1. Preconditioning protects the severely atherosclerotic mouse heart
Guohu Li, MD, Shinichi Tokuno, MD, Peeter Tähepôld, MD, Jarle Vaage, MD, PhD, Christian Löwbeer, MD, Guro Valen, MD, PhD 
The Annals of Thoracic Surgery 
Volume 71, Issue 4, Pages (April 2001)
DOI: /S (00)

2. Fig 1
(A) Transverse section of the aortic root of an Apolipoprotein E/LDL receptor double knockout mouse after being fed a diet containing 21% fat and 0.15% cholesterol for 6 months. The section is stained with Oil Red-O and counterstained with hematoxylin. Note the massive fibrofatty lesions of the aortic wall and in the right coronary artery (arrow). (Original magnification, ×200.) (B) A representative section from the middle area of the heart after 8 months on the diet. The cavity of the right ventricle with surrounding wall and septum is depicted. Note multiple lipid deposits in branches of coronary vessels (arrows). (Original magnification, ×200.) (C) Oil Red-O staining of a section from the apex region of the heart taken from an animal after 6 months on the atherogenic diet shows a coronary artery with lipid deposits caught longitudinally. (Original magnification, ×400.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

3. Fig 2
(A, B) Left ventricular developed pressure (LVDP) in Langendorff-perfused hearts of C57BL/6 and Apolipoprotein E/LDL receptor double knockout mice (ApoE/LDLr−/−) subjected to 40 minutes of global ischemia and 60 minutes reperfusion after two cycles of 2 minutes ischemia and 5 minutes reperfusion (IPC) and compared to ischemic controls (C). Additional atherosclerotic animals were exposed to 60 minutes of hyperoxia (>98% O2) prior to heart isolation and global ischemia (HPC). Values are mean ± standard error of mean of 7 to 10 animals per group. (BIPC = before ischemic preconditioning; BI = before ischemia; ∗ denotes p < ; # denotes p < in comparison of preconditioned versus ischemic control; a denotes p < when comparing C57BL/6 to ApoE/LDLr−/− ischemic controls.) (B, C) Left ventricular end-diastolic pressure (LVEDP) in the same hearts as above. (∗ denotes p < in comparison between preconditioned and control hearts; b denotes p < when comparing ApoE/LDLr−/− versus C57BL/6 controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

4. Fig 3
(A, B) Maximum positive and negative first derivative of pressure (max dP/dt and n dP/dt) in Langendorff-perfused hearts of C57BL/6 and Apolipoprotein E/LDL receptor double knockout mice (ApoE/LDLr−/−) subjected to 40 minutes global ischemia and 60 minutes reperfusion after two cycles of 2 minutes ischemia and 5 minutes reperfusion (IPC) and compared to ischemic controls (C). Additional atherosclerotic animals were exposed to 60 minutes hyperoxia (>98% O2) prior to heart isolation and global ischemia (HPC). Coronary flow is corrected for differences in heart weight as described in the Material and Methods section. Values are mean ± standard error of mean of 7 to 10 animals per group. (BIPC = before ischemic preconditioning; BI = before ischemia; ∗ denotes p < ; # denotes p < in comparison of preconditioned versus ischemic controls; d denotes p < 0.003; e denotes p < when comparing C57BL/6 to ApoE/LDLr−/− ischemic controls.) (C, D) Coronary flow (CF) in the hearts shown above. (∗ Denotes p < in comparison of preconditioned versus ischemic controls; c denotes p < when comparing C57BL/6 to ApoE/LDLr−/− ischemic controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

5. Fig 4
(A) A representative transverse section of triphenyl tetrazolium chloride stained heart from the groups shown in panel B. (B) Percentage of necrotic tissue after 60 minutes reperfusion of Langendorff-perfused hearts subjected to 40 minutes global ischemia and TTC-stained. The hearts shown are as in the x-axis on 4C: C57BL/6 ischemic control (C, C57); C57BL/6 preconditioned with two cycles of 2 minutes ischemia and 5 minutes reperfusion before sustained ischemia (IPC, C57); ischemic control of an apolipoprotein E/LDL receptor double knockout mouse after 6 months on atherogenic diet (C, ApoE); ischemic preconditioned ApoE (IPC, ApoE); and a heart of ApoE mouse subjected to 60 minutes hyperoxia prior to heart isolation and global ischemia (HPC, ApoE). Values are mean ± standard error of mean of n = 7 to 10 in each group. (∗ IPC versus C, p < 0.04; # IPC versus C, p < 0.03; § HPC versus C, p < 0.001; denotes p < when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.) (C) Release of cardiac troponin T (ΔTnT) shown as the difference between release after 30 minutes of reperfusion and release at end of stabilization (mean ± standard error of mean of 7 to 10 animals in each group). (∗ IPC, C57 versus C, C57, p < 0.05; # IPC, ApoE versus C, ApoE, p < 0.04; § HPC, ApoE versus C, C ApoE, p < 0.03; denotes p < 0.02 when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

6. Fig 4
(A) A representative transverse section of triphenyl tetrazolium chloride stained heart from the groups shown in panel B. (B) Percentage of necrotic tissue after 60 minutes reperfusion of Langendorff-perfused hearts subjected to 40 minutes global ischemia and TTC-stained. The hearts shown are as in the x-axis on 4C: C57BL/6 ischemic control (C, C57); C57BL/6 preconditioned with two cycles of 2 minutes ischemia and 5 minutes reperfusion before sustained ischemia (IPC, C57); ischemic control of an apolipoprotein E/LDL receptor double knockout mouse after 6 months on atherogenic diet (C, ApoE); ischemic preconditioned ApoE (IPC, ApoE); and a heart of ApoE mouse subjected to 60 minutes hyperoxia prior to heart isolation and global ischemia (HPC, ApoE). Values are mean ± standard error of mean of n = 7 to 10 in each group. (∗ IPC versus C, p < 0.04; # IPC versus C, p < 0.03; § HPC versus C, p < 0.001; denotes p < when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.) (C) Release of cardiac troponin T (ΔTnT) shown as the difference between release after 30 minutes of reperfusion and release at end of stabilization (mean ± standard error of mean of 7 to 10 animals in each group). (∗ IPC, C57 versus C, C57, p < 0.05; # IPC, ApoE versus C, ApoE, p < 0.04; § HPC, ApoE versus C, C ApoE, p < 0.03; denotes p < 0.02 when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

7. Fig 4
(A) A representative transverse section of triphenyl tetrazolium chloride stained heart from the groups shown in panel B. (B) Percentage of necrotic tissue after 60 minutes reperfusion of Langendorff-perfused hearts subjected to 40 minutes global ischemia and TTC-stained. The hearts shown are as in the x-axis on 4C: C57BL/6 ischemic control (C, C57); C57BL/6 preconditioned with two cycles of 2 minutes ischemia and 5 minutes reperfusion before sustained ischemia (IPC, C57); ischemic control of an apolipoprotein E/LDL receptor double knockout mouse after 6 months on atherogenic diet (C, ApoE); ischemic preconditioned ApoE (IPC, ApoE); and a heart of ApoE mouse subjected to 60 minutes hyperoxia prior to heart isolation and global ischemia (HPC, ApoE). Values are mean ± standard error of mean of n = 7 to 10 in each group. (∗ IPC versus C, p < 0.04; # IPC versus C, p < 0.03; § HPC versus C, p < 0.001; denotes p < when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.) (C) Release of cardiac troponin T (ΔTnT) shown as the difference between release after 30 minutes of reperfusion and release at end of stabilization (mean ± standard error of mean of 7 to 10 animals in each group). (∗ IPC, C57 versus C, C57, p < 0.05; # IPC, ApoE versus C, ApoE, p < 0.04; § HPC, ApoE versus C, C ApoE, p < 0.03; denotes p < 0.02 when comparing ApoE/LDLr−/− to C57BL/6 ischemic controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

8. The Annals of Thoracic Surgery 2001 71, 1296-1303DOI: (10
The Annals of Thoracic Surgery  , DOI: ( /S (00) )

9. The Annals of Thoracic Surgery 2001 71, 1296-1303DOI: (10
The Annals of Thoracic Surgery  , DOI: ( /S (00) )