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1 Department of Cardiology, University of Heidelberg, Heidelberg, Germany
* To whom correspondence should be addressed. E-mail: ctiefenbacher{at}med.uni-heidelberg.de.
Statins have a variety of cardioprotective properties following chronic treatment. In contrast, little is known about acute effects. Reperfusion acutely injures the heart by activation of neutrophils as well as endothelial cells. Since statins are known to influence the processes pathogenetically involved, we hypothesized that acute application of statins attenuates the sequelae of cardiac reperfusion. In rats, myocardial infarction (MI) was induced by ligature of the left coronary artery followed by reperfusion. Myocardial blood flow (MBF) was determined by H2-clearance and regional myocardial function (fractional thickening, FT) by pulsed doppler. MI size was measured by triphenyltetrazoliumchloride (TTC)-staining, neutrophil extravasation by determination of myeloperoxidase (MPO)-acticity and NO generation via measurement of cGMP. Treatment with fluvastatin, administered intravenously 20min before the onset of ischemia, significantly attenuated the decline of FT and MBF at the end of the reperfusion period and significantly reduced MI size. Furthermore, fluvastatin induced a significant reduction of MPO-activity and an increase of cGMP level as compared to the control group. The effect of fluvastatin was completely abolished following pretreatment of L-NAME. These findings suggest that acute application of fluvastatin reduces myocardial infarct size and attenuates reperfusion injury. We propose that the underlying mechanism is at least partially an inhibition of inflammation and endothelial dysfunction by preventing the activation and extravasation of neutrophils.
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