In:
Experimental Physiology, Wiley, Vol. 92, No. 2 ( 2007-03), p. 409-416
Abstract:
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% O 2 , 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‐α(TNFα), 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 TNFα 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.
Type of Medium:
Online Resource
ISSN:
0958-0670
,
1469-445X
DOI:
10.1113/eph.2007.92.issue-2
DOI:
10.1113/expphysiol.2006.036590
Language:
English
Publisher:
Wiley
Publication Date:
2007
detail.hit.zdb_id:
1493802-9
