Effect of severe acidosis on vasoactive effects of epinephrine and norepinephrine in human distal mammary artery  Charles Vidal, MD, Stanislas Grassin-Delyle,

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Effect of severe acidosis on vasoactive effects of epinephrine and norepinephrine in human distal mammary artery  Charles Vidal, MD, Stanislas Grassin-Delyle, PharmD, Philippe Devillier, MD, PhD, Emmanuel Naline, PharmD, Emmanuel Lansac, MD, Philippe Ménasché, MD, PhD, Christophe Faisy, MD, PhD  The Journal of Thoracic and Cardiovascular Surgery  Volume 147, Issue 5, Pages 1698-1705 (May 2014) DOI: 10.1016/j.jtcvs.2013.11.013 Copyright © 2014 The American Association for Thoracic Surgery Terms and Conditions

Figure 1 Concentration–response curves for epinephrine in human distal internal mammary arteries in absence (pH 7.40) and presence of extracellular acidosis: A and B, pH of 7.20 (n = 11); C and D, pH of 7.0 (n = 10); and E and F, pH of 6.8 (n = 11). Contraction expressed in g (A, C, and E) and percentage of the maximal contraction induced by 90 mM KCl under standard conditions (pH 7.40; B, D, and F). Data presented as mean ± standard deviation. Each experiment served as its own control. No differences between acidosis and the standard condition (pH 7.40) were statistically significant (P > .05 for all). The Journal of Thoracic and Cardiovascular Surgery 2014 147, 1698-1705DOI: (10.1016/j.jtcvs.2013.11.013) Copyright © 2014 The American Association for Thoracic Surgery Terms and Conditions

Figure 2 Concentration–response curves for norepinephrine in human distal internal mammary arteries in absence (pH 7.40) and presence of extracellular acidosis: A and B, pH of 7.20 (n = 11); C and D, pH of 7.0 (n = 10); and E and F, pH of 6.8 (n = 11). Contraction expressed in g (A, C, and E) and percentage of the maximal contraction induced by 90 mM KCl under standard conditions (pH 7.40; B, D, and F). Data presented as mean ± standard deviation. Each experiment served as its own control. No differences between acidosis and the standard condition (pH 7.40) were statistically significant (P > .05 for all). The Journal of Thoracic and Cardiovascular Surgery 2014 147, 1698-1705DOI: (10.1016/j.jtcvs.2013.11.013) Copyright © 2014 The American Association for Thoracic Surgery Terms and Conditions

Figure 3 Concentration–response curves for (A and B) methoxamine, an α1A/D-adrenoceptor agonist (n = 10); C and D, phenylephrine, an equipotent agonist of α1A/B-adrenoceptors (n = 10); and (E and F) clonidine, a peripheral α2-adrenoceptor agonist (n = 5), in human distal internal mammary arteries in the absence (pH 7.40) and presence (pH 6.80) of severe extracellular acidosis. Contraction expressed in g (A, C, and E) and percentage of the maximal contraction induced by 90 mM KCl under standard conditions (pH 7.40; B, D, and F). Acidosis sensitized human arterial rings to methoxamine but did not significantly alter the arterial responsiveness to phenylephrine and clonidine. Data presented as mean ± standard deviation. Each experiment served as its own control. *P < .05, **P < .001, acidosis vs standard condition (pH 7.40). The Journal of Thoracic and Cardiovascular Surgery 2014 147, 1698-1705DOI: (10.1016/j.jtcvs.2013.11.013) Copyright © 2014 The American Association for Thoracic Surgery Terms and Conditions