Vasodilator drug effects on internal mammary artery and saphenous vein grafts

G. Kimble Jett, Joseph M. Arcici, Charles R. Hatcher, Peter W. Abel, Robert A. Guyton

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15 Scopus citations

Abstract

The internal mammary artery is a dynamic conduit used for myocardial revascularization in which potential exists for spasm as well as for vasodilation. This study investigated vasodilator drug effects on the mammary artery using nitroprusside and nitroglycerin in vitro to measure the inhibition of contraction of human internal mammary artery and in vivo to examine blood flow through a canine mammary artery. In the in vitro study, ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 °C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated with 70 mM potassium and 10 μM norepinephrine, and inhibition of contraction by vasodilators was measured. Nitroprusside was more potent and effective than was nitroglycerin in inhibiting potassium and norepinephrine contraction. The in vivo study utilized a canine (n = 8) right heart bypass preparation that allowed precise control of cardiac output, blood pressure and heart rate, which were maintained constant. The internal mammary artery graft and the saphenous vein graft perfused the same coronary artery bed. Electromagnetic flow probes measured graft flow (with the other graft occluded) before and after 15 min of drug infusion (1 μg/kg per min). Nitroglycerin significantly increased mammary artery flow 36 ± 13%, whereas nitroprusside significantly decreased it 12 ± 2%. Saphenous vein grafts responded differently; graft blood flow decreased with nitroglycerin and increased with nitroprusside. Thus, although nitroprusside was more effective than nitroglycerin in inhibiting mammary artery contraction in vitro, it decreased internal mammary artery graft flow measured in vivo. Nitroglycerin had the opposite effect, increasing mammary graft flow. In addition, saphenous vein grafts responded differently from the mammary artery to vasodilator administration. These divergent findings in the in vivo canine and in vitro human studies may have resulted from the effects of the vasodilators on the regional vasculature. However, the in vivo response in canine vessels may not necessarily predict the in vivo response of human vessels to vasodilators.

Original languageEnglish (US)
Pages (from-to)1317-1324
Number of pages8
JournalJournal of the American College of Cardiology
Volume11
Issue number6
DOIs
StatePublished - Jun 1988

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

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