title: The in vitro reversal of histamine-induced vasodilation in the human internal mammary artery.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Anesthesiology, Emory University School of Medicine, Division of Cardiothoracic Anesthesiology and Critical Care, Emory Healthcare, Atlanta, Georgia 30322, USA.
authors.forename: A
authors.initials: A
authors.lastname: Tsuda
authors.forename: K A
authors.initials: KA
authors.lastname: Tanaka
authors.forename: C
authors.initials: C
authors.lastname: Huraux
authors.forename: F
authors.initials: F
authors.lastname: Szlam
authors.forename: N
authors.initials: N
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: J H
authors.initials: JH
authors.lastname: Levy
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000707:Anaphylaxis / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors; D006632:Histamine / Q000009:adverse effects / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008323:Mammary Arteries / Q000187:drug effects* / Q000502:physiology; D008751:Methylene Blue / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014667:Vasopressins / Q000494:pharmacology; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D000322:Adrenergic Agonists; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D014667:Vasopressins; D019323:omega-N-Methylarginine; D006632:Histamine; D006162:Guanylate Cyclase; D008751:Methylene Blue; D007213:Indomethacin; D004837:Epinephrine