The impact of pressure overload on coronary vascular changes following myocardial infarction in rats

Abstract

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.

Abnormalities of capillary microarchitecture in a rat model of coronary ischemic congestive heart failure

“…no. 07349; Polysciences; www.polysciences.com) as previously described (11). Proper fluorescent dye (www.blacklightworld.com) was mixed with red pigment (1:4 in weight) and added into casting polymer mixture.…”

“…Transient (Ͻ30 min) arterial ligation, moderate occlusion, or blockage of a small vessel leads to submyocardial infarction (MI) and minor alternation or no change in cardiac function (11). Severe ischemia (Ͼ30 min) of a major coronary artery induces a large MI and serious heart dysfunction, usually due to pathological physical geometry: large MI reduce left ventricular (LV) ejection fraction (EF) and increase LV volume as myocardial mass is replaced by the noncontractile scar tissue (9).…”

Chronic N‐Methyl‐d‐Aspartate Receptor Activation Induces Cardiac Electrical Remodeling and Increases Susceptibility to Ventricular Arrhythmias

“…After the completion of the electrophysiological experiments, the hearts were weighed and fixed in 10% formaldehyde for histologic analysis . In brief, the hearts were cut transversely close to the papillary muscles.…”

Variability in coronary artery anatomy affects consistency of cardiac damage after myocardial infarction in mice

“…Indicators of cardiac structure and function, such as LV ejection fraction (EF), fractional shortening (FS), contractility (ϮdP/dt), and MI size, are impacted by the specific pathophysiological condition induced and experience of the researcher in data acquisition and analysis (3,25). Pathological changes in the coronary artery during HF have been well studied by our laboratory and others (6,8,17). However, the physiological reason for variability in cardiac function after MI induction is unknown (5).…”