes might be associated with chronic venous insufficiency. (This is a translation of Jpn J Phlebol 2015; 26: 227–235.)


Url:
DOI: 10.3400/avd.oa.16-00122
PubMed: 28018498
PubMed Central: 5174986

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PMC:5174986

Le document en format XML

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<name sortKey="Sasaki, Takeshi" sort="Sasaki, Takeshi" uniqKey="Sasaki T" first="Takeshi" last="Sasaki">Takeshi Sasaki</name>
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<bold>Objective:</bold>
Previously, we analyzed human varicose veins (VV) using imaging mass spectrometry (IMS) and detected the abnormal accumulation of lipid molecules in the walls of VV, possibly due to insufficient lipid drainage by the lymphatic vessels. In this study, we created an animal model of lymphatic insufficiency to investigate the effects of insufficient lymph drainage on vein walls.</p>
<p>
<bold>Methods:</bold>
In rats, the lymphatic collecting vessels surrounding the femoral vein were ligated on one side (the model tissue), which caused the local retention of lymphatic fluid in the perivascular tissue. The equivalent contralateral tissue was used as a control. A histological study of the femoral vein and the surrounding perivascular tissue was conducted. IMS was used to analyze the distribution of lipid molecules in the perivascular tissue.</p>
<p>
<bold>Results:</bold>
Fourteen days after the procedure, the lymphatic vessels in the model tissue were significantly dilated. Furthermore, IMS revealed that the composition of the lipid molecules in the perivascular regions of the model tissue had altered. Compared with the control tissue, the model tissue exhibited marked perivascular accumulation of lysophosphatidylcholine (1-acyl 16:0), phosphatidylcholine (16:0/20:4), and triglycerides (52:2). Interestingly, the walls of the femoral veins running through the model tissue were 3.4-fold thicker than those of the femoral veins running through the control tissue. The number of tumor necrosis factor α-positive adipocytes was increased in the perivascular regions of the model tissue.</p>
<p>
<bold>Conclusion:</bold>
The findings of this study indicated that the accumulation of lymphatic fluid due to insufficient lymph drainage changes the structure of vein walls, and such changes might be associated with chronic venous insufficiency. (This is a translation of Jpn J Phlebol 2015; 26: 227–235.)</p>
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<name sortKey="Zaima, Nobuhiro" sort="Zaima, Nobuhiro" uniqKey="Zaima N" first="Nobuhiro" last="Zaima">Nobuhiro Zaima</name>
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<name sortKey="Sasaki, Takeshi" sort="Sasaki, Takeshi" uniqKey="Sasaki T" first="Takeshi" last="Sasaki">Takeshi Sasaki</name>
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<name sortKey="Unno, Naoki" sort="Unno, Naoki" uniqKey="Unno N" first="Naoki" last="Unno">Naoki Unno</name>
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<title xml:lang="en" level="a" type="main">Insufficient Lymph Drainage Causes Abnormal Lipid Accumulation and Vein Wall Degeneration</title>
<author>
<name sortKey="Tanaka, Hiroki" sort="Tanaka, Hiroki" uniqKey="Tanaka H" first="Hiroki" last="Tanaka">Hiroki Tanaka</name>
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<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
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<affiliation wicri:level="1">
<nlm:aff id="aff2">Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1">
<nlm:aff id="aff3">Department of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Yamamoto, Naoto" sort="Yamamoto, Naoto" uniqKey="Yamamoto N" first="Naoto" last="Yamamoto">Naoto Yamamoto</name>
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<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Suzuki, Minoru" sort="Suzuki, Minoru" uniqKey="Suzuki M" first="Minoru" last="Suzuki">Minoru Suzuki</name>
<affiliation wicri:level="1">
<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Mano, Yuuki" sort="Mano, Yuuki" uniqKey="Mano Y" first="Yuuki" last="Mano">Yuuki Mano</name>
<affiliation wicri:level="1">
<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Sano, Masaki" sort="Sano, Masaki" uniqKey="Sano M" first="Masaki" last="Sano">Masaki Sano</name>
<affiliation wicri:level="1">
<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Zaima, Nobuhiro" sort="Zaima, Nobuhiro" uniqKey="Zaima N" first="Nobuhiro" last="Zaima">Nobuhiro Zaima</name>
<affiliation wicri:level="1">
<nlm:aff id="aff2">Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1">
<nlm:aff id="aff4">Department of Applied Biological Chemistry, Graduate School of Agricultural Science, Kinki University, Osaka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Applied Biological Chemistry, Graduate School of Agricultural Science, Kinki University, Osaka</wicri:regionArea>
<wicri:noRegion>Osaka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Sasaki, Takeshi" sort="Sasaki, Takeshi" uniqKey="Sasaki T" first="Takeshi" last="Sasaki">Takeshi Sasaki</name>
<affiliation wicri:level="1">
<nlm:aff id="aff5">Department of Organ & Tissue Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Organ & Tissue Anatomy, Hamamatsu University School of Medicine, Hamamatsu</wicri:regionArea>
<wicri:noRegion>Hamamatsu</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Setou, Mitsutoshi" sort="Setou, Mitsutoshi" uniqKey="Setou M" first="Mitsutoshi" last="Setou">Mitsutoshi Setou</name>
<affiliation wicri:level="1">
<nlm:aff id="aff2">Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Unno, Naoki" sort="Unno, Naoki" uniqKey="Unno N" first="Naoki" last="Unno">Naoki Unno</name>
<affiliation wicri:level="1">
<nlm:aff id="aff1">Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka</wicri:regionArea>
<wicri:noRegion>Shizuoka</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series>
<title level="j">Annals of Vascular Diseases</title>
<idno type="ISSN">1881-641X</idno>
<idno type="eISSN">1881-6428</idno>
<imprint>
<date when="2016">2016</date>
</imprint>
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<front>
<div type="abstract" xml:lang="en">
<p>
<bold>Objective:</bold>
Previously, we analyzed human varicose veins (VV) using imaging mass spectrometry (IMS) and detected the abnormal accumulation of lipid molecules in the walls of VV, possibly due to insufficient lipid drainage by the lymphatic vessels. In this study, we created an animal model of lymphatic insufficiency to investigate the effects of insufficient lymph drainage on vein walls.</p>
<p>
<bold>Methods:</bold>
In rats, the lymphatic collecting vessels surrounding the femoral vein were ligated on one side (the model tissue), which caused the local retention of lymphatic fluid in the perivascular tissue. The equivalent contralateral tissue was used as a control. A histological study of the femoral vein and the surrounding perivascular tissue was conducted. IMS was used to analyze the distribution of lipid molecules in the perivascular tissue.</p>
<p>
<bold>Results:</bold>
Fourteen days after the procedure, the lymphatic vessels in the model tissue were significantly dilated. Furthermore, IMS revealed that the composition of the lipid molecules in the perivascular regions of the model tissue had altered. Compared with the control tissue, the model tissue exhibited marked perivascular accumulation of lysophosphatidylcholine (1-acyl 16:0), phosphatidylcholine (16:0/20:4), and triglycerides (52:2). Interestingly, the walls of the femoral veins running through the model tissue were 3.4-fold thicker than those of the femoral veins running through the control tissue. The number of tumor necrosis factor α-positive adipocytes was increased in the perivascular regions of the model tissue.</p>
<p>
<bold>Conclusion:</bold>
The findings of this study indicated that the accumulation of lymphatic fluid due to insufficient lymph drainage changes the structure of vein walls, and such changes might be associated with chronic venous insufficiency. (This is a translation of Jpn J Phlebol 2015; 26: 227–235.)</p>
</div>
</front>
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<name sortKey="Zaima, Nobuhiro" sort="Zaima, Nobuhiro" uniqKey="Zaima N" first="Nobuhiro" last="Zaima">Nobuhiro Zaima</name>
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<country xml:lang="fr">Japon</country>
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<name sortKey="Zaima, Nobuhiro" sort="Zaima, Nobuhiro" uniqKey="Zaima N" first="Nobuhiro" last="Zaima">Nobuhiro Zaima</name>
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<country xml:lang="fr">Japon</country>
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<name sortKey="Sasaki, Takeshi" sort="Sasaki, Takeshi" uniqKey="Sasaki T" first="Takeshi" last="Sasaki">Takeshi Sasaki</name>
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<name sortKey="Setou, Mitsutoshi" sort="Setou, Mitsutoshi" uniqKey="Setou M" first="Mitsutoshi" last="Setou">Mitsutoshi Setou</name>
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<name sortKey="Unno, Naoki" sort="Unno, Naoki" uniqKey="Unno N" first="Naoki" last="Unno">Naoki Unno</name>
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<front>
<div type="abstract" xml:lang="en">Objective: Previously, we analyzed human varicose veins (VV) using imaging mass spectrometry (IMS) and detected the abnormal accumulation of lipid molecules in the walls of VV, possibly due to insufficient lipid drainage by the lymphatic vessels. In this study, we created an animal model of lymphatic insufficiency to investigate the effects of insufficient lymph drainage on vein walls. Methods: In rats, the lymphatic collecting vessels surrounding the femoral vein were ligated on one side (the model tissue), which caused the local retention of lymphatic fluid in the perivascular tissue. The equivalent contralateral tissue was used as a control. A histological study of the femoral vein and the surrounding perivascular tissue was conducted. IMS was used to analyze the distribution of lipid molecules in the perivascular tissue. Results: Fourteen days after the procedure, the lymphatic vessels in the model tissue were significantly dilated. Furthermore, IMS revealed that the composition of the lipid molecules in the perivascular regions of the model tissue had altered. Compared with the control tissue, the model tissue exhibited marked perivascular accumulation of lysophosphatidylcholine (1-acyl 16:0), phosphatidylcholine (16:0/20:4), and triglycerides (52:2). Interestingly, the walls of the femoral veins running through the model tissue were 3.4-fold thicker than those of the femoral veins running through the control tissue. The number of tumor necrosis factor α-positive adipocytes was increased in the perivascular regions of the model tissue. Conclusion: The findings of this study indicated that the accumulation of lymphatic fluid due to insufficient lymph drainage changes the structure of vein walls, and such changes might be associated with chronic venous insufficiency. (This is a translation of Jpn J Phlebol 2015; 26: 227-235.).</div>
</front>
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