BACKGROUND: We hypothesized that mast cells may participate in coronary angiogenesis in acute myocardial infarction, contributing to myocardial salvage. METHODS: The left coronary artery was occluded in control (n = 30) and Ws rats (n = 30), which genetically lacked c-kit, resulting in a mast cell deficiency. Four weeks later, the infarct area, i.e., infarct core and surrounding infarct areas, and the non-infarct area were assessed histopathologically. The mast cell and small vessel densities were assessed using toluidine blue and alkaline phosphatase staining. Myocardial perfusion was assessed by myocardial contrast echocardiography (MCE). RESULTS: In Ws rats, the percentage infarct core area increased (p < 0.05) compared with the controls, whereas the percentage surrounding infarct area decreased (p < 0.01). Mast cell density increased most in the surrounding infarct area (p < 0.01) in control rats, whereas mast cells were absent in Ws rats. Compared with the controls, coronary microvessel density decreased in the surrounding infarct area in Ws rats (p < 0.01). MCE showed that the percentage infarct core area, i.e., perfusion defect, increased (p < 0.05) and the percentage surrounding infarct area, i.e., reduced perfusion area, decreased (p < 0.01) in Ws rats. CONCLUSION: Mast cells may participate in promoting coronary angiogenesis in the infarct area surrounding the infarct core, contributing to attenuation of left ventricular dysfunction.
BACKGROUND: We hypothesized that mast cells may participate in coronary angiogenesis in acute myocardial infarction, contributing to myocardial salvage. METHODS: The left coronary artery was occluded in control (n = 30) and Ws rats (n = 30), which genetically lacked c-kit, resulting in a mast cell deficiency. Four weeks later, the infarct area, i.e., infarct core and surrounding infarct areas, and the non-infarct area were assessed histopathologically. The mast cell and small vessel densities were assessed using toluidine blue and alkaline phosphatase staining. Myocardial perfusion was assessed by myocardial contrast echocardiography (MCE). RESULTS: In Ws rats, the percentage infarct core area increased (p < 0.05) compared with the controls, whereas the percentage surrounding infarct area decreased (p < 0.01). Mast cell density increased most in the surrounding infarct area (p < 0.01) in control rats, whereas mast cells were absent in Ws rats. Compared with the controls, coronary microvessel density decreased in the surrounding infarct area in Ws rats (p < 0.01). MCE showed that the percentage infarct core area, i.e., perfusion defect, increased (p < 0.05) and the percentage surrounding infarct area, i.e., reduced perfusion area, decreased (p < 0.01) in Ws rats. CONCLUSION: Mast cells may participate in promoting coronary angiogenesis in the infarct area surrounding the infarct core, contributing to attenuation of left ventricular dysfunction.
Authors: Kou Gi Shyu; Mei Ti Wang; Bao Wei Wang; Chih Chuna Chang; Jyh Gang Leu; Peiliang Kuan; Hang Chang Journal: Cardiovasc Res Date: 2002-06 Impact factor: 10.787
Authors: Stéphane Lafitte; Aya Higashiyama; Hisashi Masugata; Barry Peters; Monet Strachan; Oi Ling Kwan; Anthony N DeMaria Journal: J Am Coll Cardiol Date: 2002-05-01 Impact factor: 24.094
Authors: D Orlic; J Kajstura; S Chimenti; F Limana; I Jakoniuk; F Quaini; B Nadal-Ginard; D M Bodine; A Leri; P Anversa Journal: Proc Natl Acad Sci U S A Date: 2001-08-14 Impact factor: 11.205