Abstract
Spasm of the internal mammary artery (IMA) may occur in coronary grafting (CABG). We studied the interaction of human urotensin II (hU‐II) and vasodilators (calcium antagonists or glyceryl trinitrate (GTN)) in human IMA segments (n=102, from 46 CABG patients) in myograph (n=6 in each group). hU‐II contracted all IMA. In KCL‐contraction, full (nifedipine:98.9±3.9%) or nearly full (diltiazem:92.7±6.0%) relaxation with 18.6‐fold‐higher potency to nifedipine vs. diltiazem (EC50 −8.01±0.20 vs. −6.74±0.22 logM, p=0.002) and in hU‐II‐contraction, nearly full relaxation (nifedipine: 90.6 ±4.6%; diltiazem: 95.1±2.1%) with 6.2‐fold‐higher potency to nifedipine vs. diltiazem (EC50 −7.25±0.25 vs. −6.46±0.18 logM, p=0.014) were observed. GTN caused nearly full relaxation (95.4±5.8%) but its pretreatment failed to alter, whereas diltiazem and nifedipine pretreatment reduced contraction to hU‐II. Thus, hU‐II is a potent vasoconstrictor in human IMA. Calcium antagonists and GTN relax the contraction caused by hU‐II with different potencies. However, calcium antagonists are more effective in preventing the contraction induced by hU‐II than GTN.Supported by China Nat'l Ministry of Sci. & Tech. 2009DFB30560 & 2010CB529502(973)åTianjin Municipal Sci. & Tech. Commission 09ZCZDSF04200 &10JCYBJC26400å Hong Kong RGC (CUHK4651/07M & CUHK4789/09M); CUHK2041561, and Providence SV Med. Foundation, Portland, OR.
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