Improved functional recovery of the isolated rat heart after 24 hours of hypothermic arrest with a stable prostacyclin analogue (ZK 36 374).

Prostacyclin (PGI2) can protect the heart against ischemia, i.e. it can reduce myocardial damage [9, 10]. PGI2 protects the myocardium in vivo by preventing platelets from clumping and by dispersing preformed platelet aggregates [1,14]. However, also in the absence of platelets, PGI2 was shown to protect the myocardium against ischemia at concentrations that did not affect smooth muscle tone in the vessel wall [2]. This protective effect of PGI2 in vitro might be related to a stabilization of cell membranes in adrenergic nerve endings and hence to the prevention of ischemia-induced catecholamine release [13]. The instability of PGI2, both in vitro and in vivo, limits its application during long ischemic periods. Recently, a stable prostacyclin analogue, ZK 36 374, was demonstrated to have several prostacyclin-mimetic activities, both in vitro and in vivo [11,12]. In this communication we report upon the beneficial effect of this stable prostacyclin analogue at a low concentration (4 nM) on the extent of ischemic damage, on the recovery of myocardial function and on the occurrence of arrhythmias in the isolated rat heart after 24 h hypothermic cardiac arrest.