Effect of prostaglandin E1 on leukotriene C4-induced increases in vascular permeability of hamster cheek pouch.

Our goal was to determine whether there is a synergistic effect of prostaglandin E1 (PGE1) on leukotriene C4 (LTC4)-induced increases in vascular permeability of the hamster cheek pouch in vivo. Changes in permeability were quantified by counting venular leaky sites (LS) and calculating clearance (CLR) of fluorescein isothiocyanate (FITC)-dextran 70kDa, during suffusion of the cheek pouch with LTC4 in the absence or presence of PGE1. LTC4 produced a dose-related increase in LS and CLR, and PGE1 (0.01 microM) significantly potentiated the effect of LTC4. During suffusion with LTC4 (15.0 nM) in the absence of PGE1, LS increased from 0 to 19 +/- 3/0.11 cm2 and CLR increased from 0.3 +/- 0.1 to 1.0 +/- 0.2 x 10(-6) ml/sec. During superfusion with LTC4 (15.0 nM) in the presence of PGE1, LS increased from 0 to 40 +/- 3/0.11 cm2, and CLR increased from 0.4 +/- 0.1 to 2.1 +/- 0.5 x 10(-6) ml/sec. To determine whether the effect of PGE1 on LTC4-induced increases in vascular permeability was related to the vasodilatory effect of PGE1, we examined the effect of isoproterenol (ISO). In contrast to that observed with PGE1, ISO decreased LTC4-induced increases in LS and CLR. Our data suggest that there is a synergistic effect of PGE1 on LTC4-induced increases in venular permeability that is not mediated by a vasodilatory action of PGE1.