The Role of the Intestinal Barrier after Acute Myocardial Infarction |
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Author | WangShiQi |
Tutor | ZengQiuTang |
School | Huazhong University of Science and Technology |
Course | Internal Medicine |
Keywords | Acute myocardial infarction Intestinal barrier Inflammatory cytokines |
CLC | R542.22 |
Type | Master's thesis |
Year | 2011 |
Downloads | 5 |
Quotes | 0 |
Objective: The variation of the intestinal barrier function and inflammatory cytokines in acute myocardial infarction , for the treatment of myocardial infarction new intervention targets . Methods: 50 patients with acute myocardial infarction , serum levels of D - lactate levels ( the colorimetric quantitative detection ) , access to the intestinal barrier , which were divided into two groups , namely intestinal barrier dysfunction group (A ) and complete group (B ) of the intestinal barrier function . Respectively after admission 1,3,5 , 7 days Dynamic detection of plasma endotoxin ( chromogenic substrate Limulus reagent endpoint chromogenic method ) and inflammatory cytokines CRP ( immunofluorescence sandwich method ) , TNF -α , TGF -β1 in and the level of IL-10 ( enzyme-linked immunosorbent assay ) . Results: 36 patients with acute myocardial infarction in patients with early intestinal barrier function is impaired . Intestinal barrier function is impaired group and intestinal barrier function intact group comparison : endotoxin levels of CRP, TNF - α , TGF - β1 , IL - 10 was significantly higher ( P lt; 0.05 ) . Conclusion: acute myocardial infarction , approximately 70% of patients with intestinal barrier function is impaired . Impaired intestinal barrier function and endotoxin levels consistent , that produce gut-derived endotoxemia . Endotoxin activation and amplification of the inflammatory response produces inflammatory cytokines and further damage to the intestinal barrier function and myocardial cells , thus creating a vicious cycle . Protect the intestinal barrier treatment and regulation and intervention in the inflammatory cytokine network , may be beneficial to reduce myocardial damage , delay or even inhibit ventricular remodeling , and thus fundamental to avoid the occurrence of heart failure in acute myocardial infarction .