Inhibitors of ischemic preconditioning do not attenuate Na+/H+ exchange inhibitor mediated cardioprotection. J Cardiovasc Pharmacol 2000 Jun;35(6):949-53
Date
06/03/2000Pubmed ID
10836732DOI
10.1097/00005344-200006000-00019Scopus ID
2-s2.0-0034079168 (requires institutional sign-in at Scopus site) 21 CitationsAbstract
Pharmacologic inhibition of the K(ATP) channel with sulfonylureas or the adenosine receptor with methylxanthines has been shown to attenuate ischemic preconditioning (IPC). Both classes of compounds are widely used clinically, and several reports have demonstrated adverse outcomes in patients taking sulfonylureas. Recently inhibition of the sodium/hydrogen exchanger isozyme-1 (NHE-1) has been shown to be equal to IPC at providing myocardial protection in dogs and may be an alternative to IPC in patients taking sulfonylureas or methylxanthines. However, no experiments have examined the pharmacologic overlap between IPC and NHE-1 inhibitor-mediated cardioprotection in dogs. With an in vivo canine infarct model in which the left anterior descending coronary artery was occluded for 60 min and reperfused for 3 h, neither the K(ATP) channel antagonist glibenclamide nor the adenosine-receptor antagonist PD 115199 attenuated NHE-1 inhibitor-mediated reduction in infarct size expressed as a percentage of the area at risk produced by EMD 85131 (Control, 24.2 +/- 3.6%; EMD 85131, 6.4 +/- 2.3%; PD 115199 + EMD 85131, 6.6 +/- 2.4%; glibenclamide + EMD 85131, 3.5 +/- 1.2%). NHE-1 inhibition and IPC do not overlap pharmacologically, and NHE-1 inhibition may be an alternative for cardioprotection in patients taking sulfonylureas or methylxanthines.
Author List
Gumina RJ, Beier N, Schelling P, Gross GJMESH terms used to index this publication - Major topics in bold
AnimalsBenzamides
Dogs
Female
Glyburide
Hemodynamics
Hypoglycemic Agents
Ischemic Preconditioning
Male
Myocardial Infarction
Myocardial Reperfusion Injury
Purines
Pyrroles
Sodium-Hydrogen Exchangers
Sulfonamides
