The impact of pressure overload on coronary vascular changes following myocardial infarction in rats
| Autor: | Jagat Narula, Lifan Liang, Jiqiu Chen, Elisa Yaniz-Galende, Roger J. Hajjar, Hans J. de Haas, Artiom Petrov |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
medicine.medical_specialty Physiology Myocardial Infarction Myocardial Reperfusion Injury Rats Sprague-Dawley Coronary circulation Left coronary artery Fibrosis Physiology (medical) Internal medicine medicine.artery Coronary Circulation medicine Ventricular Pressure Animals Myocardial infarction Pressure overload Heart Failure business.industry Translational Physiology Myocardium medicine.disease Coronary Vessels Capillaries Rats Cardiac Imaging Techniques Disease Models Animal Tomography x ray computed medicine.anatomical_structure Echocardiography Heart failure Cardiology Ventricular pressure Cardiology and Cardiovascular Medicine business Tomography X-Ray Computed |
| Popis: | This study investigates the impact of pressure overload on vascular changes after myocardial infarction (MI) in rats. To evaluate the effect of pressure overload, MI was induced in three groups: 1) left coronary artery ligation for 1 mo (MI-1m), 2) ischemia 30 min/reperfusion for 1 mo (I/R-1m), and 3) ischemia-reperfusion (I/R) was performed after pressure overload induced by aortic banding for 2 mo; 1 mo post-I/R, aortic constriction was released (Ab+I/R+DeAb). Heart function was assessed by echocardiography and in vivo hemodynamics. Resin casting and three-dimensional imaging with microcomputed tomography were used to characterize changes in coronary vasculature. TTC (triphenyltetrazohum chloride) staining and Masson's Trichrome were conducted in parallel experiments. In normal rats, MI induced by I/R and permanent occlusion was transmural or subendocardial. Occluded arterial branches vanished in MI-1m rats. A short residual tail was retained, distal to the occluded site in the ischemic area in I/R-1m hearts. Vascular pathological changes in transmural MI mostly occurred in ischemic areas and remote vasculature remained normal. In pressure overloaded rats, I/R injury induced a sub-MI in which ischemia was transmural, but myocardium in the involved area had survived. The ischemic arterial branches were preserved even though the capillaries were significantly diminished and the pathological changes were extended to remote areas, characterized by fibrosis, atrial thrombus, and pulmonary edema in the Ab+I/R+DeAb group. Pressure overload could increase vascular tolerance to I/R injury, but also trigger severe global ventricular fibrosis and results in atrial thrombus and pulmonary edema. |
| Databáze: | OpenAIRE |
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