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CARDIOVASCULAR ANESTHESIA

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

Department of Anesthesiology, Emory University School of Medicine, Division of Cardiothoracic Anesthesiology and Critical Care, Emory Healthcare, Atlanta, Georgia

Address correspondence and reprint requests to Jerrold H. Levy, MD, Department of Anesthesiology, Emory University Hospital, 1364 Clifton Rd. NE, Atlanta, GA 30322.

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 ± 0.7g) 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.

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.

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