The actions of bradykinin on pial venule leaky site formation were mea
sured intra-vitally in two inbred strains of mice (BALB/c and SJL/J).
Pial venules were visualized using an open cranial window microscopy t
echnique and the microvascular leaky site formation was assessed visua
lly using a fluorescein-dextran (70 kDa) indicator. The SJL/J strain w
as found to be very sensitive to bradykinin-induced microvascular leak
age. Pial venule leaky site formation was observed after exposure to 1
0 pM of bradykinin. In contrast, the BALB/c strain was found to be ref
ractory to bradykinin-induced leakage. Pial arterioles were dilated in
response to bradykinin in both strains of mice. These results support
the concept that genetically controlled differences in vascular sensi
tivity and localization of inflammatory peptides play important roles
in the generation of vasogenic oedema and inflammation in CNS trauma a
nd disease.