Mast cells and their proteases are thought to participate in the developmen
t of skin blisters in various pathological conditions. Tn this study, sucti
on blistering was used as an experimental model to evaluate the significanc
e of mast cells in blister formation after pre-treatment of normal skin wit
h intradermal injections of 100 mu g/ml compound 48/80 (a mast cell degranu
lator) or with 0.1% capsaicin cream. Tryptic and chymotryptic enzyme activi
ties in blister fluids were measured with sensitive p-nitroanilide substrat
es, Repeated injections of compound 48/80 once a day on 3 or 5 consecutive
days or capsaicin applications 3 times a day for 7 or 10 days were used to
induce mast cell degranulation and inflammation in normal skin. Both treatm
ents ultimately led to decreased wheal and erythema reactions before suctio
n blistering, but neither treatment affected the size or formation rate of
suction blisters, No suction blister fluids had detectable levels of chymot
ryptic activity, but blister fluids from bullous pemphigoid, herpes tester
and insect bullous eruption, used as the control, revealed clear chymotrypt
ic activity. In addition, tryptic activity in suction blister fluids was no
t significantly altered after compound 48/80 and capsaicin pre-treatments.
However, if the wheal reaction was induced immediately before suction blist
ering, a significantly increased rate in blister formation together with in
creased tryptic activity was found, but, unexpectedly, no chymotryptic acti
vity could be detected in blister fluids. The results show that repeated ma
st cell degranulation in normal skin has no effect on the formation rate of
suction blisters, which developed more rapidly on acutely whealing skin. T
his is probably due to skin oedema rather than mast cell proteases, since n
o chymotryptic activity was detected in suction blisters where tryptic acti
vity exhibited high individual variation.