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Minerva Chirurgica 2009 December;64(6):559-64


language: English

Use of alprostadil, a stable prostaglandin E1 analogue, for the attenuation of rat skeletal muscle ischemia and reperfusion injury

Antonio L. G. M., Evora P. R. B., Piccinato C. E.

1 Department of Surgery, Division of Vascular and Endovascular Surgery Faculty of Medicine of Ribeirão Preto, University of São Paul, São Paul, Brazil; 2 Division of Cardiovascular Surgery, Department of Surgery and Anatomy, Faculty of Medicine of Ribeirão Preto, University of São Paul, São Paul, Brazil


AIM: Some stable prostaglandin analogues such as alprostadil have been used to attenuate the deleterious effects of ischemia and reperfusion injury. The aim of this paper was to test if alprostadil can decrease the ischemia- reperfusion injury in rat skeletal muscle using muscular enzymes as markers, such as aspartate aminotransferase (AST), creatine kinase (CPK), lactate dehydrogenase (LDH); degeneration products of cell membrane-malondialdehyde (MDA) and muscle glycogen storage.
METHODS: Thirty male Wistar rats were used in a model of hind limb ischemia achieved by infrarenal aortic cross-clamping. The animals were randomized into three equal groups (N=10) submitted to 5 hours of ischemia followed by one hour of reperfusion. The first group (control) received continuous intravenous infusion of saline solution and the second group (preischemia, GPI) received continuous intravenous infusion of alprostadil throughout the experiment starting 20 minutes before the aortic cross-clamping. The third group, prereperfusion (GPR), received alprostadil only during the reperfusion period, with intravenous infusion being started 10 min before the clamp release.
RESULTS: There was no difference in CPK, LDH, AST or tissue glycogen values between groups. However, a significant elevation in MDA was observed in the GPI and GPR groups compared to the control group, with no difference between the GPI and GPR.
CONCLUSIONS: Under conditions of partial skeletal muscle ischemia, alprostadil did not reduce the release of muscular enzymes, the consumption of tissue glycogen or the effects of ischemia and reperfusion on the cell membrane, characterized by lipid peroxidation.

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