TY - JOUR
T1 - Endothelin-1 and myocardial preconditioning
AU - Erikson, J. M.
AU - Velasco, C. E.
N1 - Funding Information:
From the Cardiology Section, Veterans Affairs Medical Center, and Department of Medicine, The University of Texas Southwestern Medical Center at Dallas Supported by a Grant-in~Aid from the American Heart Association, Texas Affiliate, Inc. (94R-132). Received for publication June 13, 1995; accepted Nov. 20, 1995. Reprint requests: Carlos E. Velasco, MD, Baylor University Medical Center, Wadley Tower, Suite 85I, 3600 Gaston Ave., Dallas, TX 75246. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/1/72013
PY - 1996
Y1 - 1996
N2 - 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 ET(A)-selective antagonist FR 139317. 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 ET(A)-receptor blockade did not alter infarct size in preconditioned animals and suggests that endothelin does not play a significant role in this process.
AB - 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 ET(A)-selective antagonist FR 139317. 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 ET(A)-receptor blockade did not alter infarct size in preconditioned animals and suggests that endothelin does not play a significant role in this process.
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U2 - 10.1016/S0002-8703(96)90394-4
DO - 10.1016/S0002-8703(96)90394-4
M3 - Article
C2 - 8701880
AN - SCOPUS:0030006106
SN - 0002-8703
VL - 132
SP - 84
EP - 90
JO - American heart journal
JF - American heart journal
IS - 1 I
ER -