Supplemental nitric oxide and its effect on myocardial injury and function in patients undergoing cardiac surgery with extracorporeal circulation Jacopo.

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Presentation transcript:

Supplemental nitric oxide and its effect on myocardial injury and function in patients undergoing cardiac surgery with extracorporeal circulation Jacopo Gianetti, MD, PhD, Paolo Del Sarto, MD, Stefano Bevilacqua, MD, Cristina Vassalle, BSc, Rossella De Filippis, BSc, Mirsad Kacila, MD, Pier Andrea Farneti, MD, Aldo Clerico, MD, Mattia Glauber, MD, Andrea Biagini, MD The Journal of Thoracic and Cardiovascular Surgery Volume 127, Issue 1, Pages 44-50 (January 2004) DOI: 10.1016/j.jtcvs.2002.08.001

Figure 1 Results of colorimetric assay for NO by-products (NO−2 and NO−3) on blood samples peripherally drawn at prefixed perioperative intervals: T1, prethoracotomy; T2, 5 minutes after aortic clamping; T3, 5 minutes after aortic unclamping; T4, 24 hours after surgery. Data shown are mean ± SEM for patients who received NO (lighter blocks) and for controls (darker blocks). *P < .05. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)

Figure 2 Analysis of myocardial injury determined in CPB patients by measurements of the release of total CK (A) and CK-MB (C) and by measurements of the cumulative release (AUC) of total CK (B) and CK-MB (D) over 48 hours postsurgery. Data shown are mean ± SEM for patients who received NO (lighter blocks) and for controls (darker blocks). *P < .05. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)

Figure 3 Analysis of myocardial injury determined in CPB patients by measurements of the release of total troponin I over 48 hours postsurgery. Data shown are mean ± SEM for patients who received NO (lighter blocks) and for controls (darker blocks). *P < .05. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)

Figure 4 Analysis of early endothelial activation in CPB patients by measurements of soluble P-selectin in blood samples taken from coronary sinus before and 5 minutes after the end of aortic clamping (A). Gradient of soluble P-selectin between pre–/post–aortic clamping in both patients groups are illustrated (B). Data shown are mean ± SEM for P-selectin measurements for patients who received NO (lighter blocks) and for controls (darker blocks). *P < .05. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)

Figure 5 BNP release in blood samples peripherally drawn at prefixed perioperative intervals: T1, prethoracotomy; T2, 5 minutes after aortic clamping; T3, 5 minutes after aortic unclamping; T4, 5 minutes after extracorporeal circulation; T5, 6 hours after surgery; T6, 24 hours after surgery. To normalize the basal values, we report the gradient of BNP release as measured by the percent of the ratio between the levels at each time (T2-T6) compared with T1. Data shown are mean ± SEM for patients who received NO (lighter blocks) and for controls (darker blocks). *P < .05. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)

Figure 6 Simple regression analysis relating the extent of myocardial injury as detected by the AUC of CK-MB to the gradient of soluble P-selectin before/after aortic clamping. The Journal of Thoracic and Cardiovascular Surgery 2004 127, 44-50DOI: (10.1016/j.jtcvs.2002.08.001)