Chronic high-
altitude hypoxia (HAH) results in compensatory pathological adaptations, especially in the cardiorespiratory system. The
oxygen enrichment technology can provide long-lasting
oxygen supply and minimize
oxygen toxicity, which has proven to be effective to increase oxygen saturation, decrease heart rate, and improve human exercise performance after ascending to high altitudes. Nevertheless, it remains unknown whether
oxygen enrichment can resist chronic HAH-induced cardiorespiratory alterations. Thirty-six male rats were equally assigned to the normal control (NC), HAH, and HAH with
oxygen enrichment (HAHO) groups. The HAH and HAHO rats were housed in a hypobaric
hypoxia chamber equivalent to 5,000 m for 4 weeks. The HAHO rats were exposed to
oxygen-enriched air for 8 h/day. We found that
oxygen enrichment mitigated the augmented skin blood flow and improved the locomotor activity of HAH-exposed rats.
Oxygen enrichment inhibited HAH-induced increase in the production of red blood cells (RBCs). The hemodynamic results showed that
oxygen enrichment decreased right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) in HAH-exposed rats. HAH-associated
right ventricular hypertrophy and cardiomyocyte enlargement were ameliorated by
oxygen enrichment.
Oxygen enrichment inhibited HAH-induced excessive expression of
cytokines associated with
cardiac hypertrophy and myocardial
fibrosis [
angiotensin-converting enzyme (ACE)/
angiotensin-converting enzyme 2 (ACE2),
angiotensin II (Ang II),
collagen type I alpha 1 (Col1α1),
collagen type III alpha 1 (Col3α1), and
hydroxyproline] in the right ventricle (RV).
Oxygen enrichment inhibited medial thickening,
stenosis and
fibrosis of pulmonary arterioles, and
cytokine expression related with
fibrosis (Col1α1, Col3α1, and
hydroxyproline) and pulmonary vasoconstriction [
endothelin-1(ET-1)] in HAH-exposed rats. This study represents the first effort testing the efficacy of the
oxygen enrichment technique on cardiopulmonary structure and function in chronic HAH animals, and we found
oxygen enrichment has the capability of ameliorating chronic HAH-induced cardiopulmonary alterations.