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J Am Coll Cardiol, 2002; 40:155-161
© 2002 by the American College of Cardiology Foundation
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urocortin promotes hemodynamic and bioenergetic recovery and improves cell survival in the isolated rat heart exposed to ischemia/reperfusion

Tiziano M. Scarabelli, MD*,*, Evasio Pasini, MD{dagger}, Anastasis Stephanou, PhD*, Laura Comini, MSc{dagger}, Salvatore Curello, MD{ddagger}, Riccardo Raddino, MD{ddagger}, Roberto Ferrari, MD, PhD{dagger}, Richard Knight, MD, PhD§ and David S. Latchman, PhD, DSc*

* Medical Molecular Biology Unit, Institute of Child Health and Great Ormond Street Hospital, University College London, London, United Kingdom
{dagger} Cardiovascular Pathophysiology Research Centre, S. Maugeri Foundation IRCCS, University of Ferrara, Ferrara, Italy
{ddagger} Cardiology Department, University of Brescia, Brescia, Italy
§ Department of Cystic Fibrosis, National Heart and Lung Institute, Imperial College London, London, United Kingdom



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Figure 1 Effects of urocortin (Ucn) on developed pressure (DP) and diastolic pressure (dP) during ischemia/reperfusion (I/R) in the isolated rat heart. Developed pressure and dP in control heart exposed to I/R are shown in a; changes in DP and dP induced by Ucn given before I, before and after R, and over R alone are reported in b, c and d, respectively. Solid triangle = DP; open square = dP.

 


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Figure 2 (a) Effects of urocortin (Ucn) administered before ischemia (I) (Ucn pre-I), before and after I (Ucn I/reperfusion) (R) and during R only (Ucn R) on the postischemic release of creatine phosphokinase (CPK). Creatine phosphokinase release by control (CTL) hearts subjected to I/R is shown by CTL I/R. (b) Effects of Ucn on adenosine triphosphate (ATP) (Solid bars) and creatine phosphate (open bars) levels at the end of I (end I) and at the end of R (end R) when given before I (Ucn pre-I), before I and during R (Ucn I/R) and only over R (Ucn R). Values for buffer (BS perf) and Ucn perfused (Ucn inf) hearts as well as for non-Ucn-treated hearts exposed to I/R (CTL I/R) are also shown. (c) Numbers of cells positive for cleaved active caspase 3 (C3) (bars) and tissue levels of C3 activity (line) assessed at the end of I/R in hearts perfused with buffer (P), infused with Ucn (P + Ucn), exposed to I/R (control) and treated with Ucn (10–8 M) before I (Ucn pre-I), both before and after I (Ucn I/R) and during R alone (Ucn R). (d) Percentages of TUNEL and cleaved active C3 positive endothelial cells (EC) (open bars and open squares) and cardiomyocytes (CM) (solid bars and open circles) in the various treatment groups. The legend for the individual groups is as described in (2c).

 




 
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