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J Thorac Cardiovasc Surg 2003;125:30-31
© 2003 The American Association for Thoracic Surgery

Editorials

Attenuation of postischemic myocardial injury by cariporide

From the Cardiovascular Research Center, University of Connecticut, School of Medicine, Farmington, Conn.

Received for publication April 18, 2002. Accepted for publication May 10, 2002. Address for reprints: Dipak K. Das, PhD, Professor and Director, Cardiovascular Research Center, University of Connecticut, School of Medicine, Farmington, CT 06030-1110 (E-mail: ddas@neuron.uchc.edu).

The first 20% of the full text of this article appears below.

See related article on page 155.

Recent evidence supports the sodium-hydrogen antiport system as an important player in the pathophysiology of myocardial ischemia-reperfusion injury. ^1-3 Accumulation of hydrogen ions in the myocyte cytosol during ischemia creates a proton gradient that promotes the efflux of hydrogen ions in exchange for the influx of sodium ions. This hydrogen ion-driven process may be self-limiting during ischemia because the hydrogen ion gradient is blunted by the accumulation of H⁺ in the interstitial (extracellular) compartment, and extracellular acidosis and accumulation of acid products attenuates activity of the exchanger. ³ However, reactivation of the antiport mechanism during early reperfusion leads to a reactivation of the exchange system. The buildup of intracellular sodium secondarily activates the Na⁺-Ca²⁺ exchange mechanism to operate in the reverse mode, resulting in a net calcium accumulation. The intracellular Ca²⁺ accumulation is thought to be the event that leads to dysfunction and cell death. Therefore, re-alkalinization of intracellular pH by the sodium-hydrogen exchange system and subsequent reversal of the sodium-calcium exchange system favoring net calcium accumulation work in concert to cause cell injury during ischemia and/or reperfusion.

Inhibition of the sodium-hydrogen exchange mechanism during ischemia (ie, . . . [Full Text of this Article]

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Blood cardioplegia supplementation with the sodium-hydrogen ion exchange inhibitor cariporide to attenuate infarct size and coronary artery endothelial dysfunction after severe regional ischemia in a canine model

Satoshi Muraki, Cullen D. Morris, Jason M. Budde, Zhi-Qing Zhao, Robert A. Guyton, and Jakob Vinten-Johansen
J. Thorac. Cardiovasc. Surg. 2003 125: 155-164. [Abstract] [Full Text] [PDF]

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