Fehr J, Bütler S
Klin Wochenschr. 1985 Feb 15;63(4):152-7. doi: 10.1007/BF01732168.
The (patho-)physiological role of prostaglandins and thromboxanes on granulocyte function remains controversial. In a combined in vitro and in vivo study, we analyzed the influence of these arachidonic acid metabolites on granulocyte adhesion and margination. A dichotomous dose-dependent effect on epinephrine-induced granulocyte demargination parallels the paradoxical effect of low (0.5 g)- and high (4 g)-dose aspirin on bleeding time. These observations suggest that prostacyclin acts as a modulator for low-affinity adhesion and margination of granulocytes. With respect to the induction of high-affinity adhesion, which is reflected in a state of hypermargination in vivo and accompanied by potentially cytotoxic cell activation, prostaglandins in general and prostacyclin in particular are without effect when such activation is induced, either by endotoxin, by formylated chemotactic peptide, or by activated complement.