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Myocardial Effects of Sodium-Hydrogen Exchange Inhibition during Resuscitation from Ventricular Fibrillation

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Myocardial Ischemia and Preconditioning

Part of the book series: Progress in Experimental Cardiology ((PREC,volume 6))

Summary

Multiple mechanisms of cell injury are unleashed during the global myocardial ischemia of cardiac arrest, and are in part responsible for the development of myocardial abnormalities that can compromise efforts to restore cardiac activity. Among these mechanisms, activation of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) with subsequent intramyocardial sodium overload has been identified as a prominent mechanism of cell injury. Using isolated heart and intact animal models of ventricular fibrillation, our group has identified various beneficial myocardial effects associated with selective NHE-1 inhibition. During ventricular fibrillation, NHE-1 inhibition attenuates the development of ischemic contracture and preserves the hemodynamic efficacy of chest compression. Immediately after restoration of cardiac activity, NHE-1 inhibition markedly reduces reperfusion arrhythmias and prevents episodes of recurrent ventricular fibrillation. During the post-resuscitation phase, NHE-1 inhibition ameliorates the severity of myocardial systolic and diastolic dysfunction and favors hemodynamic stability and improved survival. These studies suggest that NHE-1 inhibition may represent a highly effective new form of treatment for resuscitation from cardiac arrest.

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Correspondence to Raúl J. Gazmuri MD, PhD. .

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Gazmuri, R.J., Ayoub, I.M. (2003). Myocardial Effects of Sodium-Hydrogen Exchange Inhibition during Resuscitation from Ventricular Fibrillation. In: Dhalla, N.S., Takeda, N., Singh, M., Lukas, A. (eds) Myocardial Ischemia and Preconditioning. Progress in Experimental Cardiology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0355-2_26

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