Improved cardiac function after prolonged hypothermic ischemia with the Na+/H+ exchange inhibitor HOE 694
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Cited by (55)
Exploration of the optimal dose of HOE-642 for the protection of neuronal mitochondrial function after cardiac arrest in rats
2019, Biomedicine and PharmacotherapyCitation Excerpt :Na+/H+ exchanger isoform 1 (NHE1) is a plasma membrane protein that is present in all eukaryotic cells and plays a central role in the regulation of intracellular pH and cell volume by exchanging intracellular H+ with extracellular Na+ [5]. Inhibition of NHE has been shown to provide significant protection in a variety of models of myocardial ischemia-reperfusion, with consistent improvements in functional recovery, metabolic status, attenuation of arrhythmias, preservation of cellular ultrastructure and inhibition of apoptosis [6–11]. HOE-642, a selective NHE1 inhibitor, has demonstrated beneficial effects in patients with acute coronary syndromes [12].
Cardio-protective Signalling by Glyceryl Trinitrate and Cariporide in a Model of Donor Heart Preservation
2015, Heart Lung and CirculationCitation Excerpt :Short non-lethal cycles of ischaemia and reperfusion or pharmacological agents mimicking these physiological strategies that are applied before (pre-conditioning), during (per-conditioning) or after (post-conditioning) an index period of ischaemia produce significant functional improvement during subsequent reperfusion [7]. Experimental studies indicate that such protective strategies initially employed against myocardial infarction are also effective in models of donor heart preservation and transplantation [8,9]. Previous work from our laboratory has shown that ischaemic preconditioning or the presence of pharmacological agents such as nitric oxide donors (diazenium diolates or glyceryl-trinitrate (GTN)), KATP channel openers or the sodium hydrogen exchange inhibitor cariporide at cardioplegia and during hypothermic storage significantly improved post-storage cardiac function in an isolated working rat heart model of donor heart preservation [10–12].
Involvement of Na<sup>+</sup>/H<sup>+</sup> exchanger in hypoxia/re-oxygenation-induced neonatal rat cardiomyocyte apoptosis
2004, European Journal of PharmacologySodium-hydrogen inhibitor cariporide (HOE 642) improves in situ protection of hearts from non-heart-beating donors
2003, Journal of Heart and Lung TransplantationOptimal Dose and Mode of Delivery of Na<sup>+</sup>/H<sup>+</sup> Exchange-1 Inhibitor Are Critical for Reducing Postsurgical Ischemia- Reperfusion Injury
2003, Annals of Thoracic SurgeryCitation Excerpt :In the control group, there was a significantly greater relaxation response in the left circumflex coronary artery compared with the ischemic-reperfused LAD (p = 0.03). Inhibition of NHE1 during the period of cardioplegic arrest has been shown to improve postischemic recovery of LV function in isolated Langendorff preparations of the rat and rabbit [27–29]. In dogs, NHE 1 inhibitor in crystalloid cardioplegia decreases myocardial edema and preserves preload-recruitable stroke work after CPB in normal hearts [30, 31].
This study was supported by the Heart and Stroke Foundation of Ontario (HSFO grant A2400) and the Medical Research Council of Canada (grant MT-10284).