Cardioprotection exerted by rosuvastatin on rat hearts subjected to ischemia-reperfusion

Abstract

Introduction: The prophylactic use of statins in patients with cardiovascular risk has recently increased, due to its association with lower mortality and morbidity related to ischemic heart disease. The present investigation tends to clarify if the treatment with statins induces beneficial changes to increase the resistance to the damages caused by the ischemia reperfusion.
Objectives: To investigate the possible protection exerted by rosuvastatin (R) in a Langendorff perfused heart model and its relation with the regulation of the opening of the Mitochondrial Permeability Transition Pore (MPTP). Materials and methods: Hearts from female Wistar rats were used, retrograde perfused, and subjected to 25 minutes of ischemia and 60 minutes of reperfusion (RP). R was given 10 minutes prior to ischemia (R1) or throughout reperfusion (R2). Functional response, creatine kinase (CK) release, infarct size, ATP synthesis capacity and sensitivity
to MPTP opening were determined.
Results: R-treated hearts had a greater postischemic recovery than the control group ((contractility (%) at 5 min of RP: control 6.8 ± 2*; R1 24.3 ± 6; R2 19 ± 6; left ventricle end diastolic pressure (%) at 5 min of RP: control 20 ± 3**; R1 6 ± 1; R2 3.8 ± 1.5), with no differences between pre-and post-ischemia treatments. Likewise, in these hearts, we observed: lower tissue damage (CK (UI/ g.w) during the first 10 minutes of RP: control 60 ± 5; R1 32 ± 3; R2 28 ± 6; infarct size (% AR) control 62.0 ± 1.5; R1 41.6 ± 3.5*; R2 36.3 ± 3.2),