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Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
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Quantification of Atherosclerosis in Mice
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Hypoxia/reperfusion predisposes to atherosclerosis.

Richard Finsterwalder1, Minu Karthika Ganesan1, Heide Leb1

  • 1Skin and Endothelium Research Division (SERD), Department of Dermatology, Medical University of Vienna, Vienna, Austria.

Plos One
|October 6, 2018
PubMed
Summary

Surgical injury to blood vessels can cause intimal hyperplasia and atherosclerosis by altering vascular smooth muscle cell (VSMC) gene expression. Transient arterial ligation in mice induced persistent VSMC changes and atherosclerosis, especially in those with lipid metabolism issues.

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Area of Science:

  • Vascular biology
  • Surgical pathology
  • Cardiovascular research

Background:

  • Surgical interventions on blood vessels risk intimal hyperplasia and atherosclerosis.
  • A key feature of intimal hyperplasia is the loss of vascular smooth muscle cell (VSMC) differentiation gene expression.

Purpose of the Study:

  • To investigate if immediate responses following injury induce vascular remodeling.
  • To differentiate injury causes like trauma, reperfusion, and pressure changes.
  • To analyze vascular responses to carotid artery bypass grafting versus transient ligation.

Main Methods:

  • Comparison of vascular responses in mice undergoing carotid artery bypass grafting, transient ligation, or surgical opening.
  • Analysis of inflammatory responses and VSMC differentiation gene expression over time.
  • Assessment of atherosclerosis development in ApoE knockout mice following transient ligation.

Main Results:

  • Inflammatory responses were transient (peaking at 6h), but VSMC differentiation gene expression loss persisted.
  • Transient carotid artery ligation induced persistent VSMC phenotype changes for up to 28 days.
  • Transient ligation in ApoE knockout mice led to atherosclerosis in the ligated segment, particularly with perturbed lipid metabolism.

Conclusions:

  • Surgical interventions involving hypoxia/reperfusion are sufficient to induce VSMC phenotype changes and vascular remodeling.
  • Perturbed lipid metabolism in conjunction with surgical injury significantly increases the risk of atherosclerosis development.