Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo
Introduction. In the animal model, preconditioning is a powerful weapon against ischemic damage. The reason why the human heart cannot be protected from ischemic damage by preconditioning remains unclear. There are assumptions that the lack of preconditioning in humans is caused by concomitant disea...
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| Format: | Article |
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Wiley
2021-01-01
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| Series: | Cardiovascular Therapeutics |
| Online Access: | http://dx.doi.org/10.1155/2021/5596590 |
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| author | Walter Petermichl Kathrin Eglmeier Henriette Hesse Michael Gruber Bernhard Graf Andre Bredthauer Andreas Redel |
| author_facet | Walter Petermichl Kathrin Eglmeier Henriette Hesse Michael Gruber Bernhard Graf Andre Bredthauer Andreas Redel |
| author_sort | Walter Petermichl |
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| description | Introduction. In the animal model, preconditioning is a powerful weapon against ischemic damage. The reason why the human heart cannot be protected from ischemic damage by preconditioning remains unclear. There are assumptions that the lack of preconditioning in humans is caused by concomitant diseases such as dyslipoproteinemia and arteriosclerosis. This study investigates whether dyslipoproteinemia and the resulting arteriosclerosis can be a cause of a reduced precondition effect of heart in mice. Methods. LDL receptor-deficient mice were fed a long-term (14-16 weeks) high-fat atherogenic diet to induce arteriosclerosis. Arteriosclerosis was identified by histological examination and vessel contraction tests. LDLR-/- and wild-type mice were randomly assigned to anesthetic-induced, remote ischemic, or no preconditioning. All mice were subjected to 45 minutes of coronary artery occlusion and 180 minutes of reperfusion. The area at risk and infarct size were determined by Evans Blue and triphenyltetrazolium chloride staining. Results. Histopathological examination showed atherosclerosis in high-fat atherogenic fed LDLR-/- mice, and the vessel relaxation capacity was significantly reduced compared to wild-type mice. In the wild type, as expected, infarct size was significantly reduced by preconditioning compared to the control. In LDLR-/- mice, infarct size was significantly reduced by preconditioning compared to the control. Surprisingly, the LDLR-/- control group also had a significantly reduced infarct size compared to the wild-type control group. Conclusion. We were able to demonstrate that a high-fat diet morphologically and functionally triggered atherosclerosis in LDLR-/- mice. Interestingly, LDLR-/- mice with an atherogenic diet had smaller infarct sizes compared to wild-type mice. Moreover, preconditioning additionally reduced myocardial infarct size in LDLR-/- mice. A long-term high-fat atherogenic diet and preconditioning seem to result in additive cardioprotection in LDLR-/- mice. |
| format | Article |
| id | doaj-art-f869ce285aa240acb5f0b89df30c0f3e |
| institution | Kabale University |
| issn | 1755-5914 1755-5922 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
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| series | Cardiovascular Therapeutics |
| spelling | doaj-art-f869ce285aa240acb5f0b89df30c0f3e2025-02-03T06:46:42ZengWileyCardiovascular Therapeutics1755-59141755-59222021-01-01202110.1155/2021/55965905596590Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In VivoWalter Petermichl0Kathrin Eglmeier1Henriette Hesse2Michael Gruber3Bernhard Graf4Andre Bredthauer5Andreas Redel6Department of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, GermanyDepartment of Anesthesiology, Amberg Hospital, Mariahilfbergweg 7, 92224 Amberg, GermanyIntroduction. In the animal model, preconditioning is a powerful weapon against ischemic damage. The reason why the human heart cannot be protected from ischemic damage by preconditioning remains unclear. There are assumptions that the lack of preconditioning in humans is caused by concomitant diseases such as dyslipoproteinemia and arteriosclerosis. This study investigates whether dyslipoproteinemia and the resulting arteriosclerosis can be a cause of a reduced precondition effect of heart in mice. Methods. LDL receptor-deficient mice were fed a long-term (14-16 weeks) high-fat atherogenic diet to induce arteriosclerosis. Arteriosclerosis was identified by histological examination and vessel contraction tests. LDLR-/- and wild-type mice were randomly assigned to anesthetic-induced, remote ischemic, or no preconditioning. All mice were subjected to 45 minutes of coronary artery occlusion and 180 minutes of reperfusion. The area at risk and infarct size were determined by Evans Blue and triphenyltetrazolium chloride staining. Results. Histopathological examination showed atherosclerosis in high-fat atherogenic fed LDLR-/- mice, and the vessel relaxation capacity was significantly reduced compared to wild-type mice. In the wild type, as expected, infarct size was significantly reduced by preconditioning compared to the control. In LDLR-/- mice, infarct size was significantly reduced by preconditioning compared to the control. Surprisingly, the LDLR-/- control group also had a significantly reduced infarct size compared to the wild-type control group. Conclusion. We were able to demonstrate that a high-fat diet morphologically and functionally triggered atherosclerosis in LDLR-/- mice. Interestingly, LDLR-/- mice with an atherogenic diet had smaller infarct sizes compared to wild-type mice. Moreover, preconditioning additionally reduced myocardial infarct size in LDLR-/- mice. A long-term high-fat atherogenic diet and preconditioning seem to result in additive cardioprotection in LDLR-/- mice.http://dx.doi.org/10.1155/2021/5596590 |
| spellingShingle | Walter Petermichl Kathrin Eglmeier Henriette Hesse Michael Gruber Bernhard Graf Andre Bredthauer Andreas Redel Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo Cardiovascular Therapeutics |
| title | Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo |
| title_full | Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo |
| title_fullStr | Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo |
| title_full_unstemmed | Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo |
| title_short | Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo |
| title_sort | remote and anesthetic induced myocardial preconditioning is preserved in atherosclerotic ldl receptor mice in vivo |
| url | http://dx.doi.org/10.1155/2021/5596590 |
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