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Mouse Pneumonectomy Model of Compensatory Lung Growth
Published on: December 17, 2014
[Molecular and cellular mechanisms of compensation for respiratory failure in nonspecific lung diseases]
Abstract:
Some molecular and cellular mechanisms of compensation for respiratory failure (RF) were examined in 90 patients with nonspecific pulmonary diseases. In acute RF, the content of 2,3-DPH in red blood cells was increased. As RF progressed, the compensatory-adaptation reaction became less marked. In chronic RF, the 2,3-DPH content in red blood cells did not differ from the control values. The disease was characterized by cholesterol a and sphingomyelin accumulation, a reduction in red blood cell ATPase activity, and an increase in microviscosity of red blood cell membranes. Decelerated utilization of ATPases in red blood cells is of a role in the genesis of a rise of the 2,3-DPH content in acute RF.
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