Abstract
In rats, the intradermal injection of norepinephrine [NE] had a short term vasoconstricting effect and resulted in a transitory inhibition of histamine induced vasodilatation and increased capillary permeability. At delayed times, 2 to 6 hr. after norepinephrine injection, vasodilatation and increased permeability occurred. When histamine was injected intradermally 2 to 6 hr. after norepinephrine, enormous vasodilatation, vascular damage and edema formation occurred. Norepinephrine, 2 hr. after injection, provoked mast cell disruption and many ghost mast cells were found at the site of treatment. Histamine injection at this delayed time further aggravated the mast cell and vascular damage. All alterations in morphology and permeability were transitory, the cells returning to normal within 24 hr. The NE induced delayed inflammatory vascular response was the result of a local imbalance in the proportional concentration of mediators of mast cell origin, rather than a direct effect of pro- or antinflammatory mediators upon the minute vessels.