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Impaired Coronary Collateral Growth in a Mouse Model of Diabetes
Author(s) -
Cumpston Devan,
Wan Weiguo,
Chinchilla Sofia,
McCabe Caige,
Enrick Molly,
Shoenbeck Sydney,
Chilian William,
Yin Liya
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb280
Subject(s) - medicine , cardiology , collateral circulation , diabetes mellitus , ischemia , blood flow , endocrinology
Cardiovascular disease is the leading cause of death in the United States, Ischemic Heart Disease (IHD) accounts for one in seven cardiovascular related deaths. Patients with poorly developed coronary collateral networks have a poorer prognosis after a cardiovascular event than those with well‐developed collaterals. Furthermore, coronary collateral growth is impaired in metabolic syndromes such as diabetes, and obesity. The underlying mechanism(s) that is (are) causal for growth are unknown. In an attempt to elucidate a mechanistic understanding, we developed a murine model that allows us to use genetically modified mice to study the coronary collateral growth spatially and temporally. Methods a pneumatic snare was implanted and situated around the LAD (open chest surgery during anesthesia). After mice recovered from surgery, the snare was periodically inflated to occlude the LAD; thus producing episodes of ischemia or repetitive ischemia (RI). Coronary collateral growth (CCG) was measured by myocardial blood flow with contrast echocardiography and by collateral numbers by micro‐CT. Results 1) No native coronary collaterals were found in mice. 2) After the RI stimulation, extensive coronary collaterals grew. 3) Diabetic mice failed to grow coronary collaterals after RI stimulation. 4) Moreover, the coronary blood flow increased in the ischemic area when there was coronary collateral growth. 5) The quantification of vessel density by tree analysis showed an increase after RI stimulation. Figure 1 (A–C) shows the microfil pictures of the wild type mouse heart without CCG (A), the wild type mouse heart with CCG (B), and the diabetic heart without CCG (C). We believe this murine model of coronary collateral growth is very useful for future studies to investigate the mechanism of regulation of coronary collateral growth. Figure 1 (D–F) shows the micro‐CT pictures of the wild type mouse heart without CCG (D), the wild type mouse heart with CCG (E) and the diabetic heart without CCG (F). Support or Funding Information 2R01HL103227‐05( Zhang, Yin), 1R01HL135110‐01 (WMC, LY), 1 R01 HL137008‐01A1 (LY), 1R15HL115540‐01 (LY) and14BGIA18770028 from American Heart Association This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .