title: Inhibition of human internal mammary artery contractions. An in vitro study of vasodilators.
abstract: The internal mammary artery is currently the preferred conduit for myocardial revascularization; however, perioperative vasospasm of the internal mammary artery may limit its use as a bypass graft. The ability of various vasodilators to inhibit internal mammary artery contraction was investigated with the use of discarded segments of human internal mammary artery not used in coronary artery bypass grafting. Ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 degrees C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated by elevating the extracellular potassium concentration to 70 mmol/L or by exposure to a 10 mumol/L concentration of norepinephrine, and inhibition of contraction by vasodilators was measured. The order of potency to inhibit potassium-induced contraction was as follows: nifedipine > verapamil > nitroprusside > papaverine. At maximal effective doses, nifedipine, verapamil, and papaverine almost completely inhibited potassium-induced contraction, whereas nitroprusside inhibited contraction by only 55%. When norepinephrine was used to contract the arteries, a biphasic relaxation curve was seen with nifedipine, but not with other vasodilator drugs. The order of potency to inhibit norepinephrine-induced contraction was as follows: nifedipine > nitroprusside > verapamil > papaverine. Maximal inhibition of norepinephrine contraction by these vasodilators ranged from 68% to 95%. Nitroglycerin, isoproterenol, and adenosine produced little or no inhibition of internal mammary artery contraction caused by potassium or norepinephrine. Although nifedipine was the most potent vasodilator, papaverine produced the greatest maximal inhibition of both potassium- and norepinephrine-induced contraction of human internal mammary artery.
authors.affiliation: Department of Cardiothoracic Surgery, Carlyle Fraser Heart Center, Crawford W. Long Memorial Hospital, Emory University, Atlanta, Ga.
authors.forename: G K
authors.initials: GK
authors.lastname: Jett
authors.forename: R A
authors.initials: RA
authors.lastname: Guyton
authors.forename: C R
authors.initials: CR
authors.lastname: Hatcher
authors.forename: P W
authors.initials: PW
authors.lastname: Abel
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D008323:Mammary Arteries / Q000187:drug effects / Q000502:physiology*; D009119:Muscle Contraction / Q000187:drug effects*; D009543:Nifedipine / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology*; D014700:Verapamil / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D014700:Verapamil; D005996:Nitroglycerin; D009543:Nifedipine; D000241:Adenosine; D007545:Isoproterenol; D011188:Potassium; D009638:Norepinephrine