1. Failure of Preconditioning to Improve Postcardioplegia Stunning of Minimally Infarcted Hearts 
Bouchaib Faris, Jacqueline Peynet, Michel Wassef, Alain Bel, Christian Mouas, Micheline Duriez, Philippe Menasché 
The Annals of Thoracic Surgery 
Volume 64, Issue 6, Pages (December 1997)
DOI: /S (97)

2. Fig. 1
Experimental protocol. All hearts (n = 10 per group) were subjected to 60 minutes of hyperkalemic (K+) cardioplegic arrest at 37°C followed by 60 minutes of reperfusion. Before arrest, the hearts were allowed to stabilize for 20 minutes, with no further intervention for controls. In the study groups, ischemic preconditioning (PC) was elicited by either one 5-minute episode of zero-flow ischemia or a shorter similar episode (2 minutes) preceded by a 5-minute administration of the nucleoside transport inhibitor (NTI) draflazine (10−6 mol/L). In these two groups, a 5-minute period of buffer reperfusion was then instituted between the end of the preconditioning intervention and the onset of arrest. (CK = creatine kinase activity; Ino/Ado = inosine to adenosine ratio; TTC = 2,3,5-triphenyltetrazolium chloride.)
The Annals of Thoracic Surgery  , DOI: ( /S (97) )

3. Fig. 2
Effect of ischemic preconditioning (PC), alone or combined with administration of the nucleoside transport inhibitor (NTI) draflazine (10−6 mol/L), on the recovery profile of left ventricular diastolic pressure. For the sake of clarity, errors bar have been omitted. Two-way analysis of variance demonstrated a significant time-related effect (p < ) but no treatment-related effect except at the 5-minute postarrest study point (∗p < 0.03 between the control group and the draflazine + ischemic preconditioning group). Each group consisted of 10 hearts.
The Annals of Thoracic Surgery  , DOI: ( /S (97) )

4. Fig. 3
Effect of ischemic preconditioning (PC), alone or combined with administration of the nucleoside transport inhibitor (NTI) draflazine (10−6 mol/L), on the recovery profile of left ventricular pressure (LV dP/dt). For the sake of clarity, errors bar have been omitted. Two-way analysis of variance demonstrated a significant time-related effect (p < ) but no treatment-related effect except at the 5-minute postarrest study point (∗∗p < 0.01 between the control group and the ischemic preconditioning group; p < between the control group and the draflazine + ischemic preconditioning group). Each group consisted of 10 hearts.
The Annals of Thoracic Surgery  , DOI: ( /S (97) )

5. Fig. 4
Effect of ischemic preconditioning (PC), alone or combined with administration of the nucleoside transport inhibitor (NTI) draflazine (10−6 mol/L), on the extent of myocardial infarction, as assessed by creatine kinase washout during the initial 5 minutes of reperfusion (left), and on infarct size, as determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining after 60 minutes of reperfusion (right). There were no significant differences for these two markers among the three groups (LV = left ventricle.)
The Annals of Thoracic Surgery  , DOI: ( /S (97) )