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Cardiovascular (CV) adaptation to chronic mild carbon monoxide (CO) hypoxia in mice
Author(s) -
O’Neill J. Timothy,
Trentini John,
Li Andrew,
Halim Nadir,
Ren Ming,
Xing Guoqiang,
Thaker Jay,
Verma Ajay
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1287-a
Subject(s) - carboxyhemoglobin , hemoglobin , hypoxia (environmental) , medicine , oxygenation , pco2 , anesthesia , cardiology , carbon monoxide , endocrinology , oxygen , chemistry , biochemistry , organic chemistry , catalysis
Chronic mild hypoxia is encountered in many clinical settings including lung disease, anemia, and vascular disorders. Little is known about the adaptive CV responses to this stress. We have utilized a model of chronic CO hypoxia in mice to examine adaptive changes. Mice (5/group) were placed in exposure chambers with air flow containing 0, 100 or 500 ppm CO for 30 days. Twice per week the animals were transferred to another chamber for non‐invasive blood pressure measurements. Gas in the measurement chamber was the same [CO] as the housing chambers. Mean arterial pressure (MAP) was similar among groups on day 0 (121±4.8 mmHg) MAP remained stable in the 0 and 100 ppm groups but dropped by day 2 in the 500 ppm group and remained below control for at least 21 days. There were no sustained changes in heart rate in any group. At day 30 carboxyhemoglobin (HbCO) and total hemoglobin (THb), measured by tail nick immediately upon removal from the chambers, were significantly elevatedThe HIF‐1α regulated protein VEGF in brain was also found to increase with 500 ppm CO exposure. Our data suggest that mice adapt to chronic hypoxia by increasing hemoglobin and microvascular proliferation rather than cardiac output to maintain tissue oxygenation. Supported by Flight Attendants Medical Research Institute