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Inhibition of human internal mammary artery contractions. An in vitro study of vasodilators
G K Jett1, R A Guyton, C R Hatcher
1Department of Cardiothoracic Surgery, Carlyle Fraser Heart Center, Crawford W. Long Memorial Hospital, Emory University, Atlanta, Ga.
Insights
Vasospasm limits internal mammary artery grafts. Nifedipine and papaverine effectively inhibited arterial contraction, with papaverine showing the greatest maximal inhibition for myocardial revascularization bypass grafts.
Area of Science:
- Cardiovascular Surgery
- Pharmacology
- Vascular Biology
Background:
- The internal mammary artery is the preferred conduit for myocardial revascularization.
- Perioperative vasospasm can limit its effectiveness as a bypass graft.
Purpose of the Study:
- To investigate the efficacy of various vasodilators in inhibiting internal mammary artery contraction.
- To determine the potency and maximal inhibition of different vasodilators on human internal mammary artery segments.
Main Methods:
- Discarded human internal mammary artery segments were used for in vitro isometric tension measurements.
- Arterial contraction was induced using high potassium concentration or norepinephrine.
- Inhibition of contraction by vasodilators including nifedipine, verapamil, nitroprusside, and papaverine was measured.
Main Results:
- Nifedipine was the most potent vasodilator for both potassium- and norepinephrine-induced contractions.
- Papaverine demonstrated the greatest maximal inhibition of contractions.
- Nitroprusside showed moderate inhibition, while nitroglycerin, isoproterenol, and adenosine had minimal effect.
Conclusions:
- Nifedipine and papaverine are effective in inhibiting internal mammary artery vasospasm.
- Papaverine offers the greatest potential for maximal vasodilation in internal mammary artery grafts.
- These findings may help optimize vasodilator use to prevent graft failure.
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.