Inflammation-induced vasodepression detected ex vivo in the isolated perfused hindlegs in mice

The ex vivo vasoreactivity of isolated perfused hindleg blood vessels upon norepinephrine is strongly decreased in mice with anaphylactic or dextran-induced paw oedema. In the presence of the carrageenin paw oedema vasoreactivity is only slightly or not influenced. The decrease of vasoreactivity can be observed in the leg with the paw oedema but, to a somewhat lesser extent, in an animal's leg without paw oedema, i.e., general vasodepression occurs. The development of vasodepression can already be seen a few minutes after inflammation induction. It partly parallels the development of paw swelling, but, to a certain extent, overlasts the disappearance of the oedema. Vasodepressing factors (VDFs) released from the site of inflammation are obviously responsible for the vasodepression. Contrary to the rat, no vasodepression could be demonstrated by using angiotensin II as the vasoconstrictor in the dextran mouse paw oedema model.