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National Institute of Environmental Health Sciences

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Publication Detail

Title: Vasoconstrictor potential of coronary aspirate from patients undergoing stenting of saphenous vein aortocoronary bypass grafts and its pharmacological attenuation.

Authors: Kleinbongard, Petra; Bose, Dirk; Baars, Theodor; Mohlenkamp, Stefan; Konorza, Thomas; Schoner, Sandra; Elter-Schulz, Miriam; Eggebrecht, Holger; Degen, Hubertus; Haude, Michael; Levkau, Bodo; Schulz, Rainer; Erbel, Raimund; Heusch, Gerd

Published In Circ Res, (2011 Feb 4)

Abstract: Stent implantation into atherosclerotic plaques releases, apart from particulate debris, soluble substances that contribute to impaired microvascular perfusion. Objective: To quantify the release of vasoconstrictors and to determine the efficacy of coronary dilators to attenuate their action.Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stenting in 22 patients with severe saphenous vein aorto-coronary bypass stenoses. The release of catecholamines, endothelin, serotonin, thromboxane B(2), and tumor necrosis factor (TNF)ýý was measured. The response of rat mesenteric arteries with intact (+E) and denuded (-E) endothelium to aspirate plasma was normalized to that by KCl. Responses to selective receptor blockade, adenosine, nitroprusside, and verapamil against the aspirate-induced constriction were determined. The coronary arterial plasma withdrawn before stenting induced 21ýý5% and the aspirate plasma after stenting induced 95ýý8% of maximum KCl-induced vasoconstriction. Serotonin, thromboxane B(2), and TNFýý release into aspirate plasma increased by 1.9ýý0.2 ýýmol/L, 25.6ýý3.1 pg/mL, and 19.7ýý6.1 pg/mL, respectively, during stenting. The aspirate-induced vasoconstriction was largely antagonized by selective serotonin receptor blockade, with little further antagonism by additional thromboxane receptor blockade. TNFýý did not induce constriction per se but potentiated the constriction with serotonin and the thromboxane-analog U-46619 in arteries +E. The concentrations to induce half-maximal vasodilation were comparable for nitroprusside (+E, 3.3ýý10(-8); -E, 1.9ýý10(-8) mol/L) and verapamil (+E, 8.3ýý10(-8); -E, 7.8ýý10(-8) mol/L), and the vasoconstriction was eventually eliminated. The vasodilator response to adenosine was dependent on functional endothelium and weaker.Serotonin is the main coronary vasoconstrictor after stenting, and thromboxane and TNFýý somewhat potentiate the serotonin response. Nitroprusside and verapamil are more potent than adenosine to attenuate the aspirate plasma-induced vasoconstriction, and they are not dependent on functional endothelium.

PubMed ID: 21183739 Exiting the NIEHS site

MeSH Terms: Adenosine/pharmacology; Aged; Animals; Coronary Artery Bypass*; Endothelins/pharmacology*; Female; Humans; Male; Mesenteric Arteries/drug effects*; Mesenteric Arteries/physiopathology; Middle Aged; Models, Animal; Nitroprusside/pharmacology; Rats; Rats, Inbred Lew; Saphenous Vein/transplantation*; Serotonin/pharmacology; Stents*; Thromboxane B2/pharmacology; Tumor Necrosis Factor-alpha/pharmacology; Vasodilation/drug effects*; Vasodilation/physiology; Vasodilator Agents/pharmacology*; Verapamil/pharmacology

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