Acute intravenous application of fluvastatin significantly reduced myocardial infarct size and attenuated the decline of myocardial blood flow and function in rats.
Does acute intravenous administration of fluvastatin reduce myocardial infarct size and attenuate reperfusion injury in a rat model of ischemia-reperfusion?
Acute intravenous administration of fluvastatin before ischemia reduces myocardial infarct size and attenuates reperfusion injury in a rat model, likely via inhibition of inflammation and endothelial dysfunction.
Statins have a variety of cardioprotective properties following chronic treatment. In contrast, little is known about the acute effects. Reperfusion acutely injures the heart by activation of neutrophils as well as endothelial cells. Because 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 triphenyltetrazolium chloride (TTC) staining, neutrophil extravasation by determination of myeloperoxidase (MPO) activity, and nitric oxide generation via measurement of cGMP. Treatment with fluvastatin, administered intravenously 20 min 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 compared with the control group. The effect of fluvastatin was completely abolished following pretreatment of NG-nitro-l-arginine methyl ester (l-NAME). These findings suggest that acute application of fluvastatin reduces MI 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.
Tiefenbacher et al. (Tue,) conducted a other in Myocardial infarction and reperfusion injury. Fluvastatin vs. Control group was evaluated on Myocardial infarct size, myocardial blood flow, and regional myocardial function. Acute intravenous application of fluvastatin significantly reduced myocardial infarct size and attenuated the decline of myocardial blood flow and function in rats.