Hyperglycemia exaggerates ischemia-reperfusion–induced cardiomyocyte injury: Reversal with endothelin antagonism Subodh Verma, MD, PhD, Andrew Maitland, MD, Richard D. Weisel, MD, Shu-Hong Li, MSc, Paul W.M. Fedak, MD, Neil C. Pomroy, 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 1120-1124 (June 2002) DOI: 10.1067/mtc.2002.121973 Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions
Fig. 1 Cellular injury (assessed by means of trypan blue uptake) in human ventricular heart cells subjected to simulated ischemia-reperfusion. Cells subjected to 48 hours of hyperglycemia exhibited increased cellular damage. This response was prevented by BQ-123 (an ETA antagonist) and bosentan (an ETA/B antagonist). *P =.01 versus normoglycemic group and hyperglycemic group plus BQ-123 and hyperglycemic group plus bosentan. The Journal of Thoracic and Cardiovascular Surgery 2002 123, 1120-1124DOI: (10.1067/mtc.2002.121973) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions
Fig. 2 Effects of normoglycemia versus hyperglycemia on human heart cell ET-1 production. Hyperglycemic heart cells elaborate more ET-1 after ischemia-reperfusion when compared with those in the normoglycemic group. *P =.02 versus normoglycemic group. The Journal of Thoracic and Cardiovascular Surgery 2002 123, 1120-1124DOI: (10.1067/mtc.2002.121973) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions