Endothelial Plasticity Drives Arterial Remodeling Within the Endocardium After Myocardial Infarction

Rats with myocardial infarction (MI) after coronary artery ligation (n = 75) and sham operated rats (n = 40) were treated with captopril (2 g/l drinking water), hydralazine (80 mg/l drinking water), or untreated water for 3 wk. Arterial hemodynamics, carotid artery mechanical properties, and water permeability were measured. Arterial wall stress and interstitial fluid velocity were calculated. In infarcted rats, the characteristic impedance at matched pressure was increased by 135% (P < 0.02); captopril and hydralazine decreased characteristic impedance (P < 0.015). MI altered the material constants; captopril but not hydralazine normalized these constants. Water permeability was increased by 221% (P < 0.001) in infarcted rats; captopril but not hydralazine reversed water permeability (P < 0.05). MI resulted in a 59% increase (P < 0.05) in the arterial collagen area and a 22% decrease (P < 0.05) in the media thickness. Captopril but not hydralazine decreased (P < 0.03) collagen area. In conclusion, 1) arterial remodeling defined by alterations in the passive mechanical properties, water permeability, and structure occurs in rats after MI; and 2) captopril but not hydralazine reverses the arterial remodeling.

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Abstract 679: Pdgf/snail-mediated Endothelial Plasticity Drives Non-productive Neovascularization and Impedes Tissue Repair After Myocardial Infarction

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.38.suppl_1.679 ◽

2018 ◽

Vol 38 (Suppl_1) ◽

Author(s):

Yi Fan ◽

Menggui Huang ◽

Fan Yang ◽

Hao Duan

Keyword(s):

Myocardial Infarction ◽

Tissue Repair ◽

Endothelial Plasticity

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An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010008328x ◽

1978 ◽

Vol 36 (2) ◽

pp. 484-485

Author(s):

Masahiro Ono ◽

Kaoru Aihara ◽

Gompachi Yajima

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Coronary Vessels ◽

Vascular Wall ◽

Vascular Changes ◽

Electron Microscopic ◽

Main Trunk ◽

Mechanical Destruction ◽

Transmission Electron ◽

Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

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