Remote and Anesthetic-Induced Myocardial Preconditioning Is Preserved in Atherosclerotic LDL Receptor-/- Mice In Vivo

URN to cite this document:: urn:nbn:de:bvb:355-epub-461733
DOI to cite this document:: 10.5283/epub.46173

Petermichl, Walter ; Eglmeier, Kathrin ; Hesse, Henriette ; Gruber, Michael

; Graf, Bernhard ; Bredthauer, Andre

; Redel, Andreas ; Ptaszynski, Pawel

Preview

License: Creative Commons Attribution 4.0
PDF - Published Version
(668kB)

Date of publication of this fulltext: 25 Jun 2021 19:23

Alternative links to fulltext:DOI Publisher

Details

Preview

Indexed in

Export bibliographical data

Abstract

Abstract

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.

Owner only: item control page

Download Statistics

Altmetric

Alternative Statistics (altmetrics)

More literature (via CORE)

Details

Preview

Indexed in

Export bibliographical data

Abstract

Abstract

Download Statistics

Downloads

Alternative Statistics (altmetrics)

More literature (via CORE)

University Library