Increased endothelin-1 production in diabetic patients after cardioplegic arrest and reperfusion impairs coronary vascular reactivity: Reversal by means.

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Increased endothelin-1 production in diabetic patients after cardioplegic arrest and reperfusion impairs coronary vascular reactivity: Reversal by means of endothelin antagonism Subodh Verma, MD, PhD, Andrew Maitland, MD, Richard D. Weisel, MD, Paul W.M. Fedak, MD, Shu-Hong Li, MSc, Donald A.G. Mickle, MD, Ren-Ke Li, MD, PhD, Lawrence Ko, BSc, Vivek Rao, MD, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 123, Issue 6, Pages 1114-1119 (June 2002) DOI: 10.1067/mtc.2002.121972 Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 1 Plasma ET levels at baseline and after 1 and 10 minutes of reperfusion (removal of the aortic crossclamp) in diabetic and case-matched nondiabetic patients. ET-1 levels are similar at baseline; however, after reperfusion, the coronary sinus effluent ET-1 release was higher in the diabetic than in the nondiabetic group. *P =.01 versus the nondiabetic group. MIN R, Minutes of reperfusion. The Journal of Thoracic and Cardiovascular Surgery 2002 123, 1114-1119DOI: (10.1067/mtc.2002.121972) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 2 Percentage decrease in internal diameter (vasoconstriction) in response to 10−10 mol/L ET-1 and the ETA antagonist BQ-123. Atrial microvessels were studied in a pressurized fashion by using videomicroscopy before cardioplegia, and the results 15 minutes after removal of the aortic crossclamp were depicted. ET-1-mediated vasoconstriction was higher in both diabetic (n = 10) and nondiabetic (n = 11) microvessels; however, the vasoconstrictor effects of ET-1 were greater in diabetic arterioles. BQ-123 attenuated the increased constrictor responses to ET-1 in both control and diabetic groups. **P =.01 versus control group; ##P =.02 versus control-reperfusion group; #P =.02 versus control and diabetic groups; *P =.03 versus control-reperfusion and diabetic-reperfusion groups. R, Reperfusion. The Journal of Thoracic and Cardiovascular Surgery 2002 123, 1114-1119DOI: (10.1067/mtc.2002.121972) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 3 Percentage increase in internal diameter (vasodilatation) in response to 10−8 mol/L substance P and the ETA antagonist BQ-123 in arterioles precontracted to 40% to 50% of baseline internal diameter achieved either spontaneously or with additions of U46619. Substance P-mediated vasodilatation was similar at baseline between the control and diabetic groups. The results after reperfusion are depicted. Substance P-mediated responses were attenuated in both the control and diabetic groups, but the relaxation was greater in the diabetic vessels. BQ-123 prevented the decrease in substance P responses in both control and nondiabetic groups. **P =.02 versus control, diabetic, and diabetic-reperfusion groups; #P =.01 versus control, diabetic, and control-reperfusion groups; *P =.01, versus control-reperfusion and diabetic-reperfusion groups. The Journal of Thoracic and Cardiovascular Surgery 2002 123, 1114-1119DOI: (10.1067/mtc.2002.121972) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions