Role of prostaglandins and histamine in reactive hyperemia: in-vivo studies on single mesenteric arterioles.

Direct, in vivo microcirculatory experiments were undertaken with anesthetized rats to determine whether prostaglandin (PG)-like compounds and histamine may mediate post-occlusion hyperemia in single mesenteric arterioles. Superfusion of the mesenteric vasculature with two structurally different PG synthetase inhibitors, indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA), was found to markedly inhibit postocclusion vasodilator responses in arterioles 20-22 micrometer i.d. Superfusion of mesentery with an H2-histamine receptor antagonist, metiamide, resulted in a 40% inhibition of the postocclusion vasodilator responses in arterioles. Superfusion of the mesenteric vasculature with a combination of indomethacin and metiamide resulted in a 95% suppression of the postocclusion dilator responses. Administration of either the PG synthetase inhibitors, metiamide, or a combination of both types of drugs did not, however, influence resting arteriolar tone or responsiveness to PGE1 or epinephrine. Although the results of these experiments implicate a role for PG-like substances and histamine in reactive or postocclusion hypermia, they do not provide evidence for a role of these humoral substances in the normal moment-to-moment regulation of arteriolar tone.