Modulation of macromolecular permeability by immune-complexes and a beta-adrenoceptor stimulant.

The suffused, noneverted cheek pouch of ovalbumin (OA)-immunized hamsters was employed to study changes in vascular permeability utilizing intravital light microscopy and direct measurements of plasma to suffusate tracer efflux. Suffusion of the cheek pouches of immunized animals with OA for 10 min stimulated the formation of focal venular fluorescein isothiocyanate dextran (FITC-D, 70,000 Da) leakage sites and produced increases in the plasma to suffusate FITC-D efflux resulting in marked increases in concentration of FITC-D in suffusate ([FITC-D]s). The intravenous injection of the FITC-D 15 to 60 min after the start of the OA suffusion failed to reveal the formation of vascular FITC-D leakage sites or increases in [FITC-D]s. In contrast, the intravenous injection of the tracer at the start or 10 min after the start of the OA suffusion revealed the formation of venular FITC-D leakage sites and marked increases in [FITC-D]s. Treatment with diphenhydramine or isoproterenol completely inhibited the antigen-stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]s. It is concluded that antigen-antibody reactions resulting in the production of immune complexes trigger immediate increases in the plasma to suffusate FITC-D clearance via the formation of venular FITC-D leakage sites subsequent to the release of endogenous histamine. The increase in venular permeability is marked but transient, lasting approximately 10 min, and is subject to inhibition by either diphenhydramine or isoproterenol.