Intramyocardial Small Arteries Remodeling In Spontaneously Hypertensive Rats And The Effects Of Telmisartan On Them

ObjectiveTo investigate cytological mechanisms of intramyocardial small arteries (IMSAs) remodeling in spontaneously hypertensive rats, to study the effects of telmisartan and to explore the relationship between inflammation and IMSAs remodeling. Methods12-week-old male SHRs were randomized to 3 groups (all n=10), including untreated SHR group, telmisartan low dose(TelL) group, telmisartan high dose(TelH) group.Rats of TelL and TelH received telmisartan 0.8 mg·kg-1·d-1, 8mg·kg-1 ·d-1 by intragastric administration respectively. Age and sex matched Wistar Kyoto rats were served as control group (WKY, n= 10). After 18 weeks intervention, hemodynamics index of rats were measured before rats being sacrificed. Morphological characteristics were evaluated with HE, Sirus—red, elasticity fibrin and collagen fibrin double staining (P/VB). Wall area (WA), lumen area (LA) and percent wall area (%WA) of IMSAs were assessed with the compute-assisted image analysis system. Immunohistochemistry staining was performed to lable macrophages, vascular smooth muscle cells and ICAM-1. The apoptosis and proliferation of intramyocardial arterial smooth muscle cells were detected by in situ end labeling technique (TUNEL) and proliferating cell nuclear antigen (PCNA) immunohistochemistry staining respectively. Mast cells were demonstrated with toluidine blue staining. Results1. Mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricular end—diastolic pressure (LVEDP) and the maximum rate of left ventricular pressure rise (dp/dt_max) of SHR group were much higher than those of WKY group (P<0.01); MAP, LVSP, and dp/dtmax of TelH group (P<0.01) were significantly decreased compared to those of SHR group; However, the same effects were scarcely found in TelL group, except LVEDP.