title: Tissue ACE inhibition improves microcirculation in remote myocardium after coronary stenosis: MR imaging study in rats.
abstract: ACE inhibition has been shown to improve left ventricular (LV) and myocardial blood flow. Previous data regarding changes in capillary density and angiogenesis during ACE inhibition are controversial. The aim of the following study was to determine myocardial microcirculation and heart function in the rat after coronary stenosis using non invasive MR imaging techniques. MR spin labeling and cine techniques have been performed in female Wistar rats 2weeks after coronary artery stenosis. In one group, animals were treated with quinapril in a dose of 6mg/kg/day. Perfusion, relative blood volume (RBV), LV mass and function were determined non-invasively 2weeks after treatment. Finally, fibrosis and capillary density were analyzed histologically. Additionally, hemodynamic measurements were realized in a further group in order to calculate systemic vascular resistance (SVR). Quinapril resulted in a significant increase in perfusion at rest in the remote and the poststenotic myocardium with improved systolic function and a decrease in SVR compared to the non treated control group. Additionally, maximum perfusion and RBV were slightly elevated whereas capillary density was unchanged among the groups. MRI allows for non-invasive quantification of functional microcirculation and heart function. In addition to the well known effect of ACE inhibition on systolic function, treatment with the tissue specific ACE inhibitor quinapril revealed an important microvascular improvement, especially at arteriolar level. These findings may support the use of tissue ACE inhibitors to improve cardiac microcirculation after ischemia.
authors.affiliation: MRB Research Center Magnetic-Resonance-Bavaria, Würzburg, Germany.
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Hiller
authors.forename: Philipp
authors.initials: P
authors.lastname: Ruile
authors.forename: Günter
authors.initials: G
authors.lastname: Kraus
authors.forename: Wolfgang R
authors.initials: WR
authors.lastname: Bauer
authors.forename: Christiane
authors.initials: C
authors.lastname: Waller
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D005355:Fibrosis; D006439:Hemodynamics / Q000187:drug effects; D019028:Magnetic Resonance Imaging, Cine; D008833:Microcirculation / Q000187:drug effects*; D055414:Myocardial Perfusion Imaging / Q000379:methods*; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000097:blood*; D000077583:Quinapril; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function; D044005:Tetrahydroisoquinolines / Q000494:pharmacology*; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D044005:Tetrahydroisoquinolines; D007703:Peptidyl-Dipeptidase A; D000077583:Quinapril