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BioMed Research International
Volume 2013 (2013), Article ID 201614, 10 pages
Research Article

The Cardioprotective Effect of Hypertonic Saline Is Associated with Inhibitory Effect on Macrophage Migration Inhibitory Factor in Sepsis

1Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan
2Department of Pharmacology, Taipei Medical University, Taipei, Taiwan
3Department of Anesthesiology, Catholic Mercy Hospital, Hsinchu, Taiwan
4Department of Physiology & Biophysics, National Defense Medical Center, Taipei, Taiwan
5Department of Nursing, Tzu Chi College of Technology, Hualien, Taiwan
6Department of Nursing, HungKuang University, Taichung, Taiwan
7Department of Pharmacology, National Defense Medical Center, 160 Min-Chuan E. Road, Taipei 114, Taiwan
8Division of Cardiology, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
9Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Chi-Mei Medical Center, 901 Chung Hwa Road, Tainan 710, Taiwan
10Chia Nan University of Pharmacy & Science, Tainan, Taiwan

Received 2 October 2013; Accepted 8 November 2013

Academic Editor: Joen-Rong Sheu

Copyright © 2013 Yi-Li Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sepsis can cause myocardial dysfunction, which contributes to the high mortality of sepsis. Hypertonic saline (HS) has been reported to increase myocardial contractility in sepsis. In the present study, mechanisms of action of HS resuscitation (4 mL of 7.5% NaCl per kilogram) on cardiac function have been evaluated in septic rats. HS was administered 1 h after LPS (10 mg/kg, i.v.) challenge. The mean arterial blood pressure significantly decreased 4 h after LPS challenge, and septic shock was observed at the end of experiment (6 h). Posttreatment with HS prevented hypotension caused by LPS and significantly improved cardiac function, evidenced by increases in left ventricular developed pressure, mean and . The amplitude of electrical-stimulated intracellular Ca2+ transient in isolated single cardiomyocytes was significantly reduced after 6 h LPS insult, which was recovered by HS. In addition, LPS resulted in significant increases in neutrophil myeloperoxidase activity, macrophage migration inhibitory factor (MIF), and NF- B phospho-p65 protein levels in myocardium at 6 h, which were significantly attenuated by HS. In conclusion, HS improved myocardial contractility and prevented circulatory failure induced by endotoxemia, which may attribute to improvement of intracellular calcium handling process and inhibitory effects on neutrophil infiltration and MIF production in hearts.