1. 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 (June 2002)
DOI: /mtc
Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

2. 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  , DOI: ( /mtc )
Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

3. 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  , DOI: ( /mtc )
Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions