Chronic intermittent hypobaric hypoxia prevents cardiac dysfunction through enhancing antioxidation in fructose-fed rats

Author:

Zhou Jing-Jing1,Wei Yan1,Zhang Li2,Zhang Jiao1,Guo Lan-Ying3,Gao Chao4,Li De-Pei5,Zhang Yi1

Affiliation:

1. Department of Physiology, Hebei Medical University, Hebei Key Laboratory of Medical Biotechnology, Hebei 050017, People’s Republic of China.

2. Third Affiliated Hospital, Hebei Medical University, Hebei 050017, People’s Republic of China.

3. Dental Hospital, Hebei Medical University, Hebei 050017, People’s Republic of China.

4. Department of Radiation Oncology, the Fourth Hospital of Hebei Medical University, Shijiazhang 050017, People’s Republic of China.

5. Department of Critical Care, The University of Texas, M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.

Abstract

High-fructose intake induces metabolic syndrome and cardiac dysfunction. Chronic intermittent hypobaric hypoxia (CIHH) preserves cardiac function during ischemia. We hypothesized that CIHH restores the impaired cardiac function in fructose-fed rats. Sprague–Dawley rats were randomly subject to treatment with fructose (10% fructose in drinking water for 6 weeks), CIHH (simulated 5000 m altitude, 6 h/day for 6 weeks in a hypobaric chamber), and CIHH plus fructose groups. In addition to an increase in blood pressure, fructose feeding caused elevated serum levels of glucose, fasting insulin and insulin C peptide, triglyceride, cholesterol, and mass ratio of heart to body. CIHH treatment decreased the arterial blood pressure, serum levels of biochemical markers, and cardiac hypertrophy in fructose-fed rats. Furthermore, CIHH treatment improved the recovery of left ventricular function after ischemia–reperfusion procedure (30 min global no-flow ischemia followed by 60 min of reperfusion) in rats with or without fructose feeding. In addition, CIHH treatment caused a significant increase in superoxide dismutase (SOD) activity and decrease in malondialdehyde level in cardiac myocardium experiencing ischemia–reperfusion in control and fructose-fed rats. Collectively, these data suggest that CIHH improve impaired cardiac function in fructose-fed rats through enhancing antioxidation in the myocardium.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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