The in vitro reversal of histamine-induced vasodilation in the human internal mammary artery.

Journal Article (Journal Article)

UNLABELLED: 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, N(G)-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 +/- 0.7 g) compared with vasopressin (2.6 +/- 0.7 g). 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. IMPLICATIONS: Epinephrine only partially reverses histamine-induced vasodilation in human internal mammary arteries, whereas vasopressin, methylene blue, and drugs involved in the inhibition of nitric oxide and prostaglandin generation lead to a complete reversal of the vascular relaxation.

Full Text

Duke Authors

Cited Authors

  • Tsuda, A; Tanaka, KA; Huraux, C; Szlam, F; Sato, N; Yamaguchi, K; Levy, JH

Published Date

  • December 2001

Published In

Volume / Issue

  • 93 / 6

Start / End Page

  • 1453 - 1459

PubMed ID

  • 11726422

International Standard Serial Number (ISSN)

  • 0003-2999

Digital Object Identifier (DOI)

  • 10.1097/00000539-200112000-00020


  • eng

Conference Location

  • United States