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Updated: May 30, 2026
Myocardial Infarction by Percutaneous Embolization Coil Deployment in a Swine Model
Published on: November 4, 2021
No-reflow disrupts the expression and distribution of connexin 43 in a swine model
Yu-tong Cheng1, Yue-jin Yang, Hai-tao Zhang
1Department of Cardiology, Fuwai Hospital and Cardiovascular Institute, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100037, China.
Introduction And Objectives:
Ischemia and ischemia/reperfusion can dephosphorylate and redistribute connexin 43 (Cx43). But it is unknown whether no-reflow phenomenon has an effect on the expression and distribution of Cx43 after acute infarction and reperfusion.
Methods:
21 open-chest pigs were divided into three groups. Left anterior descending artery (LAD) occlusion for 90 min before 180 min of reperfusion was made in ischemia/reperfusion group. The pigs in ischemia groups were either subjected to LAD ligation for 90 min or for 270 min. No-reflow and risk regions were determined pathologically by dye staining. Cx43 expression was measured by western blotting and quantitative RT-PCR analysis. Cx43 spatial distribution was shown by immunofluorescence examination.
Results:
The content of phosphorylated and mRNA of Cx43 were higher in reflow region than in the no-reflow or sustained ischemic region. The distribution of Cx43 was also altered in no-reflow region.
Conclusions:
There are some differences in synthesis, expression and distribution of myocardial Cx43 at microvascular level after ischemia/reperfusion. Cx43 is partially rephosphorylated with reperfusion only in the reflow myocardium.