1-O-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC) inducedin vitro a slowly-developing contraction of rabbit lung parenchymal strips by a mechanism distinct from those of histamine, acetylcholine and C5a. AGEPC appeared more potent on a molar basis than histamine, acetylcholine and C5a. However, rabbit lung tissue appeared more sensitive in terms of magnitude of maximal contraction to histamine-dependent agents (histamine and C5a). Priorin vitro exposure of lung tissue to AGEPC resulted in desensitization to AGEPC, but not to histamine, acetylcholine and C5a. Thein vivo infusion of AGEPC in the rabbit, which resulted in cardio-vascular and respiratory changes characteristic of an anaphylactoid reaction, induced complete desensitization of lung parenchymal strips, obtained 30 min after infusion, to AGEPC but not to histamine, acetylcholine and C5a. These data suggest anin vivo interaction between the injected AGEPC and the lung smooth muscle receptors.

Synthetic platelet-activating factor (PAF) (1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, AGEPC) has been shown to induce a slowly developing contraction of rabbit lung parenchymal strips in an isolated organ bath. The spasmogenic effect of AGEPC appeared to be mediated by specific receptors distinct from H1, H2, cholinergic and C5a anaphylatoxin receptors. Prior exposure to AGEPC induced specific desensitization of lung parenchymal strips. Experiments with several pharmacological agents indicated that AGEPC-induced contraction was independent from cyclooxygenase, but was blocked when phosopholipase A2 and lipoxygenase were inhibited and when the Ca++ channels were antagonized. Corticosteroids exhibited an inhibitory effect specific for AGEPC. Intracellular levels of cyclic AMP or cyclic GMP seemed to have a modulatory role in AGEPC-induced contraction of rabbit lung parenchymal strips.