The mechanism of pulmonary hypertension in rats with high-altitude hypoxia

Abstract

Morphofunctional examinations of the lungs of rats exposed to high-altitude conditions for 3 to 300 days revealed that systolic pulmonary hypertension observed during the entire period of study is caused by a total increase of the elastic resistance of pulmonary arteries. Adequate bloodflow in such a case is provided by intensive work of the right-ventricular myocardium against this resistance.High-altitude hypoxia is regularly associated with rise of pressure in the pulmonary artery [4]. Usually hypertension in the pulmonary circulation is diagnosed from a rise of the mean pressure, and the actual process of pressure change is modeled on the basis of Poiseuille's model of the circulation, according to which a pressure rise in this vascular bed with the bloodflow decreased or intact means an increase of the pulmonary peripheral resistance (PPR). However, structural changes in the pulmonary network of vessels are diverse and cannot be interpreted unequivocally solely as an increase of PPR.Therefore, the purpose of our study was to analyze the pulmonary hemodynamics under high-altitude conditions on the basis of natural pressure values in the pulmonary artery together with other hemodynamic Institute of Physiology, Siberian Division of the Russian Academy of Medical Sciences; Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk (Presented by V. A. Trufakin, Member of the Russian Academy of Medical Sciences) parameters and data on the structural changes developing in the lungs during the exposure of animals to a mountain environment. MATERIALS AND METHODSExperiments were carried out in summer with male Wistar rats brought to an altitude of 3200 m above sea level beforehand and kept at room temperature on the standard diet. Animals kept under the same conditions on the plain were controls.The pressure was measured and pulmonary bloodflow, blood filling, and air content in the lungs per unit volume of the organ were assessed by catheterization of a lung artery through the jugular vein and transbronchial electroplethysmography. The parameters were recorded using a Siemens-Elema Mingograf-34 ink-jet recorder. The methods of investigation were described in detail previously [3]. The animals were exposed to the mountain altitude for 3, 10, 20, 30, 60, 150, and 300 days. After the experiments the lungs