Urotensin II (UII) was first isolated from the marine Goby fish and subsequently found active in the mammalian cardiovascular system. UII interaction with its receptor UT is pseudo-irreversible suggesting that alterations in UT expression may be an important determinant of functionality. More recently UII has been implicated in diseases such as diabetes, renal dysfunction and in particular heart failure. Indeed there is evidence of upregulation of UII and possibly UT in heart failure.\ud Data from 40 elective coronary artery bypass surgery patients are presented. Ejection fraction (EF) was assessed using pre-operative trans-thoracic echocardiography and ventriculography. Intra-operative trans-oesophageal echocardiography (TOE) was performed in 22 cases. The following questions have been addressed;\ud 1. Using quantitative polymerase chain reaction (Q-PCR) is there a relationship between myocardial or aortic UT and plasma UII and left ventricular systolic function?\ud 2. Is there any relationship between atrial and aortic UT expression?\ud 3. Is there a relationship between myocardial or aortic UT and plasma UII and preoperative\ud New York Heart Association Grade of Dyspnoea (NYHA) or Canadian Cardiovascular Society Angina Severity (CCSA) score? According to pre-operative EF (Normal>50%, Moderate 30-50% and Poor<30%) right atrial and thoracic aortic UT expression was similar in patients with normal, moderate and poor systolic function. Using intra-operative TOE (mid-oesophageal 2-chamber view) there was an inverse relationship between right atrial UT and EF. Mean plasma UII was elevated compared with healthy (historical) controls. No significant correlation was detected between right atrial and thoracic aortic UT. Right atrial and thoracic aortic UT was similar in patients with increasing dypsnoea (NYHA) and angina (CCSA) severity.\ud This is the first study to simultaneously measure UT, UII and cardiovascular function in pre-bypass patients. Collectively these data suggest that UT is not globally up-regulated and may even be down-regulated within the right atrium of patients with systolic left ventricular dysfunction
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