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  • Title: Postoperative hemodynamics depend on cardiopulmonary bypass temperature: the potential role of endothelin-1.
    Author: Tönz M, Mihaljevic T, von Segesser LK, Shaw S, Lüscher TF, Turina M.
    Journal: Eur J Cardiothorac Surg; 1997 Jan; 11(1):157-61. PubMed ID: 9030805.
    Abstract:
    OBJECTIVE: There is a growing body of evidence that perfusion temperature during cardiopulmonary bypass (CPB) influences postoperative systemic vascular resistance (SVR). The reason for this is not clear. Extracorporeal circulation can provoke raised plasma levels of endothelin-1 (ET-1), a very potent vasoconstrictor peptide produced by endothelial cells. We therefore analysed the effect of CPB temperature on postoperative vascular resistance and plasma concentrations of ET-1. METHODS: Thirty four patients undergoing elective coronary artery bypass grafting procedures were randomly assigned for either normothermic (37 degrees C, n = 17) or hypothermic CPB (28 degrees C, n = 17). Serial measurements of SVR and plasma ET-1 concentrations were performed before, during, and until 9 h after CPB measured. RESULTS: As a consequence of CPB, plasma ET-1 levels increased slightly in both groups. In normothermic patients, ET-1 reached maximal levels at the end of CPB whereas ET-1 levels in patients after hypothermic CPB had a tendency to further increase during the stay in the intensive care unit. Plasma ET-1 levels were significantly higher in patients 9 h postoperatively after hypothermic CPB (1.94 +/- 0.28 vs. 1.30 +/- 0.12 pg/ml, P = 0.033), which was associated with significantly higher systemic vascular resistance index (SVRI) in these patients (area under the curve; 1978 +/- 76 vs. 1626 +/- 69 dyne s/cm5 per m2, P = 0.003). Plasma ET-1 levels showed a positive correlation with postoperative SVRI (P = 0.008, r = 0.51) and a negative correlation with minimal rectal temperature during CPB (P = 0.006, r = 0.55). CONCLUSIONS: These results suggests that the hemodynamic differences after normothermic and hypothermic CPB might be mediated, at least in part, by temperature dependent changes in ET-1 plasma levels.
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