The In Vitro Reversal of Histamine-Induced Vasodilation in the Human Internal Mammary Artery

Anaphylactic shock therapy includes the use of catecholamines but they may not always be effective. Because vasodilation during anaphylaxis is a result of the endothelial release of multiple mediators, we investigated the effects of epinephrine, vasopressin, and inhibitors of nitric oxide and prostanoid pathways on histamine-induced relaxation in human internal mammary artery. The vessel segments were obtained intraoperatively and were suspended in organ chambers to record isometric tension. Norepinephrine (10−6 M) was used to precontract the rings followed by histamine (10−6.5 M) to relax the vessels and mimic vascular collapse. Epinephrine, vasopressin, methylene blue, NG-monomethyl-L-arginine (L-NMA) and indomethacin were added in a cumulative fashion to reverse the histamine-induced vasodilation. The internal mammary artery segments exhibited greater contraction in the presence of the epinephrine (4.9 ± 0.7g) compared with vasopressin (2.6 ± 0.7g). Vasopressin (10−11 to 10−7 M), methylene blue (10−7 to 10−5 M), L-NMA (10−6 to 10−4 M), and indomethacin (10−7 to 10−5 M) were only partially effective. These findings suggest that vasopressin and methylene blue may offer a potential therapeutic option in the treatment of histamine-induced vasodilatory shock.