This study investigates the action of intravenous
PGE1 on
myocardial reperfusion injury and the possible involvement of antineutrophil activities. Cats were subjected to 3 h of temporary
ligation of the left anterior descending coronary artery, followed by 2 h of reperfusion. Animals were treated with
PGE1 (5 micrograms/kg x min) or vehicle (
saline solution), starting 0.5 h after coronary artery occlusion. Vehicle-treated cats exhibited a significant loss of cardiac
creatine phosphokinase specific activity at 5 h, accompanied by a significant
ischemia-induced rise in the ST segment of the ECG and development of a Q wave after starting reperfusion. All of these alterations were largely prevented by
PGE1 treatment.
PGE1 exerted some blood-pressure-lowering activity at 5 h (P greater than 0.05) but did not reduce myocardial contractile force and oxygen consumption.
PGE1 modestly antagonized
ischemia-induced formation of platelet aggregates. However,
PGE1 prevented the rise in peripheral white blood cell count during
ischemia and reperfusion and inhibited the generation of
reactive oxygen species (
myeloperoxidase assay) from
zymosan-stimulated whole blood ex vivo. The ratio of generation of
reactive oxygen species/white blood count remained unchanged. It is concluded that
PGE1 protects the ischemic myocardium from acute
reperfusion injury and that this effect involves an action of the compound on neutrophils, probably by improved myocardial tissue preservation, resulting in reduced formation of chemotactic products and, consequently, less local neutrophil accumulation and release of noxious metabolites.