Endothelin-1 and myocardial preconditioning - 11/09/11
Reprint requests: Carlos E. Velasco, MD, Baylor University Medical Center, Wadley Tower, Suite 851, 3600 Gaston Ave., Dallas, TX 75246.Abstract |
This study attempted to define the role of endothelin (ET) in preconditioning. We previously showed that ET is produced during myocardial ischemia and reperfusion. Because both preconditioning and ET act through protein kinase C, ET could play a role in preconditioning. Dogs were randomized to three groups subjected to 40 minutes of ischemia, with (groups A and B) or without (group C) preconditioning, followed by 4 hours of reperfusion. Groups A and C received saline infusions; group B received continuous infusions of the ETA-selective antagonist FR139317. Both preconditioned groups had smaller infarct sizes (group A, 7.9% ± 2.5%; group B, 8.4% ± 2.6%) than the nonpreconditioned group (group C, 16.2% ± 3.3%). Administration of the ETA antagonist FR139317 did not alter infarct size. This study demonstrated that ETA-receptor blockade did not alter infarct size in preconditioned animals and suggests that endothelin does not play a significant role in this process.
Le texte complet de cet article est disponible en PDF. | Supported by a Grant-in-Aid from the American Heart Association, Texas Affiliate, Inc. (94R-132). |
Vol 132 - N° 1P1
P. 84-90 - juillet 1996 Retour au numéro
Article précédent
- Ventricular premature beat—driven intermittent restoration of coronary blood flow reduces the incidence of reperfusion-induced ventricular fibrillation in a cat model of regional ischemia
- Heung Sik Na, Yang In Kim, Young Wook Yoon, Hee Chul Han, Sook Hyun Nahm, Seung Kil Hong
- l-Arginine decreases infarct size in rats exposed to environmental tobacco smoke
- Bo-qing Zhu, Yi-ping Sun, Richard E. Sievers, Jonathan L. Shuman, Stanton A. Glantz, Kanu Chatterjee, William W. Parmley, Christopher L. Wolfe
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