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This Article Full Text Full Text (PDF) All Versions of this Article: 92/2/409    most recent expphysiol.2006.036590v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, L.-M. Articles by Lee, S.-D. Search for Related Content PubMed PubMed Citation Articles by Chen, L.-M. Articles by Lee, S.-D.

¹ Center of General Education, Central Taiwan University of Science & Technology, Taichung, Taiwan ² Departments of Internal Medicine⁹ Division of Cardiology, Armed Forces Taichung General Hospital, Taichung, Taiwan ³ Department of Biological Science and Technology, China Medical University, Taichung, Taiwan Schools of ⁴ Dentistry⁸ Psychology, Chung-Shan Medical University, Taichung, Taiwan ⁵ Department of Physiology, National Yang-Ming University, Taipei, Taiwan ⁶ Department of Pathology, Changhua Christian Hospital, Changua, Taiwan ⁷ Department of Pediatrics, Medical Research and Medical Genetics, China Medical University Hospital, Taichung, Taiwan ¹⁰ Graduate Institute of Chinese Medical Science¹¹ Institute of Medical Science¹² Department of Physical Therapy, China Medical University, Taichung, Taiwan

It is unclear whether cardiac hypertrophy and hypertrophy-related pathways will be induced by long-term intermittent hypoxia. Thirty-six Sprague–Dawley rats were randomly assigned into three groups: normoxia, and long-term intermittent hypoxia (12% O₂, 8 h per day) for 4 weeks (4WLTIH) or for 8 weeks (8WLTIH). Myocardial morphology, trophic factors and signalling pathways in the three groups were determined by heart weight index, histological analysis, Western blotting and reverse transcriptase-polymerase chain reaction from the excised left ventricle. The ratio of whole heart weight to body weight, the ratio of left ventricular weight to body weight, the gross vertical cross-section of the heart and myocardial morphological changes were increased in the 4WLTIH group and were further augmented in the 8WLTIH group. In the 4WLTIH group, tumour necrosis factor-(TNF), insulin-like growth factor (IGF)-II, phosphorylated p38 mitogen-activated protein kinase (P38), signal transducers and activators of transcription (STAT)-1 and STAT-3 were significantly increased in the cardiac tissues. However, in the 8WLTIH group, in addition to the above factors, interleukin-6, mitogen-activated protein kinase (MEK)5 and extracellular signal-regulated kinase (ERK)5 were significantly increased compared with the normoxia group. We conclude that cardiac hypertrophy associated with TNF and IGF-II was induced by intermittent hypoxia. The longer duration of intermittent hypoxia further activated the eccentric hypertrophy-related pathway, as well as the interleukin 6-related MEK5–ERK5 and STAT-3 pathways, which could result in the development of cardiac dilatation and pathology.

(Received 11 November 2006; accepted after revision 20 December 2006; first published online 21 December 2006)
Corresponding author Shin-Da Lee: Department of Physical Therapy, China Medical University, 91 Hsueh-Shih Road, Taichung 40202, Taiwan. Email: shinda{at}mail.cmu.edu.tw

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