Intermittent high altitude hypoxia - induced structural changes in the pulmonary myocardium in young mice.
Seven-day-old mice, strain H, were exposed to intermittent high altitude hypoxia (IHA) in a barochamber (7,000 m, 4 h/day, 5 days a week); a total number of exposures was 10. It has been shown that the layer of cardiac musculature in the adventitia of the pulmonary veins, the so-called pulmonary myocardium, reacts to IHA hypoxia by enlargement even sooner than the right ventricular myocardium. The average thickness of the layer of pulmonary myocardium was significantly greater in animals exposed to IHA hypoxia as compared with the controls. Furthermore, IHA hypoxia induces the extension of the pulmonary myocardium to the periphery of the pulmonary venous bed. Ultrastructural investigation of the pulmonary myocardium in hypoxic animals revealed the presence of unoriented myofilaments in the peripheral myofibril-free sarcoplasma, increase in the number of ribosomes and appearance of profiles of granular endoplasmic reticulum. Our data provide quantitative support for the hypothesis that it is not only the contraction of pulmonary arteries, but also venoconstriction which contribute to the hypoxic pressure response in mice.
D000531:Altitude; D000818:Animals; D006332:Cardiomegaly / Q000473:pathology; D003599:Cytoskeleton / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006984:Hypertrophy; D000860:Hypoxia / Q000473:pathology*; D008297:Male; D051379:Mice; D008854:Microscopy, Electron; D009206:Myocardium / Q000648:ultrastructure*; D011667:Pulmonary Veins / Q000648:ultrastructure*; D012270:Ribosomes / Q000648:ultrastructure; D013997:Time Factors